Diagnostic Ultrasound, 2-Volume Set [5th edition] 9780323401715, 2017019887, 0323401716, 9780323529631, 0323529631

Table of contents :
I. Physics. Physics of ultrasound --
Biologic effects and safety --
Contrast agents for ultrasound imaging and Doppler --
II. Abdominal, pelvic, and thoracic sonography. The liver --
The spleen --
The biliary tree and gallbladder --
The pancreas --
The gastrointestinal tract --
The kidney and urinary tract --
The prostrate --
The adrenal glands --
The retroperitoneum --
Dynamic ultrasound of hernias of the groin and anterior abdominal wall --
The peritoneum --
The uterus --
The adnexa --
Ultrasound-guided biopsy of chest abdomen and pelvis --
Organ transplantation --
III. Small parts, carotid artery, and peripheral vessel sonography. The thyroid gland --
The parathyroid glands --
The breast --
The scrotum --
Overview of musculoskeletal ultrasound techniques and applications --
The shoulder --
Musculoskeletal interventions --
The extracranial cerebral vessels --
The peripheral vessels --
IV. Obstetric and fetal sonography. Overview of obstetric imaging --
Bioeffects and safety of ultrasound in obstetrics --
The first trimester --
Chromosomal abnormalities --
Multifetal pregnancy --
The fetal face and neck --
The fetal brain --
The fetal spine --
The fetal chest --
The fetal heart --
The fetal abdominal wall and gastrointestinal tract --
The fetal urogenital tract --
The fetal musculoskeletal system --
Fetal hydrops --
Fetal measurements: normal and abnormal fetal growth and assessment of fetal well-being --
Sonographic evaluation of the placenta --
Cervical ultrasound and preterm birth --
V. Pediatric sonography. Neonatal and infant brain imaging --
Doppler sonography of the neonatal and infant brain --
Doppler sonography of the brain in children --
The pediatric head and neck --
The pediatric spinal canal --
The pediatric chest --
The pediatric liver and spleen --
The pediatric kidney and adrenal glands --
The pediatric gastrointestinal tract --
Pediatric pelvic sonography --
The pediatric hip and musculoskeletal ultrasound --
Pediatric interventional sonography.

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DIAGNOSTIC ULTRASOUND

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DIAGNOSTIC ULTRASOUND 5TH EDITION CAROL M. RUMACK, MD, FACR Vice Chair of Education and Professional Development Professor of Radiology and Pediatrics Associate Dean for GME University of Colorado School of Medicine Denver, Colorado

DEBORAH LEVINE, MD, FACR Co-Chief of Ultrasound Director of OB/Gyn Ultrasound Vice Chair of Academic Afairs Department of Radiology Beth Israel Deaconess Medical Center Professor of Radiology Harvard Medical School Boston, Massachusetts

1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103-2899

DIAGNOSTIC ULTRASOUND, FIFTH EDITION

ISBN: 978-0-323-40171-5

Copyright © 2018 by Elsevier, Inc. All rights reserved. Chapter 32: Mary C. Frates retains copyright for the original igures appearing in the chapter. Chapter 42: Carol B. Benson and Peter M. Doubilet retain copyright for their original igures appearing in the chapter. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. his book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).

Notices Knowledge and best practice in this ield are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identiied, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. Previous editions copyrighted 2011, 2005, 1998, and 1993. Library of Congress Cataloging-in-Publication Data Names: Rumack, Carol M., editor. | Levine, Deborah, 1962- editor. Title: Diagnostic ultrasound / [edited by] Carol M. Rumack, Deborah Levine. Other titles: Diagnostic ultrasound (Rumack) Description: 5th edition. | Philadelphia, PA : Elsevier, [2018] | Includes bibliographical references and index. Identiiers: LCCN 2017019887 | ISBN 9780323401715 (hardcover : alk. paper) Subjects: | MESH: Ultrasonography Classiication: LCC RC78.7.U4 | NLM WN 208 | DDC 616.07/543–dc23 LC record available at https://lccn.loc.gov/2017019887 Executive Content Strategist: Robin Carter Senior Content Development: Manager: Taylor Ball Publishing Services Manager: Catherine Jackson Senior Project Manager: Daniel Fitzgerald Design Manager: Amy Buxton Illustrations Manager: Nichole Beard Printed in China. Last digit is the print number: 9

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ABOUT THE EDITORS

Carol M. Rumack, MD, FACR, is Professor of Radiology and Pediatrics at the University of Colorado School of Medicine in Denver, Colorado. Her clinical practice is based at the University of Colorado Hospital. Her primary research has been in neonatal sonography of high-risk infants, particularly the brain, on which she has published and lectured widely. She is a Fellow, previous Chair of the Ultrasound Commission, past president of the American College of Radiology, and American Association for Women Radiologists, and a Fellow of both the American Institute of Ultrasound in Medicine and the Society of Radiologists in Ultrasound. She and her husband, Barry, have two children, Becky and Marc, and ive grandchildren.

Deborah Levine, MD, FACR, is Professor of Radiology at Beth Israel Deaconess Medical Center, Boston, and Harvard Medical School. At Beth Israel Deaconess Medical Center she is Vice Chair of Academic Afairs of the Department of Radiology, Co-Chief of Ultrasound, and Director of Ob/Gyn Ultrasound. Her main areas of clinical and research interest are obstetric and gynecologic imaging. She is a Fellow and past Vice President of the American College of Radiology and a Fellow (and 2016-2017 President) of the Society of Radiologists in Ultrasound. She and her husband, Alex, have two children, Becky and Julie.

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Contributors

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CONTRIBUTORS Jacques S. Abramowicz, MD, FACOG, FAIUM Professor and Director Ultrasound Services Department of Obstetrics and Gynecology University of Chicago Chicago, Illinois United States

Diane S. Babcock, MD Professor Emerita of Radiology and Pediatrics University of Cincinnati College of Medicine Cincinnati Children’s Hospital Medical Center Cincinnati, Ohio United States

Ronald S. Adler, MD, PhD Professor of Radiology New York University School of Medicine Department of Radiology NYU Langone Medical Center New York, New York United States

Beryl Benacerraf, MD Clinical Professor of Obstetrics and Gynecology and Radiology Brigham and Women’s Hospital Clinical Professor of Obstetrics and Gynecology Massachusetts General Hospital Harvard Medical School Boston, Massachusetts United States

Allison Aguado, MD Assistant Professor Department of Radiology Cincinnati Children’s Hospital Medical Center Cincinnati, Ohio United States Rochelle Filker Andreotti, MD Professor of Clinical Radiology Associate Professor of Clinical Obstetrics and Gynecology Department of Radiology and Radiological Sciences Vanderbilt University Nashville, Tennessee United States Elizabeth Asch, MD Instructor in Radiology Harvard Medical School Brigham and Women’s Hospital Boston, Massachusetts United States homas D. Atwell, MD Professor of Radiology Department of Radiology Mayo Clinic Rochester, Minnesota United States Amanda K. Auckland, BS, RT(R), RDMS, RVT, RDCS Diagnostic Medical Sonographer Division of Ultrasound/Prenatal Diagnosis and Genetics University of Colorado Hospital Aurora, Colorado United States

Carol B. Benson, MD Professor of Radiology Harvard Medical School Director of Ultrasound and Co-Director of High Risk Obstetrical Ultrasound Department of Radiology Brigham and Women’s Hospital Boston, Massachusetts United States Raymond E. Bertino, MD, FACR, FSRU Medical Director of Vascular and General Ultrasound OSF Saint Francis Medical Center Clinical Professor of Radiology and Surgery University of Illinois College of Medicine Peoria, Illinois United States Edward I. Bluth, MD, FACR, FSRU Chairman Emeritus Ochsner Clinic Foundation Professor Ochsner Clinical School University of Queensland, School of Medicine New Orleans, Louisiana United States Bryann Bromley, MD Professor of Obstetrics, Gynecology and Reproductive Biology, part time Harvard Medical School Department of Obstetrics and Gynecology Massachusetts General Hospital Brigham and Women’s Hospital Boston, Massachusetts United States

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Contributors

Olga R. Brook, MD Assistant Professor Harvard Medical School Associate Director of CT Department of Radiology Beth Israel Deaconess Medical Center Boston, Massachusetts United States Douglas Brown, MD Professor of Radiology Department of Radiology Mayo Clinic College of Medicine and Science Rochester, Minnesota United States Dorothy Bulas, MD Professor of Pediatrics and Radiology George Washington University Medical Center Pediatric Radiologist Children’s National Health Systems Washington DC United States Peter N. Burns, PhD Professor and Chairman Department of Medical Biophysics University of Toronto Senior Scientist, Imaging Research Sunnybrook Research Institute Toronto, Ontario Canada Vito Cantisani, MD, PhD Department of Radiologic, Oncologic and Pathologic Sciences Policlinic Umberto I Sapienza University Rome Italy Ilse Castro-Aragon, MD Assistant Professor of Radiology Boston University School of Medicine Section Head, Pediatric Radiology Boston Medical Center Boston, Massachusetts United States J. William Charboneau, MD Emeritus Professor of Radiology Department of Radiology Mayo Clinic Rochester, Minnesota United States

Humaira Chaudhry, MD Section Chief, Abdominal Imaging Assistant Professor Department of Radiology Rutgers-New Jersey Medical School Newark, NJ United States Tanya Punita Chawla, MBBS, FRCR, MRCP, FRCPC Assistant Professor and Staf Radiologist Joint Department of Medical Imaging University of Toronto Toronto, Ontario Canada Christina Marie Chingkoe, MD Department of Radiology Beth Israel Deaconess Medical Center Boston, Massachusetts United States David Chitayat, MD Professor Department of Pediatrics, Obstetrics and Gynecology, Molecular Genetics and Laboratory Medicine and Pathobiology Medical Director he MSc program in Genetic Counselling, Department of Molecular Genetics University of Toronto Head he Prenatal Diagnosis and Medical Genetics Program Mount Sinai Hospital Staf Pediatrics, Division of Clinical and Metabolic Genetics Hospital for Sickkids Toronto, Ontario Canada Peter L. Cooperberg, OBC, MDCM, FRCP(C), FACR Professor Emeritus Department of Radiology University of British Columbia Vancouver, British Columbia Canada Lori A. Deitte, MD, FACR Vice Chair of Education and Professor Department of Radiology and Radiological Sciences Vanderbilt University Nashville, Tennessee United States

Contributors Peter M. Doubilet, MD, PhD Professor of Radiology Harvard Medical School Senior Vice Chair Department of Radiology Brigham and Women’s Hospital Boston, Massachusetts United States Julia A. Drose, RDMS, RDCS, RVT Associate Professor Department of Radiology University of Colorado Hospital Aurora, Colorado United States Alexia Eglof, MD Diagnostic Imaging and Radiology Children’s National Health Systems Washington DC United States Judy A. Estrof, MD Instructor Boston University School of Medicine Department of Radiology Boston Children’s Hospital Boston, Massachusetts United States Katherine W. Fong, MBBS, FRCPC Associate Professor Medical Imaging and Obstetrics and Gynecology University of Toronto Co-director, Centre of Excellence in Obstetric Ultrasound Mount Sinai Hospital Toronto, Ontario Canada J. Brian Fowlkes, PhD Professor Department of Radiology University of Michigan Ann Arbor, Michigan United States Mary C. Frates, MD Associate Professor of Radiology Department of Radiology Harvard Medical School Brigham and Women’s Hospital Boston, Massachusetts United States

Hournaz Ghandehari, MD, FRCPC Department of Medical Imaging Abdominal Division University of Toronto Sunnybrook Health Sciences Centre Toronto, Ontario Canada Phyllis Glanc, MDCM Associate Professor University of Toronto Department Medical Imaging, Obstetric & Gynecology Sunnybrook Health Sciences Centre Toronto, Ontario Canada S. Bruce Greenberg, MD Professor of Radiology and Pediatrics Department of Radiology University of Arkansas for Medical Sciences Little Rock, Arkansas United States Leslie E. Grissom, MD Clinical Professor of Radiology and Pediatrics Department of Radiology Sidney Kimmel Medical College at homas Jeferson University Philadelphia, Pennsylvania Attending Radiologist Department of Medical Imaging Nemours Alfred I. duPont Hospital for Children Wilmington, Delaware United States Anthony E. Hanbidge, MB, BCh, FRCPC Associate Professor Department of Medical Imaging University of Toronto Site Director, Abdominal Imaging Toronto Western Hospital Joint Department of Medical Imaging University Health Network, Mount Sinai Hospital and Women’s College Hospital Toronto, Ontario Canada H. heodore Harcke, MD, FACR, FAIUM Sidney Kimmel Medical College at homas Jeferson University Chairman, Emeritus Department of Medical Imaging Nemours/A I duPont Hospital for Children Wilmington, Delaware United States

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Christy K. Holland, PhD Scientiic Director of the Heart, Lung, and Vascular Institute Professor Department of Internal Medicine Division of Cardiovascular Health and Disease University of Cincinnati Cincinnati, Ohio United States hierry A.G.M. Huisman, MD Professor of Radiology, Pediatrics, Neurology, and Neurosurgery Director Pediatric Radiology and Pediatric Neuroradiology Russell H. Morgan Department of Radiology and Radiological Science he Johns Hopkins University School of Medicine Baltimore, Maryland United States Bonnie J. Huppert, MD Assistant Professor of Radiology Consultant in Radiology Department of Radiology Mayo Clinic Rochester, Minnesota United States

Anne Kennedy, MB, BCh Vice Chair Clinical Operations Department of Radiology University of Utah Salt Lake City, Utah United States Julia Eva Kfouri, BSc, MD, FRCSC-MFM Clinical Associate Division of Maternal Fetal Medicine Department of Obstetrics and Gynecology Mount Sinai Hospital Toronto, Ontario Canada Korosh Khalili, MD, FRCPC Associate Professor Department of Medical Imaging University of Toronto University Health Network Princess Margaret Hospital Toronto, Ontario Canada

Alexander Jesurum, PhD Weston, Massachusetts United States

Beth M. Kline-Fath, MD Professor of Radiology Department of Radiology Cincinnati Children’s Hospital Medical Center Cincinnati, Ohio United States

Susan D. John, MD Professor and Chair Department of Diagnostic and Interventional Imaging University of Texas Medical School Houston Houston, Texas United States

Elizabeth Lazarus, MD Associate Professor Department of Diagnostic Imaging Warren Alpert Medical School of Brown University Providence, Rhode Island United States

Neil Johnson, MBBS, FRANZCR, MMed Professor Department of Radiology and Pediatrics Cincinnati Children’s Hospital Medical Center Cincinnati, Ohio United States

Deborah Levine, MD, FACR Co-Chief of Ultrasound Director of OB/Gyn Ultrasound Vice Chair of Academic Afairs Department of Radiology Beth Israel Deaconess Medical Center Professor of Radiology Harvard Medical School Boston, Massachusetts United States

Stephen I. Johnson, MD Staf Radiologist Department of Radiology Ochsner Clinic Foundation New Orleans, Louisiana United States

Mark E. Lockhart, MD, MPH Professor of Radiology and Chief, Body Imaging Department of Radiology University of Alabama at Birmingham Birmingham, Alabama United States

Contributors Ana P. Lourenco, MD Associate Professor of Diagnostic Imaging Diagnostic Imaging Alpert Medical School of Brown University Providence, Rhode Island United States Martha Mappus Munden, MD Associate Professor of Radiology Department of Pediatric Radiology Texas Children’s Hospital Houston, Texas United States John R. Mathieson, MD Clinical Associate Professor University of British Columbia Vancouver, British Columbia Medical Director and Department Head Vancouver Island Health Authority Victoria, British Columbia Canada Giovanni Mauri, MD Division of Interventional Radiology European Institute of Oncology Milan Italy Colm McMahon, MB, BAO, BCh, MRCPI, FFR(RCSI) Assistant Professor Department of Radiology Harvard Medical School Beth Israel Deaconess Medical Center Brookline, Massachusetts United States Rashmi J. Mehta, MD, MBA Clinical Radiology Fellow Department of Radiology Beth Israel Deaconess Medical Center Boston, Massachusetts United States Nir Melamed, MD, MSc Associate Professor Department of Obstetrics and Gynecology University of Toronto Sunnybrook Health Sciences Center Toronto, Ontario Canada Christopher R.B. Merritt, MD New Orleans, Louisiana United States

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Derek Muradali, MD, FRCPC Associate Professor and Staf Radiologist Department of Medical Imaging St Michaels Hospital University of Toronto Toronto, Ontario Canada Elton Mustafaraj, DO Resident, Department of Radiology University of Illinois College of Medicine Peoria, Illinois United States Lisa Napolitano, RDMS Department of Radiology Beth Israel Deaconess Medical Center Boston, Massachusetts United States Sara M. O’Hara, MD Professor of Radiology & Pediatrics Department of Radiology Cincinnati Children’s Hospital Cincinnati, Ohio United States Harriet J. Paltiel, MDCM Associate Professor of Radiology Harvard Medical School Department of Radiology Boston Children’s Hospital Boston, Massachusetts United States Jordana Phillips, MD Department of Radiology Beth Israel Deaconess Medical Center Boston, Massachusetts United States Andrea Poretti, MD Assistant Professor of Radiology Section of Pediatric Neuroradiology Division of Pediatric Radiology Russell H. Morgan Department of Radiology and Radiological Science he Johns Hopkins University School of Medicine Baltimore, Maryland United States heodora A. Potretzke, MD Assistant Professor Department of Radiology Mayo Clinic Rochester, Minnesota United States

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Contributors

Rupa Radhakrishnan, MBBS Assistant Professor Department of Radiology Cincinnati Children’s Hospital Medical Center Cincinnati, Ohio United States Carl Reading, MD Professor of Radiology Department of Radiology Mayo Clinic Rochester, Minnesota United States Michelle L. Robbin, MD, MS Professor of Radiology and Biomedical Engineering Department of Radiology University of Alabama at Birmingham Birmingham, Alabama United States Henrietta Kotlus Rosenberg, MD Radiologist-in-Chief Kravis Children’s Hospital at Mount Sinai Director of Pediatric Radiology Department of Radiology Mount Sinai Hospital Professor of Radiology and Pediatrics Icahn School of Medicine at Mount Sinai New York, New York United States Carol M. Rumack, MD, FACR Vice Chair of Education and Professional Development Professor of Radiology and Pediatrics Associate Dean for GME University of Colorado School of Medicine Denver, Colorado United States Eric Sauerbrei, BSc, MSc, MD, FRCPC Professor of Radiology Diagnostic Imaging Queens University Kingston, Ontario Canada Chetan Chandulal Shah, MD, MBA Faculty, Department of Radiology Mayo Clinic Pediatric Radiologist Department of Pediatric Radiology Nemours Wolfson Children’s Hospital Jacksonville, Florida United States

homas D. Shipp, MD Associate Professor of Obstetrics, Gynecology & Reproductive Biology Harvard Medical School Department of Obstetrics & Gynecology Brigham & Women’s Hospital Boston, Massachusetts United States William L. Simpson, Jr., MD Associate Professor Department of Radiology Icahn School of Medicine at Mount Sinai New York, New York United States Luigi Solbiati, MD Professor of Radiology Department of Radiology Humanitas University and Research Hospital Rozzano (Milan) Italy Daniel Sommers, MD Associate Professor Department of Radiology University of Utah Salt Lake City, Utah United States Elizabeth R. Stamm, MD Associate Professor Department of Radiology University of Colorado Hospital Aurora, Colorado United States A. homas Stavros, MD, FACR Medical Director Ultrasound Invision Sally Jobe Breast Center Englewood, Colorado United States Maryellen R.M. Sun, MD Department of Radiology Lowell General Hospital Lowell, Massachusetts United States

Contributors Wendy hurston, MD Assistant Professor Department of Medical Imaging University of Toronto Chief, Diagnostic Imaging Department of Diagnostic Imaging St. Joseph’s Health Centre Courtesy Staf Department of Medical Imaging University Health Network Toronto, Ontario Canada Ants Toi, MD, FRCPC, FAIUM Professor of Radiology and of Obstetrics and Gynecology University of Toronto Radiologist Medical Imaging Mt. Sinai Hospital Toronto, Ontario Canada Laurie Troxclair, BS, RDMS, RVT Ochsner Clinic Foundation New Orleans, Louisiana United States Mitchell Tublin, MD Professor and Vice Chair Department of Radiology University of Pittsburgh School of Medicine Pittsburgh, Pennsylvania United States Heidi R. Umphrey, MD, MS Associate Professor of Radiology Department of Radiology University of Alabama at Birmingham Birmingham, Alabama United States Sheila Unger, MD University of Lausanne Lausanne Switzerland Patrick M. Vos, MD Clinical Assistant Professor Department of Radiology University of British Columbia Vancouver, British Columbia Canada

herese M. Weber, MD, MS Professor of Radiology Department of Radiology University of Alabama at Birmingham Birmingham, Alabama United States Kirsten L. Weind Matthews, PhD, MBBS, FRCPC Lecturer, Medical Imaging University of Toronto Department of Medical Imaging Mount Sinai Hospital Toronto, Ontario Canada Stephanie R. Wilson, MD Clinical Professor Department of Radiology Department of Medicine, Division of Gastroenterology University of Calgary Calgary, Alberta Canada homas Winter, MD Professor and Chief of Abdominal Imaging Department of Radiology University of Utah Salt Lake City, Utah United States Cynthia E. Withers, MD Radiologist (retired) Sansum Clinic and Santa Barbara Cottage Hospital Santa Barbara, California United States Corrie Yablon, MD Assistant Professor Department of Radiology University of Michigan Ann Arbor, Michigan United States Hojun Yu, MD Radiologist Department of Diagnostic Imaging Queen Elizabeth II Hospital Grande Prairie, Alberta Canada

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In memory of my parents, Drs. Ruth and Raymond Masters, who encouraged me to enjoy the intellectual challenge of medicine and the love of making a diference in patients’ lives. Carol M. Rumack To Alex, Becky, and Julie—your love and support made this work possible. Debbie Levine

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Preface

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PREFACE he ith edition of Diagnostic Ultrasound is a major revision. Previous editions have been very well accepted as reference textbooks and have been the most commonly used reference in ultrasound education and practices worldwide. he text and references have all been updated and are now all available online. We are pleased to provide over 2500 new/revised images (with over 5800 images total) and over 380 new videos (with 480 total videos). he display of real-time ultrasound has helped to capture those abnormalities that require a sweep through the pathology to truly appreciate the lesion as well. Daily we ind that cine or video clips show important areas between still images that help to make certain a diagnosis or relationships between lesions. Now we rarely need to go back to reevaluate a lesion with another scan, making patient imaging more eicient. Another new ofering in this textbook is a completely online “virtual” chapter on artifacts. PowerPoint videos explain many of the artifacts that are linked to images and videos in the text. he ith edition was a major change for our editorial team, as we said a fond farewell to Stephanie Wilson and Bill Charboneau. heir expertise is still felt in this edition, as they have contributed chapters on gastrointestinal ultrasound (liver, biliary tree, and gastrointestinal tract, which are all some of Stephanie’s passions) and thyroid and interventional ultrasound (just some of Bill’s areas of expertise). Nearly 100 outstanding new and continuing authors have contributed to this edition, and all are recognized experts in the ield of ultrasound. As in prior editions, we have emphasized the use of collages to show many examples of similar anatomy and pathology. hese images relect the spectrum of sonographic changes that may occur in a given disease, instead of the most common manifestation only. he book’s format has been redesigned with key points in addition to the outline at the beginning of each chapter. here

are again colored boxes to highlight the important or critical features of sonographic diagnoses. Key terms and concepts are emphasized in boldface type. To direct the readers to other research and literature of interest, comprehensive reference lists are provided. Diagnostic Ultrasound is again divided into two volumes. Volume I consists of Parts I to III. Part I contains chapters on physics and biologic efects of ultrasound and includes descriptions of elastography and contrast agents. Part II covers abdominal sonography and includes two completely revised chapters on pelvic sonography, along with chapters on interventional procedures (including those in the thorax) and organ transplantation. Part III presents small parts imaging, including thyroid, breast, scrotum, carotid, a completely revised chapter on imaging of the extracranial vessels, and two completely revised musculoskeletal imaging chapters, as well as an updated chapter on musculoskeletal intervention. Volume II begins with Part IV, with obstetric ultrasound, which has important updates in irst-trimester scanning and screening for aneuploidy including cell-free DNA. Part V comprehensively covers pediatric sonography, including pediatric interventional sonography. Completely revised chapters on the pediatric spinal canal and pediatric kidney are replete with new images and scanning techniques. Diagnostic Ultrasound is for practicing physicians, residents, medical students, sonographers, and others interested in understanding the vast applications of diagnostic sonography in patient care. Our goal is for Diagnostic Ultrasound to continue to be the most comprehensive reference book available in the sonographic literature, with a highly readable style and superb images. Carol M. Rumack, MD, FACR Deborah Levine, MD, FACR

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Acknowledgments

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ACKNOWLEDGMENTS We wish to express our deepest appreciation and sincerest gratitude: To all of our outstanding authors, who have contributed extensive, newly updated, and authoritative text and images and videos. We cannot thank them enough for their eforts on this project. To Alexander Jesurum, PhD, whose outstanding eforts kept the references updated for all of our authors and who helped in author contact and communication. To Lisa Napolitano, RDMS, who spent hours inding and cropping videos to supplement our online edition. To Robin Carter, Executive Content Strategist at Elsevier, who has worked closely with us on this project from the very beginning of the ith edition. To Taylor Ball and Dan Fitzgerald at Elsevier, who kept us on track for the process of updating and copyediting the entire manuscript. It has been an intense year for everyone, and we are very proud of this superb edition of Diagnostic Ultrasound.

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Contents

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CONTENTS VOLUME I

15 The Uterus, 528

PART I Physics

16 The Adnexa, 564

Douglas Brown and Deborah Levine

Rochelle Filker Andreotti and Lori A. Deitte

1 Physics of Ultrasound, 1 Christopher R.B. Merritt

2 Biologic Effects and Safety, 34 J. Brian Fowlkes and Christy K. Holland

3 Contrast Agents for Ultrasound, 53 Peter N. Burns

PART II Abdominal and Pelvic Sonography 4 The Liver, 74 Stephanie R. Wilson and Cynthia E. Withers

5 The Spleen, 139 Patrick M. Vos, John R. Mathieson, and Peter L. Cooperberg

6 The Biliary Tree and Gallbladder, 165 Korosh Khalili and Stephanie R. Wilson

7 The Pancreas, 210 Thomas Winter and Maryellen R.M. Sun

8 The Gastrointestinal Tract, 256 Stephanie R. Wilson

9 The Kidney and Urinary Tract, 310 Mitchell Tublin, Deborah Levine, Wendy Thurston, and Stephanie R. Wilson

10 The Prostate and Transrectal Ultrasound, 381 Ants Toi

11 The Adrenal Glands, 416 Christina Marie Chingkoe, Olga R. Brook, and Deborah Levine

12 The Retroperitoneum, 432 Raymond E. Bertino and Elton Mustafaraj

13 Dynamic Ultrasound of Hernias of the Groin and Anterior Abdominal Wall, 470 Deborah Levine, Lisa Napolitano, and A. Thomas Stavros

17 Ultrasound-Guided Biopsy of Chest, Abdomen, and Pelvis, 597 Theodora A. Potretzke, Thomas D. Atwell, J. William Charboneau, and Carl Reading

18 Organ Transplantation, 623 Derek Muradali and Tanya Punita Chawla

PART III Small Parts, Carotid Artery, and Peripheral Vessel Sonography 19 The Thyroid Gland, 691 Luigi Solbiati, J. William Charboneau, Vito Cantisani, Carl Reading, and Giovanni Mauri

20 The Parathyroid Glands, 732 Bonnie J. Huppert and Carl Reading

21 The Breast, 759 Jordana Phillips, Rashmi J. Mehta, and A. Thomas Stavros

22 The Scrotum, 818 Daniel Sommers and Thomas Winter

23 Overview of Musculoskeletal Ultrasound Techniques and Applications, 856 Colm McMahon and Corrie Yablon

24 The Shoulder, 877 Colm McMahon and Corrie Yablon

25 Musculoskeletal Interventions, 898 Ronald S. Adler

26 The Extracranial Cerebral Vessels, 915 Edward I. Bluth, Stephen I. Johnson, and Laurie Troxclair

27 Peripheral Vessels, 964 Mark E. Lockhart, Heidi R. Umphrey, Therese M. Weber, and Michelle L. Robbin

14 The Peritoneum, 504 Anthony E. Hanbidge, Korosh Khalili, and Stephanie R. Wilson

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Contents

VOLUME II PART IV Obstetric and Fetal Sonography 28 Overview of Obstetric Imaging, 1015 Deborah Levine

29 Bioeffects and Safety of Ultrasound in Obstetrics, 1034 Jacques S. Abramowicz

30 The First Trimester, 1048 Elizabeth Lazarus and Deborah Levine

31 Chromosomal Abnormalities, 1088 Bryann Bromley and Beryl Benacerraf

32 Multifetal Pregnancy, 1115 Mary C. Frates

33 The Fetal Face and Neck, 1133 Ana P. Lourenco and Judy A. Estroff

34 The Fetal Brain, 1166 Ants Toi and Deborah Levine

35 The Fetal Spine, 1216 Elizabeth Asch and Eric Sauerbrei

36 The Fetal Chest, 1243 Dorothy Bulas

37 The Fetal Heart, 1270 Elizabeth R. Stamm and Julia A. Drose

38 The Fetal Gastrointestinal Tract and Abdominal Wall, 1304 Nir Melamed, Anne Kennedy, and Phyllis Glanc

39 The Fetal Urogenital Tract, 1336 Katherine W. Fong, Julia Eva Kfouri, and Kirsten L. Weind Matthews

40 The Fetal Musculoskeletal System, 1376 Phyllis Glanc, David Chitayat, and Sheila Unger

41 Fetal Hydrops, 1412 Deborah Levine

42 Fetal Measurements: Normal and Abnormal Fetal Growth and Assessment of Fetal Well-Being, 1443 Carol B. Benson and Peter M. Doubilet

43 Sonographic Evaluation of the Placenta, 1465 Thomas D. Shipp

44 Cervical Ultrasound and Preterm Birth, 1495 Hournaz Ghandehari and Phyllis Glanc

PART V Pediatric Sonography 45 Neonatal and Infant Brain Imaging, 1511 Carol M. Rumack and Amanda K. Auckland

46 Duplex Sonography of the Neonatal and Infant Brain, 1573 Thierry A.G.M. Huisman and Andrea Poretti

47 Doppler Sonography of the Brain in Children, 1591 Dorothy Bulas and Alexia Egloff

48 The Pediatric Head and Neck, 1628 Rupa Radhakrishnan and Beth M. Kline-Fath

49 The Pediatric Spinal Canal, 1672 Ilse Castro-Aragon, Deborah Levine, and Carol M. Rumack

50 The Pediatric Chest, 1701 Chetan Chandulal Shah and S. Bruce Greenberg

51 The Pediatric Liver and Spleen, 1730 Sara M. O’Hara

52 The Pediatric Urinary Tract and Adrenal Glands, 1775 Harriet J. Paltiel and Diane S. Babcock

53 The Pediatric Gastrointestinal Tract, 1833 Susan D. John and Martha Mappus Munden

54 Pediatric Pelvic Sonography, 1870 William L. Simpson, Jr., Humaira Chaudhry, and Henrietta Kotlus Rosenberg

55 The Pediatric Hip and Other Musculoskeletal Ultrasound Applications, 1920 Leslie E. Grissom and H. Theodore Harcke

56 Pediatric Interventional Sonography, 1942 Neil Johnson and Allison Aguado

Appendix: Ultrasound Artifacts: A Virtual Chapter Korosh Khalili, Hojun Yu, Alexander Jesurum, and Deborah Levine

Index, I-1

Video Contents

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VIDEO CONTENTS 4 The Liver Stephanie R. Wilson and Cynthia E. Withers Video 4.1 Normal liver, sagittal sweep Video 4.2 Normal liver, subcostal sweep Video 4.3 Focal fat in the liver Video 4.4 Geographic fatty iniltration of the liver Video 4.5 CEUS of FNH with classic enhancement features Video 4.6 CEUS of the lash-illing hemangioma shown in Fig. 4.47 Video 4.7 CEUS of focal nodular hyperplasia Video 4.8 CEUS of focal nodular hyperplasia Video 4.9 CEUS of hepatic adenoma in a young woman Video 4.10 CEUS of small hepatocellular carcinoma Video 4.11 CEUS of hepatocellular carcinoma Video 4.12 Classic colorectal metastasis Video 4.13 CEUS of liver metastasis Video 4.14 CEUS of liver metastasis

5 The Spleen Patrick M. Vos, John R. Mathieson, and Peter L. Cooperberg Video 5.1 Normal spleen in sagittal plane Video 5.2 Normal spleen in transverse plane Video 5.3 Contrast study of lymphoma manifesting as a hypoechoic solitary splenic lesion

6 The Biliary Tree and Gallbladder Korosh Khalili and Stephanie R. Wilson Video 6.1 Distal common bile duct and ampulla of Vater Video 6.2 Intrahepatic bile duct stones Video 6.3 Distal common bile duct stone Video 6.4 Choledochoduodenal istula Video 6.5 Primary sclerosing cholangitis Video 6.6 Primary sclerosing cholangitis Video 6.7 Cholangiocarcinoma complicating primary sclerosing cholangitis Video 6.8 Cholangiocarcinoma complicating primary sclerosing cholangitis Video 6.9 Cholelithiasis Video 6.10 Acute cholecystitis Video 6.11 Perforated cholecystitis with liver abscess

7 The Pancreas Thomas Winter and Maryellen R.M. Sun Video 7.1 Normal pancreas Video 7.2 Acute pancreatitis Video 7.3 Acute pancreatitis Video 7.4 Chronic pancreatitis Video 7.5 Chronic pancreatitis Video 7.6 Pancreatic pseudocyst Video 7.7 Pancreatic carcinoma Video 7.8 Pancreatic carcinoma Video 7.9 Intraductal papillary mucinous neoplasm Video 7.10 Mucinous cystic neoplasm

8 The Gastrointestinal Tract Stephanie R. Wilson Video 8.1 An incidentally detected neuroendocrine tumor (carcinoid) of the small bowel Video 8.2 Classic features of Crohn disease on a sweep through the terminal ileum Video 8.3 Loss of stratiication of the bowel wall layers in severe subacute inlammation of the sigmoid colon in a patient with Crohn disease Video 8.4 Stricture in Crohn disease Video 8.5 Color Doppler shows hyperemia in thickened bowel wall in Crohn disease Video 8.6 Contrast-enhanced longitudinal image of Crohn disease Video 8.7 Contrast-enhanced cross-sectional image of Crohn disease Video 8.8 Severe ixation and acute angulation of the ileum with stricture and enteroenteric istula Video 8.9 Incomplete small bowel obstruction in patient with Crohn disease Video 8.10 Dysfunctional and excess peristalsis Video 8.11 Localized perforation with a phlegmonous inlammatory mass Video 8.12 Enteroenteric istula Video 8.13 Normal appendix Video 8.14 Perforated appendix Video 8.15 Acute diverticulitis in second trimester of pregnancy Video 8.16 Paralytic ileus Video 8.17 Incomplete bowel obstruction due to an inlammatory stricture from Crohn disease seen only on endovaginal scan

9 The Kidney and Urinary Tract Mitchell Tublin, Deborah Levine, Wendy Thurston, and Stephanie R. Wilson Video 9.1 Video 9.2 Video 9.3 Video 9.4

Doppler jet Renal cell carcinoma Transitional cell carcinoma of the bladder Bladder diverticula

11 The Adrenal Glands Christina Marie Chingkoe, Olga R. Brook, and Deborah Levine Video 11.1 Video 11.2 Video 11.3 Video 11.4

Normal adrenal gland Adrenal adenoma Adrenal adenoma Adrenal gland with calciication

12 The Retroperitoneum Raymond E. Bertino and Elton Mustafaraj Video 12.1 Video 12.2 scan Video 12.3 Video 12.4 Video 12.5 image Video 12.6 Video 12.7 artery

Type 2 endoleak from inferior mesenteric artery–aorta Type 2 endoleak on enhanced computed tomography Type 3 endoleak, transverse image Type 3 endoleak, longitudinal image Aortic pseudoaneurysm (contained rupture), longitudinal Restenosis of stented accessory left renal artery Angiogram of restenosis of stented accessory left renal

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Video 12.8 Angiogram of stented accessory left renal artery restenosis after restenting Video 12.9 Normal right renal artery Video 12.10 Left renal artery stenosis with color bruit and aliasing throughout cardiac cycle Video 12.11 Nutcracker syndrome Video 12.12 Nutcracker syndrome after stent placement Video 12.13 Prominent arcuate veins Video 12.14 Mildly prominent arcuate veins Video 12.15 Angiogram of left ovarian vein during coil placement

13 Dynamic Ultrasound of Hernias of the Groin and Anterior Abdominal Wall Deborah Levine, Lisa Napolitano, and A. Thomas Stavros Video 13.1 Fat-containing indirect inguinal hernia Video 13.2 Direct inguinal hernia with intraperitoneal and preperitoneal fat Video 13.3 Note bowel peristalsis in this inguinal hernia Video 13.4 Large fat-containing direct inguinal hernia Video 13.5 Change in hernia contents during Valsalva maneuver Video 13.6 Completely reducible large wide-necked fat-containing ventral hernia Video 13.7 Partially reducible indirect inguinal hernia containing fat and bowel Video 13.8 Nonreducible fat-containing epigastric linea alba hernia Video 13.9 Large bowel-containing indirect inguinal hernia extending into scrotum Video 13.10 Fat-containing femoral hernia Video 13.11 Moderate-sized fat-containing nonreducible left spigelian hernia Video 13.12 Large fat- and bowel-containing incompletely reducible spigelian hernia Video 13.13 Diastasis recti abdominis Video 13.14 Fat-containing ventral hernia Video 13.15 Small fat-containing nonreducible epigastric linea alba hernia Video 13.16 Two adjacent moderate-sized fat-containing incompletely reducible epigastric linea alba hernias Video 13.17 Mesh with strong shadow makes evaluation for recurrent hernia dificult Video 13.18 Two adjacent moderate-sized fat-containing incisional hernias in patient after transverse rectus abdominis myocutaneous (TRAM) lap breast reconstruction Video 13.19 Fat-containing incisional hernia Video 13.20 Moderate-sized fat-containing reducible incisional hernia Video 13.21 Moderate-sized fat-containing reducible recurrent inguinal hernia at the edge of mesh Video 13.22 Pantaloon hernias Video 13.23 Strangulated right femoral hernia Video 13.24 Round ligament and inguinal canal (canal of Nuck) in a female with hydrocele

Video 14.7 Peritoneal mesothelioma Video 14.8 Endometrioma in the pouch of Douglas Video 14.9 Endometriotic plaque Video 14.10 Endometriotic plaque

15 The Uterus Douglas Brown and Deborah Levine Video 15.1 Unicornuate uterus Video 15.2 Bicornuate uterus Video 15.3 Fibroid with cystic necrotic change Video 15.4 Adenomyosis Video 15.5 Prolapsing polyp Video 15.6 Endometrial polyp Video 15.7 Endometrial polyp Video 15.8 Endometrial carcinoma Video 15.9 Endometrial carcinoma with hematometra Video 15.10 Synechia Video 15.11 Low position of intrauterine device (IUD) Video 15.12 Vascularized retained products of conception Video 15.13 Bladder lap hematoma and sutures after cesarean section

16 The Adnexa Rochelle Filker Andreotti and Lori A. Deitte Video 16.1 Bowel peristalsis Video 16.2 Hemorrhagic cyst Video 16.3 Endometrioma Video 16.4 Atypical endometrioma Video 16.5 Deep iniltrating endometriosis Video 16.6 Ovarian torsion Video 16.7 Clear cell carcinoma in endometrioma Video 16.8 Yolk sac tumor Video 16.9 Hydrosalpinx in 70-year-old woman with adnexal cyst Video 16.10 Hydrosalpinx in 35-year-old with complex left adnexal cyst Video 16.11 Pelvic inlammatory disease caused by Neisseria Gonorrhoeae

17 Ultrasound-Guided Biopsy of Chest, Abdomen, and Pelvis Theodora A. Potretzke, Thomas D. Atwell, J. William Charboneau, and Carl Reading Video 17.1 Ultrasound-guided omental core biopsy Video 17.2 Ultrasound-guided liver core biopsy Video 17.3 Ultrasound-guided liver mass biopsy using “freehand” technique Video 17.4 Ultrasound-guided liver mass biopsy using “freehand” technique Video 17.5 Power Doppler imaging improving drain conspicuity Video 17.6 Transvaginal adnexal cyst local anesthesia Video 17.7 Transvaginal adnexal cyst aspiration

18 Organ Transplantation 14 The Peritoneum Anthony E. Hanbidge, Korosh Khalili, and Stephanie R. Wilson Video 14.1 Video 14.2 Video 14.3 Video 14.4 Video 14.5 Video 14.6

Tumor iniltration of the omentum Tumor implant in the pouch of Douglas Tumor implant in the pouch of Douglas Peritoneal carcinomatosis—parietal peritoneum Peritoneal carcinomatosis—visceral peritoneum Peritoneal carcinomatosis—visceral peritoneum

Derek Muradali and Tanya Punita Chawla Video 18.1 Normal renal transplant, sagittal Video 18.2 Normal renal transplant, transverse Video 18.3 Arteriovenous malformation renal transplant Video 18.4 Partially thrombosed pseudoaneurysm in hilum of renal transplant Video 18.5 Normal pancreas transplant, sagittal Video 18.6 Normal pancreas transplant, transverse

Video Contents 19 The Thyroid Gland Luigi Solbiati, J. William Charboneau, Vito Cantisani, Carl Reading, and Giovanni Mauri Video 19.1 Video 19.2 Video 19.3 Video 19.4 Video 19.5 Video 19.6 Video 19.7

Colloid cysts Honeycomb pattern of benign nodule Adenoma Papillary carcinoma: ine calciications Papillary carcinoma: coarse and ine calciications Fine-needle aspiration (FNA) Hashimoto thyroiditis

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23 Overview of Musculoskeletal Ultrasound Techniques and Applications Colm McMahon and Corrie Yablon Video 23.1 Video 23.2 Video 23.3 Video 23.4 Video 23.5

Normal biceps muscle and distal tendon Normal Achilles tendon Normal inger lexor tendons—dynamic imaging Dynamic ulnar nerve subluxation Short-axis imaging of a Baker cyst

24 The Shoulder Colm McMahon and Corrie Yablon

20 The Parathyroid Glands Bonnie J. Huppert and Carl Reading Video 20.1 Cystic and solid parathyroid adenoma Video 20.2 Small parathyroid adenoma Video 20.3 Multiple gland parathyroid hyperplasia Video 20.4 Multiple gland parathyroid hyperplasia Video 20.5 Superior parathyroid adenoma Video 20.6 Superior parathyroid adenoma Video 20.7 Inferior parathyroid adenoma Video 20.8 Inferior parathyroid adenoma Video 20.9 Ectopic superior parathyroid adenoma Video 20.10 Intrathyroid parathyroid adenoma Video 20.11 Intrathyroid parathyroid adenoma Video 20.12 Ectopic parathyroid adenoma Video 20.13 Parathyromatosis in the postoperative neck Video 20.14 Parathyroid adenoma Video 20.15 Small inferior parathyroid adenoma and multinodular goiter Video 20.16 Small inferior parathyroid adenoma and multinodular thyroid Video 20.17 Ectopic intrathyroid parathyroid adenoma biopsy Video 20.18 Ectopic parathyroid adenoma biopsy Video 20.19 Ethanol ablation of recurrent graft-dependent hyperparathyroidism

21 The Breast Jordana Phillips, Rashmi J. Mehta, and A. Thomas Stavros Video 21.1 Importance of light pressure for color Doppler examination Video 21.2 Importance of light pressure for color Doppler examination Video 21.3 Normal cyst Video 21.4 Intraductal papilloma Video 21.5 Percutaneous biopsy using spring-loaded biopsy device

22 The Scrotum Daniel Sommers and Thomas Winter Video 22.1 Atrophic testis with seminoma Video 22.2 Epidermoid cyst Video 22.3 Varicocele in patient performing a Valsalva maneuver, with gray-scale and color Doppler sonography Video 22.4 Postvasectomy appearance of epididymis and vas deferens Video 22.5 “Dancing sperm” postvasectomy image of scrotum Video 22.6 Acute orchitis Video 22.7 Inferior traumatic tunica albuginea rupture, hematoma in testis, and extrusion of seminiferous tubules

Video 24.1 Dynamic assessment for subcoracoid impingement Video 24.2 Illustration of imaging the supraspinatus in long axis and the transition to infraspinatus posteriorly Video 24.3 Dynamic assessment for subacromial impingement Video 24.4 Dynamic imaging showing increased prominence of glenohumeral effusion on external rotation Video 24.5 Short-axis imaging of the supraspinatus tendon

25 Musculoskeletal Interventions Ronald S. Adler Video 25.1 Intraarticular injection of a hip under ultrasound guidance Video 25.2 Biceps tendon sheath injection using a rotator interval approach Video 25.3 Aspiration of a spinoglenoid notch cyst Video 25.4 Injection of calciic tendinosis Video 25.5 Autologous blood injection of 50-year-old woman with lateral epicondylitis Video 25.6 Depiction of Tenex procedure Video 25.7 Posthydrodissection of sural nerve in a 59-year-old female patient

26 The Extracranial Cerebral Vessels Edward I. Bluth, Stephen I. Johnson, and Laurie Troxclair Video 26.1 Minimal homogeneous plaque at carotid bulb (gray-scale) Video 26.2 Considerable homogenous plaque at ICA (gray-scale) Video 26.3 Type 3 homogeneous plaque with less than 50% sonolucency (gray-scale) Video 26.4 Type 3 homogeneous plaque with low-grade stenosis of the ICA (gray-scale) Video 26.5 Calciied plaque in the CCA (gray-scale) Video 26.6 Heterogeneous plaque in the left ICA (type 1) (gray-scale) Video 26.7 Heterogeneous plaque (type 1) with greater than 50% sonolucency within the plaque of the left ICA (gray-scale) Video 26.8 Heterogeneous plaque (type 2) in the ICA (gray-scale) Video 26.9 High-grade stenosis in the proximal right ICA (color Doppler) Video 26.10 Heterogeneous plaque in the ICA (color Doppler) Video 26.11 Heterogeneous plaque in the left ICA (power Doppler) Video 26.12 High-grade stenosis in the ICA (power Doppler) Video 26.13 High-grade stenosis of the ICA (power Doppler) Video 26.14 Low-grade stenosis in the ICA (color Doppler) Video 26.15 Normal spectral waveform of the proximal ICA Video 26.16 Normal spectral waveform of the mid ICA Video 26.17 Normal spectral waveform of the distal ICA Video 26.18 Normal spectral waveform of the right distal CCA Video 26.19 High-grade stenosis in the ICA (power Doppler)

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Video Contents

Video 26.20 High-grade stenosis in the ICA (color Doppler) Video 26.21 High-grade stenosis with spectral broadening (color and spectral Doppler) Video 26.22 Color and spectral Doppler of low-grade stenosis in the ICA

27 Peripheral Vessels Mark E. Lockhart, Heidi R. Umphrey, Therese M. Weber, and Michelle L. Robbin Video 27.1 Acute thrombus in the supericial femoral artery Video 27.2 Occlusion of the supericial femoral artery with a large collateral exiting proximal to the occlusion Video 27.3 Severe calciication of the supericial femoral artery limits ability to see within the artery lumen with gray-scale imaging Video 27.4 Common femoral artery pseudoaneurysm Video 27.5 Common femoral artery to common femoral vein arteriovenous istula (AVF) Video 27.6 Arterial bypass graft stenosis on grayscale and color Doppler Video 27.7 Large radial artery pseudoaneurysm with rent in arterial wall Video 27.8 Large radial artery pseudoaneurysm Video 27.9 Subclavian steal Video 27.10 Normal femoral vein compression during study to assess for deep venous thrombosis Video 27.11 Acute common femoral vein (CFV) thrombus Video 27.12 Nonocclusive slightly mobile thrombus within the great saphenous vein (GSV) with extension into the common femoral vein (CFV) Video 27.13 Acute deep venous thrombosis in right lower extremity Video 27.14 Chronic vein occlusion with collaterals Video 27.15 Chronic common femoral vein (CFV) occlusion with normal antegrade low in the femoral vein, and low reversal in the profunda femoral vein Video 27.16 Slow low in patent, compressible vein without deep venous thrombosis, longitudinal cine clip Video 27.17 Slow low in patent, compressible vein without deep venous thrombosis, transverse cine clip Video 27.18 Thrombus in one of paired femoral veins Video 27.19 Normal femoral vein valve Video 27.20 Normal internal jugular vein (IJV) on gray scale compression cine clip Video 27.21 Acute internal jugular thrombus Video 27.22 Nonocclusive thrombus in one brachial vein in the paired brachial veins Video 27.23 Acute thrombus around peripherally inserted central catheter (PICC) line in the basilic vein Video 27.24 Acute thrombus around peripherally inserted central catheter (PICC) line in the basilic vein Video 27.25 Thick-walled cephalic vein with chronic thrombus Video 27.26 Large hematoma adjacent to arteriovenous istula (AVF) Video 27.27 Small AVF basilic vein pseudoaneurysm Video 27.28 Graft wall irregularity and degeneration from repeated punctures Video 27.29 Graft venous anastomosis stenosis with peak systolic velocity measuring 6.1 m/sec in highest velocity portion of jet

28 Overview of Obstetric Imaging Deborah Levine Video 28.1 Normal 6-week embryo with cardiac activity Video 28.2 Normal irst-trimester embryo with rhombencephalon appearing as a luid collection in the region of the head Video 28.3 Sagittal view of uterus with 17-week gestational age fetus in cephalic presentation and anterior placenta Video 28.4 Normal intracranial anatomy at 19 weeks’ gestation Video 28.5 Four-chamber view of beating fetal heart Video 28.6 Scan through the heart Video 28.7 Normal kidneys and lumbosacral spine Video 28.8 Transverse fetal spine Video 28.9 Bladder and umbilical arteries

30 The First Trimester Elizabeth Lazarus and Deborah Levine Video 30.1 Early embryonic cardiac activity Video 30.2 Early pregnancy failure at 7 weeks Video 30.3 Expanded amnion in nonviable pregnancy Video 30.4 Ten-week demise with calciied yolk sac Video 30.5 Small subchorionic hemorrhage Video 30.6 Right ectopic pregnancy with adnexal mass separating from the ovary with manual pressure Video 30.7 Ruptured ectopic pregnancy Video 30.8 Cesarean section implantation in retrolexed uterus Video 30.9 Normal rhombencephalon Video 30.10 Persistent trophoblastic neoplasia Video 30.11 Choriocarcinoma

31 Chromosomal Abnormalities Bryann Bromley and Beryl Benacerraf Video 31.1 Nuchal translucency Video 31.2 Cystic hygroma Video 31.3 Nasal bone in irst trimester Video 31.4 Echogenic bowel Video 31.5 Amniocentesis needle being withdrawn from amniotic luid cavity

32 Multifetal Pregnancy Mary C. Frates Video 32.1 Quintuplets, 9 weeks’ gestational age Video 32.2 Conjoined embryos, 7 weeks’ gestational age Video 32.3 Monochorionic monoamniotic twins, 26 weeks’ gestational age Video 32.4 Three separate placentas in a trichorionic triplet pregnancy at 13 weeks’ gestational age Video 32.5 Velamentous cord insertion in a twin, 34 weeks’ gestational age Video 32.6 Growth and luid discrepancies in dichorionic twins, 24 weeks’ gestational age Video 32.7 Twin-twin transfusion syndrome, 22 weeks’ gestational age Video 32.8 Twin reversed arterial perfusion sequence, 16 weeks’ gestational age Video 32.9 Monochorionic monoamniotic twins, 12 weeks’ gestational age Video 32.10 Monochorionic monoamniotic twins, 28 weeks’ gestational age Video 32.11 Monochorionic monoamniotic conjoined twins, 35 weeks’ gestational age

Video Contents 33 The Fetal Face and Neck Ana P. Lourenco and Judy A. Estroff Video 33.1 Left 2 complete cleft lip, cleft alveolus, and cleft palate in sagittal plane in 20-week gestational age fetus Video 33.2 Left unilateral complete cleft lip, cleft alveolus, and cleft palate in axial plane in 20-week gestational age fetus Video 33.3 Left unilateral complete cleft lip, cleft alveolus, and cleft palate in coronal plane in 20-week gestational age fetus Video 33.4 Micrognathia at gestational age 20 weeks

34 The Fetal Brain Ants Toi and Deborah Levine Video 34.1 Normal brain, axial Video 34.2 Normal brain, coronal Video 34.3 Normal brain, sagittal Video 34.4 Choroid plexus cysts Video 34.5 Bilateral ventriculomegaly Video 34.6 Chiari malformation in fetus with spinal neural tube defect Video 34.7 Holoprosencephaly Video 34.8 Second trimester agenesis of corpus callosum Video 34.9 Agenesis of corpus callosum in coronal plane Video 34.10 Agenesis of corpus callosum in sagittal plane Video 34.11 Agenesis of corpus callosum in axial plane with midline cyst Video 34.12 Absence of septal lealets

35 The Fetal Spine Elizabeth Asch and Eric Sauerbrei Video 35.1 Video 35.2 Video 35.3 Video 35.4 Video 35.5 Video 35.6

Normal transaxial spine Normal longitudinal spine Myelomeningocele Closed neural tube defect: transaxial Closed neural tube defect: longitudinal Sacrococcygeal teratoma

36 The Fetal Chest

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Video 37.7 Aortic arch Video 37.8 Aortic arch Video 37.9 Atrioventricular septal defect Video 37.10 Hypoplastic left heart syndrome Video 37.11 Hypoplastic right heart Video 37.12 Ebstein anomaly Video 37.13 Tetralogy of Fallot

38 The Fetal Gastrointestinal Tract and Abdominal Wall Nir Melamed, Anne Kennedy, and Phyllis Glanc Video 38.1 Esophageal atresia Video 38.2 Gastric debris Video 38.3 Gastric debris Video 38.4 Duodenal atresia Video 38.5 Jejunal atresia Video 38.6 Duplication cyst Video 38.7 Meconium peritonitis Video 38.8 Echogenic bowel Video 38.9 Normal gallbladder Video 38.10 Annular pancreas Video 38.11 Splenic cyst Video 38.12 Gastroschisis Video 38.13 Omphalocele Video 38.14 Bladder exstrophy Video 38.15 Cloacal exstrophy

39 The Fetal Urogenital Tract Katherine W. Fong, Julia Eva Kfouri, and Kirsten L. Weind Matthews Video 39.1 “Lying down” adrenal sign due to unilateral renal agenesis Video 39.2 Bilateral renal agenesis Video 39.3 Pelvic kidney Video 39.4 Cross-fused renal ectopia Video 39.5 Horseshoe kidney Video 39.6 Autosomal recessive polycystic kidney disease Video 39.7 Perinephric urinoma Video 39.8 Primary megaureter Video 39.9 Megalourethra Video 39.10 Cloacal dysgenesis Video 39.11 Ovarian cyst

Dorothy Bulas Video 36.1 Congenital pulmonary adenomatoid malformation Video 36.2 Small pleural effusion at 16 weeks’ gestational age Video 36.3 Left-sided congenital diaphragmatic hernia at 32 weeks’ gestational age (transverse view) Video 36.4 Left-sided congenital diaphragmatic hernia at 32 weeks’ gestational age (sagittal view) Video 36.5 Large left-sided congenital diaphragmatic hernia with large amount of liver in chest Video 36.6 Right-sided congenital diaphragmatic hernia

37 The Fetal Heart Elizabeth R. Stamm and Julia A. Drose Video 37.1 Normal apical four-chamber view Video 37.2 Normal sub-costal four-chamber view Video 37.3 Normal appearance of the aorta and pulmonary artery Video 37.4 Color Doppler of the aorta and pulmonary artery Video 37.5 Short-axis view of the color Doppler of the ventricles and great arteries Video 37.6 Three-vessel and trachea view

40 The Fetal Musculoskeletal System Phyllis Glanc, David Chitayat, and Sheila Unger Video 40.1 Thanatophoric dysplasia Video 40.2 Clubfeet at 21 weeks

41 Fetal Hydrops Deborah Levine Video 41.1 Fetal abdomen at 30 weeks gestational age in fetus with a small amount of ascites and polyhydramnios Video 41.2 Bilateral pleural effusions, left greater than right Video 41.3 Large unilateral pleural effusion inverts the hemidiaphragm and is associated with ascites Video 41.4 Small pericardial effusion in fetus with poorly contractile and echogenic heart Video 41.5 Anasarca in fetus with congenital pulmonary airway malformation Video 41.6 Middle cerebral artery Doppler Video 41.7 Poorly contractile heart abnormal appearing heart, bilateral pleural effusions, and marked anasarca

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42 Fetal Measurements: Normal and Abnormal Fetal Growth and Assessment of Fetal Well-Being Carol B. Benson and Peter M. Doubilet Video 42.1 Early embryonic heartbeat Video 42.2 Fetal movement Video 42.3 Fetal breathing movements

43 Sonographic Evaluation of the Placenta Thomas D. Shipp Video 43.1 Placental lake Video 43.2 Thick placenta Video 43.3 Placenta accreta Video 43.4 Placenta increta Video 43.5 Placenta percreta Video 43.6 Abruption Video 43.7 Abruption Video 43.8 Preplacental hematoma Video 43.9 Preplacental hematoma Video 43.10 Placental infarction Video 43.11 Placental infarction Video 43.12 Circumvallate placenta Video 43.13 Circumvallate placenta Video 43.14 Bilobed placenta Video 43.15 Velamentous cord insertion and two-vessel cord Video 43.16 Umbilical cord insertion into placenta Video 43.17 Vasa previa

44 Cervical Ultrasound and Preterm Birth Hournaz Ghandehari and Phyllis Glanc Video 44.1 Open cervix with large funnel and bulging membranes Video 44.2 Closed cervix with mobile debris at the internal os Video 44.3 Open cervix with mobile debris in the dilated cervical canal and adjacent to the external os

Video 45.16 Video 45.17 Video 45.18 Video 45.19

Cystic periventricular leukomalacia Cytomegalovirus with punctate calciications Multiple focal calciications Ventricular septation

47 Doppler Sonography of the Brain in Children Dorothy Bulas and Alexia Egloff Video 47.1 Normal color Doppler of circle of Willis in 6-year-old Video 47.2 Spectral wave form of the right middle cerebral artery Video 47.3 Normal spectral Doppler of right bifurcation Video 47.4 Four-year-old pending brain death after fall from second story Video 47.5 Eight-year-old pending brain death after motor vehicle accident postcraniectomy for hematoma

48 The Pediatric Head and Neck Rupa Radhakrishnan and Beth M. Kline-Fath Video 48.1 Video 48.2 Video 48.3 Video 48.4

Wharton duct stone Multinodular goiter Infantile hemangioma Lymphatic malformation

49 The Pediatric Spinal Canal Ilse Castro-Aragon, Deborah Levine, and Carol M. Rumack Video 49.1 Normal cauda equina Video 49.2 Normal ilum terminale Video 49.3 Skin dimple and hypoechoic tract in subcutaneous tissues extending to normal coccyx Video 49.4 Lipomyelocele in sagittal view Video 49.5 Sagittal lipomyelocele Video 49.6 Lipomyelocele in transverse view Video 49.7 Lipomyelomeningocele Video 49.8 Segmental spinal dysgenesis in sagittal view Video 49.9 Segmental spinal dysgenesis patient with fatty ilum

50 The Pediatric Chest 45 Neonatal and Infant Brain Imaging Carol M. Rumack and Amanda K. Auckland Video 45.1 Normal coronal sweep Video 45.2 Normal sagittal sweep Video 45.3 Normal mastoid sweep Video 45.4 Chiari II malformation Video 45.5 Ventriculomegaly in association with Chiari II malformation (seen in Video 45.4) Video 45.6 Chiari II malformation, pointed frontal and large occipital horn; partial absence of corpus callosum (same neonate as in Videos 45.4 and 45.5) Video 45.7 Tethered cord in patient with Chiari II malformation, sagittal scan Video 45.8 Absence of cavum septi pellucidi, coronal scan Video 45.9 Right subacute subependymal, intraventricular, and right frontal intraparenchymal hemorrhages, coronal scan Video 45.10 Right subependymal, caudothalamic groove, and hemorrhage and intraventricular hemorrhage, sagittal scan Video 45.11 Cisterna magna clot Video 45.12 Acute intraventricular echogenic blood Video 45.13 Bilateral intraventricular hemorrhage and intraparenchymal hemorrhage Video 45.14 Acute highly echogenic hemorrhage Video 45.15 Intraventricular hemorrhage

Chetan Chandulal Shah and S. Bruce Greenberg Video 50.1 Video 50.2 Video 50.3 child Video 50.4 surgery

Moving septations within pleural luid Hemidiaphragmatic motion in an infant Hemidiaphragmatic movement in healthy 31-month-old Hemidiaphragmatic paralysis in an infant after cardiac

51 The Pediatric Liver and Spleen Sara M. O’Hara Video 51.1 Normal porta hepatis showing portal vein, hepatic artery, and common bile duct Video 51.2 Neonatal hepatitis Video 51.3 Steatosis from obesity Video 51.4 Multiple cutaneous hemangiomas in a 1-month-old infant Video 51.5 Multiple cutaneous hemangiomas in a 1-month-old infant Video 51.6 Hepatic abscess Video 51.7 Normal low in the main portal vein Video 51.8 Normal branching vessels in the liver Video 51.9 Normal third- and fourth-order branches in the liver Video 51.10 Cavernous transformation of the portal vein Video 51.11 Pneumobilia, an expected inding following portoenterostomy

Video Contents 52 The Pediatric Urinary Tract and Adrenal Glands Harriet J. Paltiel and Diane S. Babcock Video 52.1 Crossed renal ectopia Video 52.2 Contrast-enhanced urosonography depicts a normal bladder Video 52.3 Contrast-enhanced urosonography demonstrates vesicoureteral relux Video 52.4 Contrast-enhanced urosonography shows a normal male urethra Video 52.5 Inlammatory pseudotumor Video 52.6 Laceration of the mid-lateral aspect of the left kidney and perirenal hematoma Video 52.7 Multicystic dysplastic kidney Video 52.8 Burkitt lymphoma involving kidney Video 52.9 Neuroblastoma

54 Pediatric Pelvic Sonography William L. Simpson, Jr., Humaira Chaudhry, and Henrietta Kotlus Rosenberg Video 54.1 Video 54.2 Video 54.3 Video 54.4 Video 54.5

Water vaginogram Normal postpubertal ovary Polycystic ovarian morphology Normal postpubertal testis Testicular microlithiasis

55 The Pediatric Hip and Other Musculoskeletal Ultrasound Applications Leslie E. Grissom and H. Theodore Harcke Video 55.1 Video 55.2 Video 55.3 Video 55.4 Video 55.5 Video 55.6 Video 55.7 Video 55.8

Normal coronal/lexion view, midacetabulum Normal coronal/lexion view, posterior lip Subluxation, coronal/lexion view, midacetabulum Dislocatable hip, coronal/lexion view, midacetabulum Dislocatable hip, coronal/lexion view, posterior lip Normal transverse/lexion view Subluxation, transverse/lexion view Dislocation, transverse/lexion view

56 Pediatric Interventional Sonography Neil Johnson and Allison Aguado Video 56.1 Peripherally inserted central catheter (PICC) line placement

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Video 56.2 Video loops showing debris attached to and obstructing the drainage catheter during diagnostic and therapeutic aspiration of heavily bloodstained abdominal luid with loating debris Video 56.3 Video loops showing debris attached to and obstructing the drainage catheter during diagnostic and therapeutic aspiration of heavily bloodstained abdominal luid with loating debris Video 56.4 Appendiceal abscess with catheter touching fecalith Video 56.5 Gaucher disease patient rib biopsy Video 56.6 Gaucher rib osteomyelitis drain catheter being advanced Video 56.7 Gaucher rib prebiopsy showing pus and displaceable rib Video 56.8 Juvenile rheumatoid arthritis tendon sheath steroid injection

Appendix: Ultrasound Artifacts: A Virtual Chapter Korosh Khalili, Hojun Yu, Alexander Jesurum, and Deborah Levine Video A.1 Propagation velocity artifact Video A.2 Attenuation-related artifacts Video A.3 Shadowing Video A.4 Showing in region of cauda equina Video A.5 Increased through transmission Video A.6 Path of sound assumption Video A.7 Mirror image artifact Video A.8 Comet-tail artifact Video A.9 Comet-tail artifact in adenomyomatosis Video A.10 Refraction from the anterior abdominal wall Video A.11 Anisotropy Video A.12 Anisotropy at supraspinatus tendon insertion Video A.13 Reverberation artifact from free intraperitoneal gas Video A.14 Ring-down artifact Video A.15 Ring-down artifact from air in bile ducts Video A.16 Dirty shadowing Video A.17 Side lobe artifact Video A.18 Partial volume averaging explanation Video A.19 Tissue vibration artifact Video A.20 Tissue vibration artifact from left renal artery stenosis with color bruit and aliasing Video A.21 Aliasing seen in common femoral artery to common femoral vein arteriovenous istula Video A.22 Twinkle explanation Video A.23 Twinkle

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DIAGNOSTIC ULTRASOUND

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PART ONE: Physics CHAPTER

1

Physics of Ultrasound Christopher R.B. Merritt

SUMMARY OF KEY POINTS • Quality imaging requires an understanding of basic acoustic principles. • Image interpretation requires recognition and understanding of common artifacts. • Special modes of operation, including harmonic imaging, compounding, elastography, and Doppler, expand the

capabilities of conventional gray-scale imaging. • Knowledge of mechanical and thermal bioeffects of ultrasound is necessary for prudent use. • High-intensity focused ultrasound has potential therapeutic applications.

CHAPTER OUTLINE BASIC ACOUSTICS Wavelength and Frequency Propagation of Sound Distance Measurement Acoustic Impedance Relection Refraction Attenuation INSTRUMENTATION Transmitter Transducer Receiver Image Display Mechanical Sector Scanners Arrays Linear Arrays Curved Arrays Phased Arrays

A

Two-Dimensional Arrays Transducer Selection IMAGE DISPLAY AND STORAGE SPECIAL IMAGING MODES Tissue Harmonic Imaging Spatial Compounding Three-Dimensional Ultrasound Ultrasound Elastography Strain Elastography Shear Wave Elastography IMAGE QUALITY Spatial Resolution IMAGING PITFALLS Shadowing and Enhancement DOPPLER SONOGRAPHY Doppler Signal Processing and Display Doppler Instrumentation Power Doppler

ll diagnostic ultrasound applications are based on the detection and display of acoustic energy relected from interfaces within the body. hese interactions provide the information needed to generate high-resolution, gray-scale images of the body, as well as display information related to blood low. Its unique imaging attributes have made ultrasound an important and versatile medical imaging tool. However, expensive stateof-the-art instrumentation does not guarantee the production of high-quality studies of diagnostic value. Gaining maximum beneit from this complex technology requires a combination of skills, including knowledge of the physical principles that

Interpretation of the Doppler Spectrum Interpretation of Color Doppler Other Technical Considerations Doppler Frequency Wall Filters Spectral Broadening Aliasing Doppler Angle Sample Volume Size Doppler Gain OPERATING MODES: CLINICAL IMPLICATIONS Bioeffects and User Concerns THERAPEUTIC APPLICATIONS: HIGH-INTENSITY FOCUSED ULTRASOUND

empower ultrasound with its unique diagnostic capabilities. he user must understand the fundamentals of the interactions of acoustic energy with tissue and the methods and instruments used to produce and optimize the ultrasound display. With this knowledge the user can collect the maximum information from each examination, avoiding pitfalls and errors in diagnosis that may result from the omission of information or the misinterpretation of artifacts.1 Ultrasound imaging and Doppler ultrasound are based on the scattering of sound energy by interfaces of materials with diferent properties through interactions governed by acoustic

1

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physics. he amplitude of relected energy is used to generate ultrasound images, and frequency shits in the backscattered ultrasound provide information relating to moving targets such as blood. To produce, detect, and process ultrasound data, users must manage numerous variables, many under their direct control. To do this, operators must understand the methods used to generate ultrasound data and the theory and operation of the instruments that detect, display, and store the acoustic information generated in clinical examinations. his chapter provides an overview of the fundamentals of acoustics, the physics of ultrasound imaging and low detection, and ultrasound instrumentation with emphasis on points most relevant to clinical practice. A discussion of the therapeutic application of high-intensity focused ultrasound concludes the chapter.

BASIC ACOUSTICS Wavelength and Frequency Sound is the result of mechanical energy traveling through matter as a wave producing alternating compression and rarefaction. Pressure waves are propagated by limited physical displacement of the material through which the sound is being transmitted. A plot of these changes in pressure is a sinusoidal waveform (Fig. 1.1), in which the Y axis indicates the pressure at a given point and the X axis indicates time. Changes in pressure with time deine the basic units of measurement for sound. he distance between corresponding points on the time-pressure curve is deined as the wavelength (λ), and the time (T) to complete a single cycle is called the period. he number of complete cycles in a unit of time is the frequency (f) of the sound. Frequency and period are inversely related. If the period (T) is expressed in seconds, f = 1/T, or f = T × sec−1. he unit of acoustic frequency

is the hertz (Hz); 1 Hz = 1 cycle per second. High frequencies are expressed in kilohertz (kHz; 1 kHz = 1000 Hz) or megahertz (MHz; 1 MHz = 1,000,000 Hz). In nature, acoustic frequencies span a range from less than 1 Hz to more than 100,000 Hz (100 kHz). Human hearing is limited to the lower part of this range, extending from 20 to 20,000 Hz. Ultrasound difers from audible sound only in its frequency, and it is 500 to 1000 times higher than the sound we normally hear. Sound frequencies used for diagnostic applications typically range from 2 to 15 MHz, although frequencies as high as 50 to 60 MHz are under investigation for certain specialized imaging applications. In general, the frequencies used for ultrasound imaging are higher than those used for Doppler. Regardless of the frequency, the same basic principles of acoustics apply.

Propagation of Sound In most clinical applications of ultrasound, brief bursts or pulses of energy are transmitted into the body and propagated through tissue. Acoustic pressure waves can travel in a direction perpendicular to the direction of the particles being displaced (transverse waves), but in tissue and luids, sound propagation is primarily along the direction of particle movement (longitudinal waves). Longitudinal waves are important in conventional ultrasound imaging and Doppler, while transverse waves are measured in shear wave elastography. he speed at which pressure waves move through tissue varies greatly and is afected by the physical properties of the tissue. Propagation velocity is largely determined by the resistance of the medium to compression, which in turn is inluenced by the density of the medium and its stifness or elasticity. Propagation velocity is increased by increasing stifness and reduced by decreasing density. In the body, propagation velocity of longitudinal waves may be regarded as constant for a given tissue and is not afected by the frequency or wavelength of the sound. his is in contrast to transverse (shear) waves for

FIG. 1.1 Sound Waves. Sound is transmitted mechanically at the molecular level. In the resting state the pressure is uniform throughout the medium. Sound is propagated as a series of alternating pressure waves producing compression and rarefaction of the conducting medium. The time for a pressure wave to pass a given point is the period, T. The frequency of the wave is 1/T. The wavelength, λ, is the distance between corresponding points on the time-pressure curve.

CHAPTER 1

Air

330

Fat

1450

Water

1480

Soft tissue (average)

1540

Liver

1550

Kidney

1560

Blood

1570

Muscle

1580

Bone

4080

1400

1500

1600

1700

Physics of Ultrasound

3

1800

Propagation velocity (meters/second) FIG. 1.2 Propagation Velocity. In the body, propagation velocity of sound is determined by the physical properties of tissue. As shown, this varies considerably. Medical ultrasound devices base their measurements on an assumed average propagation velocity of soft tissue of 1540 m/sec.

which the velocity is determined by Young modulus, a measure of tissue stifness or elasticity. Fig. 1.2 shows typical longitudinal propagation velocities for a variety of materials. In the body the propagation velocity of sound is assumed to be 1540 meters per second (m/sec). his value is the average of measurements obtained from normal sot tissue.2,3 Although this value represents most sot tissues, such tissues as aerated lung and fat have propagation velocities signiicantly less than 1540 m/sec, whereas tissues such as bone have greater velocities. Because a few normal tissues have propagation values signiicantly diferent from the average value assumed by the ultrasound scanner, the display of such tissues may be subject to measurement errors or artifacts (Fig. 1.3). he propagation velocity of sound (c) is related to frequency and wavelength by the following simple equation: c= fλ hus a frequency of 5 MHz can be shown to have a wavelength of 0.308 mm in tissue: λ = c/f = 1540 m/sec × 5,000,000 sec−1 = 0.000308 m = 0.308 mm. Wavelength is an important determinant of spatial resolution in ultrasound imaging, and selection of transducer frequency for a given application is a key user decision.

Distance Measurement Propagation velocity is a particularly important value in clinical ultrasound and is critical in determining the distance of a relecting interface from the transducer. Much of the information used to generate an ultrasound scan is based on the precise measurement of time and employs the principles of echo-ranging (Fig. 1.4). If an ultrasound pulse is transmitted into the body and the time until an echo returns is measured, it is simple to calculate the depth of the interface that generated the echo, provided the

FIG. 1.3 Propagation Velocity Artifact. When sound passes through a lesion containing fat, echo return is delayed because fat has a propagation velocity of 1450 m/sec, which is less than the liver. Because the ultrasound scanner assumes that sound is being propagated at the average velocity of 1540 m/sec, the delay in echo return is interpreted as indicating a deeper target. Therefore the inal image shows a misregistration artifact in which the diaphragm and other structures deep to the fatty lesion are shown in a deeper position than expected (simulated image).

propagation velocity of sound for the tissue is known. For example, if the time from the transmission of a pulse until the return of an echo is 0.000145 seconds and the velocity of sound is 1540 m/ sec, the distance that the sound has traveled must be 22.33 cm (1540 m/sec × 100 cm/m × 0.000145 sec = 22.33 cm). Because the time measured includes the time for sound to travel to the interface and then return along the same path to the transducer, the distance from the transducer to the relecting interface is 22.33 cm/2 = 11.165 cm. By rapidly repeating this process, a two-dimensional (2-D) map of relecting interfaces is created to form the ultrasound image. he accuracy of this measurement is therefore highly inluenced by how closely the presumed velocity of sound corresponds to the true velocity in the tissue being observed (see Figs. 1.2 and 1.3), as well as by the important assumption that the sound pulse travels in a straight path to and from the relecting interface.

Acoustic Impedance Current diagnostic ultrasound scanners rely on the detection and display of relected sound or echoes. Imaging based on transmission of ultrasound is also possible, but this is not used clinically at present. To produce an echo, a relecting interface must be present. Sound passing through a totally homogeneous medium encounters no interfaces to relect sound, and the medium appears anechoic or cystic. he junction of tissues or materials with diferent physical properties produces an acoustic interface. hese interfaces are responsible for the relection of variable amounts of the incident sound energy. hus when ultrasound passes from one tissue to another or encounters a vessel wall or circulating blood cells, some of the incident sound

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ms

× ×

FIG. 1.4 Ultrasound Ranging. The information used to position an echo for display is based on the precise measurement of time. Here the time for an echo to travel from the transducer to the target and return to the transducer is 0.145 ms (0.000145 seconds). Multiplying the velocity of sound in tissue (1540 m/sec) by the time shows that the sound returning from the target has traveled 22.33 cm. Therefore the target lies half this distance, or 11.165 cm, from the transducer. By rapidly repeating this process, a two-dimensional map of relecting interfaces is created to form the ultrasound image.

energy is relected. he amount of relection or backscatter is determined by the diference in the acoustic impedances of the materials forming the interface. Acoustic impedance (Z) is determined by product of the density (ρ) of the medium propagating the sound and the propagation velocity (c) of sound in that medium (Z = ρc). Interfaces with large acoustic impedance diferences, such as interfaces of tissue with air or bone, relect almost all the incident energy. Interfaces composed of substances with smaller diferences in acoustic impedance, such as a muscle and fat interface, relect only part of the incident energy, permitting the remainder to continue onward. As with propagation velocity, acoustic impedance is determined by the properties of the tissues involved and is independent of frequency.

Relection he way ultrasound is relected when it strikes an acoustic interface is determined by the size and surface features of the interface (Fig. 1.5). If large and relatively smooth, the interface relects sound much as a mirror relects light. Such interfaces are called specular relectors because they behave as “mirrors for sound.” he amount of energy relected by an acoustic interface can be expressed as a fraction of the incident energy; this is termed the relection coeicient (R). If a specular relector is perpendicular to the incident sound beam, the amount of energy relected is determined by the following relationship: R = (Z 2 − Z1 )2 (Z 2 + Z1 )2 where Z1 and Z2 are the acoustic impedances of the media forming the interface. Because ultrasound scanners only detect relections that return to the transducer, display of specular interfaces is highly dependent

Examples of Specular Relectors Diaphragm Vessel wall Wall of urine-illed bladder Endometrial stripe

on the angle of insonation (exposure to ultrasound waves). Specular relectors will return echoes to the transducer only if the sound beam is perpendicular to the interface. If the interface is not at a near 90-degree angle to the sound beam, it will be relected away from the transducer, and the echo will not be detected (see Fig. 1.5A). Most echoes in the body do not arise from specular relectors but rather from much smaller interfaces within solid organs. In this case the acoustic interfaces involve structures with individual dimensions much smaller than the wavelength of the incident sound. he echoes from these interfaces are scattered in all directions. Such relectors are called difuse relectors and account for the echoes that form the characteristic echo patterns seen in solid organs and tissues (see Fig. 1.5B). he constructive and destructive interference of sound scattered by difuse relectors results in the production of ultrasound speckle, a feature of tissue texture of sonograms of solid organs (Fig. 1.6). For some diagnostic applications, the nature of the relecting structures creates important conlicts. For example, most vessel walls behave as specular relectors that require insonation at a 90-degree angle for best imaging, whereas Doppler imaging requires an angle of less than 90 degrees between the sound beam and the vessel.

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Physics of Ultrasound

5

B

FIG. 1.5 Specular and Diffuse Relectors. (A) Specular relector. The diaphragm is a large and relatively smooth surface that relects sound like a mirror relects light. Thus sound striking the diaphragm at nearly a 90-degree angle is relected directly back to the transducer, resulting in a strong echo. Sound striking the diaphragm obliquely is relected away from the transducer, and an echo is not displayed (yellow arrow). (B) Diffuse relector. In contrast to the diaphragm, the liver parenchyma consists of acoustic interfaces that are small compared to the wavelength of sound used for imaging. These interfaces scatter sound in all directions, and only a portion of the energy returns to the transducer to produce the image.

propagation velocities of sound in the media forming the interface (Fig. 1.7). Refraction is important because it is one cause of misregistration of a structure in an ultrasound image (Fig. 1.8). When an ultrasound scanner detects an echo, it assumes that the source of the echo is along a ixed line of sight from the transducer. If the sound has been refracted, the echo detected may be coming from a diferent depth or location than the image shown in the display. If this is suspected, increasing the scan angle so that it is perpendicular to the interface minimizes the artifact.

Attenuation

FIG. 1.6 Ultrasound Speckle. Close inspection of an ultrasound image of the breast containing a small cyst reveals it to be composed of numerous areas of varying intensity (speckle). Speckle results from the constructive (red) and destructive (green) interaction of the acoustic ields (yellow rings) generated by the scattering of ultrasound from small tissue relectors. This interference pattern gives ultrasound images their characteristic grainy appearance and may reduce contrast. Ultrasound speckle is the basis of the texture displayed in ultrasound images of solid tissues.

As the acoustic energy moves through a uniform medium, work is performed and energy is ultimately transferred to the transmitting medium as heat. he capacity to perform work is determined by the quantity of acoustic energy produced. Acoustic power, expressed in watts (W) or milliwatts (mW), describes the amount of acoustic energy produced in a unit of time. Although measurement of power provides an indication of the energy as it relates to time, it does not take into account the spatial distribution of the energy. Intensity (I) is used to describe the spatial distribution of power and is calculated by dividing the power by the area over which the power is distributed, as follows: I (W/cm2 ) = Power (W) Area (cm2 )

Refraction When sound passes from a tissue with one acoustic propagation velocity to a tissue with a higher or lower sound velocity, there is a change in the direction of the sound wave. his change in direction of propagation is called refraction and is governed by Snell law: sin θ1 sin θ2 = c1 c2 where θ1 is the angle of incidence of the sound approaching the interface, θ2 is the angle of refraction, and c1 and c2 are the

he attenuation of sound energy as it passes through tissue is of great clinical importance because it inluences the depth in tissue from which useful information can be obtained. his in turn afects transducer selection and a number of operatorcontrolled instrument settings, including time (or depth) gain compensation, power output attenuation, and system gain levels. Attenuation is measured in relative rather than absolute units. he decibel (dB) notation is generally used to compare diferent levels of ultrasound power or intensity. his value is 10 times the log10 of the ratio of the power or intensity values being

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θ1 = 20°

Tissue A c1 = 1540 m/sec Tissue B c2 = 1450 m/sec

A

B

8 18.8° θ2 = 18

FIG. 1.7 Refraction. When sound passes from tissue A with propagation velocity (c1) to tissue B with a different propagation velocity (c2), there is a change in the direction of the sound wave because of refraction. The degree of change is related to the ratio of the propagating velocities of the media forming the interface (sinθ1/sinθ2 = c1/c2).

compared. For example, if the intensity measured at one point in tissues is 10 mW/cm2 and at a deeper point is 0.01 mW/cm2, the diference in intensity is as follows: (10)(log10 0.01 10) = (10)(log10 0.001) = (10)(− log10 1000) = (10)(−33) = −30 dB As it passes through tissue, sound loses energy, and the pressure waves decrease in amplitude as they travel farther from their source. Contributing to the attenuation of sound are the transfer of energy to tissue, resulting in heating (absorption), and the removal of energy by relection and scattering. Attenuation is therefore the result of the combined efects of absorption, scattering, and relection. Attenuation depends on the insonating frequency as well as the nature of the attenuating medium. High frequencies are attenuated more rapidly than lower frequencies, and transducer frequency is a major determinant of the useful depth from which information can be obtained with ultrasound. Attenuation determines the eiciency with which ultrasound

C FIG. 1.8 Refraction Artifact. (A) and (B) Production of an artifact by refraction of sound in a transverse scan of the mid abdomen. The direct sound path properly depicts the location of the object. (B) A “ghost image” (red) produced by refraction at the edge of the rectus abdominis muscle. The transmitted and relected sound travels along the path of the black arrows. The scanner assumes the returning signal is from a straight line (red arrow) and displays the structure at the incorrect location. (C) Axial transabdominal image of the uterus showing a small gestational sac (A) and what appears to be a second sac (B) due to refraction artifact.

CHAPTER 1

Water

0.18

Fat

0.63

Soft tissue (average)

0.70

Liver

0.94

Kidney

1.00

Muscle (parallel) Muscle (transverse)

Transducer

1.30 3.30

Bone

5.00

Air

10.00 0

2

7

PRF determines the time interval between ultrasound pulses and is important in determining the depth from which unambiguous data can be obtained both in imaging and Doppler modes. he ultrasound pulses must be spaced with enough time between the pulses to permit the sound to travel to the depth of interest and return before the next pulse is sent. For imaging, PRFs from 1 to 10 kHz are used, resulting in an interval of 0.1 to 1 ms between pulses. hus a PRF of 5 kHz permits an echo to travel and return from a depth of 15.4 cm before the next pulse is sent.

0.00

Blood

Physics of Ultrasound

4

6

8

10

Attenuation (dB/cm/MHz) FIG. 1.9 Attenuation. As sound passes through tissue, it loses energy through the transfer of energy to tissue by heating, relection, and scattering. Attenuation is determined by the insonating frequency and the nature of the attenuating medium. Attenuation values for normal tissues show considerable variation. Attenuation also increases in proportion to insonating frequency, resulting in less penetration at higher frequencies.

penetrates a speciic tissue and varies considerably in normal tissues (Fig. 1.9).

INSTRUMENTATION Ultrasound scanners are complex and sophisticated imaging devices, but all consist of the following basic components to perform key functions: • Transmitter or pulser to energize the transducer • Ultrasound transducer • Receiver and processor to detect and amplify the backscattered energy and manipulate the relected signals for display • Display that presents the ultrasound image or data in a form suitable for analysis and interpretation • Method to record or store the ultrasound image

Transmitter Most clinical applications use pulsed ultrasound, in which brief bursts of acoustic energy are transmitted into the body. he source of these pulses, the ultrasound transducer, is energized by application of precisely timed, high-amplitude voltage. he maximum voltage that may be applied to the transducer is limited by federal regulations that restrict the acoustic output of diagnostic scanners. Most scanners provide a control that permits attenuation of the output voltage. Because the use of maximum output results in higher exposure of the patient to ultrasound energy, prudent use dictates use of the output attenuation controls to reduce power levels to the lowest levels consistent with the diagnostic problem.4 he transmitter also controls the rate of pulses emitted by the transducer, or the pulse repetition frequency (PRF). he

A transducer is any device that converts one form of energy to another. In ultrasound the transducer converts electric energy to mechanical energy, and vice versa. In diagnostic ultrasound systems the transducer serves two functions: (1) converting the electric energy provided by the transmitter to the acoustic pulses directed into the patient and (2) serving as the receiver of relected echoes, converting weak pressure changes into electric signals for processing. Ultrasound transducers use piezoelectricity, a principle discovered by Pierre and Jacques Curie in 1880.5 Piezoelectric materials have the unique ability to respond to the action of an electric ield by changing shape. hey also have the property of generating electric potentials when compressed. Changing the polarity of a voltage applied to the transducer changes the thickness of the transducer, which expands and contracts as the polarity changes. his results in the generation of mechanical pressure waves that can be transmitted into the body. he piezoelectric efect also results in the generation of small potentials across the transducer when the transducer is struck by returning echoes. Positive pressures cause a small polarity to develop across the transducer; negative pressure during the rarefaction portion of the acoustic wave produces the opposite polarity across the transducer. hese tiny polarity changes and the associated voltages are the source of all the information processed to generate an ultrasound image or Doppler display. When stimulated by the application of a voltage diference across its thickness, the transducer vibrates. he frequency of vibration is determined by the transducer material. When the transducer is electrically stimulated, a range or band of frequencies results. he preferential frequency produced by a transducer is determined by the propagation speed of the transducer material and its thickness. In the pulsed wave operating modes used for most clinical ultrasound applications, the ultrasound pulses contain additional frequencies that are both higher and lower than the preferential frequency. he range of frequencies produced by a given transducer is termed its bandwidth. Generally, the shorter the pulse of ultrasound produced by the transducer, the greater is the bandwidth. Most modern digital ultrasound systems employ broadbandwidth technology. Ultrasound bandwidth refers to the range of frequencies produced and detected by the ultrasound system. his is important because each tissue in the body has a characteristic response to ultrasound of a given frequency, and diferent tissues respond diferently to diferent frequencies. he range of frequencies arising from a tissue exposed to ultrasound is referred to as the frequency spectrum bandwidth of the tissue, or tissue

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signature. Broad-bandwidth technology provides a means to capture the frequency spectrum of insonated tissues, preserving acoustic information and tissue signature. Broad-bandwidth beam formers reduce speckle artifact by a process of frequency compounding. his is possible because speckle patterns at different frequencies are independent of one another, and combining data from multiple frequency bands (i.e., compounding) results in a reduction of speckle in the inal image, leading to improved contrast resolution. he length of an ultrasound pulse is determined by the number of alternating voltage changes applied to the transducer. For continuous wave (CW) ultrasound devices, a constant alternating current is applied to the transducer, and the alternating polarity produces a continuous ultrasound wave. For imaging, a single, brief voltage change is applied to the transducer, causing it to vibrate at its preferential frequency. Because the transducer continues to vibrate or “ring” for a short time ater it is stimulated by the voltage change, the ultrasound pulse will be several cycles long. he number of cycles of sound in each pulse determines the pulse length. For imaging, short pulse lengths are desirable because longer pulses result in poorer axial resolution. To reduce the pulse length, damping materials are used in the construction of the transducer. In clinical imaging applications, very short pulses are applied to the transducer, and the transducers have highly eicient damping. his results in very short pulses of ultrasound, generally consisting of only two or three cycles of sound. he ultrasound pulse generated by a transducer must be propagated in tissue to provide clinical information. Special transducer coatings and ultrasound coupling gels are necessary to allow eicient transfer of energy from the transducer to the body. Once in the body, the ultrasound pulses are propagated, relected, refracted, and absorbed, in accordance with the basic acoustic principles summarized earlier. he ultrasound pulses produced by the transducer result in a series of wavefronts that form a three-dimensional (3-D) beam of ultrasound. he features of this beam are inluenced by

constructive and destructive interference of the pressure waves, the curvature of the transducer, and acoustic lenses used to shape the beam. Interference of pressure waves results in an area near the transducer where the pressure amplitude varies greatly. his region is termed the near ield, or Fresnel zone. Farther from the transducer, at a distance determined by the radius of the transducer and the frequency, the sound ield begins to diverge, and the pressure amplitude decreases at a steady rate with increasing distance from the transducer. his region is called the far ield, or Fraunhofer zone. In modern multielement transducer arrays, precise timing of the iring of elements allows correction of this divergence of the ultrasound beam and focusing at selected depths. Only relections of pulses that return to the transducer are capable of stimulating the transducer with small pressure changes, which are converted into the voltage changes that are detected, ampliied, and processed to build an image based on the echo information.

Receiver When returning echoes strike the transducer face, minute voltages are produced across the piezoelectric elements. he receiver detects and ampliies these weak signals. he receiver also provides a means for compensating for the diferences in echo strength, which result from attenuation by diferent tissue thickness by control of time gain compensation (TGC) or depth gain compensation (DGC). Sound is attenuated as it passes into the body, and additional energy is removed as echoes return through tissue to the transducer. he attenuation of sound is proportional to the frequency and is constant for speciic tissues. Because echoes returning from deeper tissues are weaker than those returning from more supericial structures, they must be ampliied more by the receiver to produce a uniform tissue echo appearance (Fig. 1.10). his adjustment is accomplished by TGC controls that permit the user to selectively amplify the signals from deeper structures or to suppress the signals from supericial tissues, compensating for tissue attenuation. Although many newer machines provide

FIG. 1.10 Time Gain Compensation (TGC). Without TGC, tissue attenuation causes gradual loss of display of deeper tissues (A). In this example, tissue attenuation of 1 dB/cm/MHz is simulated for a transducer of 10 MHz. At a depth of 2 cm, the intensity is −20 dB (1% of initial value). By applying increasing ampliication or gain to the backscattered signal to compensate for this attenuation, a uniform intensity is restored to the tissue at all depths (B).

CHAPTER 1

Physics of Ultrasound

9

FIG. 1.11 Dynamic Range. The ultrasound receiver must compress the wide range of amplitudes returning to the transducer into a range that can be displayed to the user. Here, compression and remapping of the data to display dynamic ranges of 35, 40, 50, and 60 dB are shown. The widest dynamic range shown (60 dB) permits the best differentiation of subtle differences in echo intensity and is preferred for most imaging applications. The narrower ranges increase conspicuity of larger echo differences.

for some means of automatic TGC, the manual adjustment of this control is one of the most important user controls and may have a profound efect on the quality of the ultrasound image provided for interpretation. Another important function of the receiver is the compression of the wide range of amplitudes returning to the transducer into a range that can be displayed to the user. he ratio of the highest to the lowest amplitudes that can be displayed may be expressed in decibels and is referred to as the dynamic range. In a typical clinical application, the range of relected signals may vary by a factor of as much as 1 : 1012, resulting in a dynamic range of up to 120 dB. Although the ampliiers used in ultrasound machines are capable of handling this range of voltages, gray-scale displays are limited to display a signal intensity range of only 35 to 40 dB. Compression and remapping of the data are required to adapt the dynamic range of the backscattered signal intensity to the dynamic range of the display (Fig. 1.11). Compression is performed in the receiver by selective ampliication of weaker signals. Additional manual postprocessing controls permit the user to map selectively the returning signal to the display. hese controls afect the brightness of diferent echo levels in the image and therefore determine the image contrast.

Image Display Ultrasound signals may be displayed in several ways. Over the years, imaging has evolved from simple A-mode (amplitudemode) and bistable display to high-resolution, real-time, grayscale imaging. he earliest A-mode devices displayed the voltage produced across the transducer by the backscattered echo as a vertical delection on the face of an oscilloscope. he horizontal time sweep of the oscilloscope was calibrated to indicate the distance from the transducer to the relecting surface. In this form of display, the strength or amplitude of the relected sound is indicated by the height of the vertical delection displayed on the oscilloscope. With A-mode ultrasound, only the position and strength of a relecting structure are recorded. Another simple form of imaging, M-mode (motion-mode) ultrasound, displays echo amplitude and shows the position of

A

C

B

A

C

B

FIG. 1.12 M-Mode Display. M-mode ultrasound displays changes of echo amplitude and position with time. Display of changes in echo position is useful in the evaluation of rapidly moving structures such as cardiac valves and chamber walls. Here, the three major moving structures in the upper gray-scale image of the fetus are recorded in the corresponding M-mode image and include the near ventricular wall (A), the interventricular septum (B), and the far ventricular wall (C). The baseline is a time scale that permits the calculation of heart rate from the M-mode data.

moving relectors (Fig. 1.12). M-mode imaging uses the brightness of the display to indicate the intensity of the relected signal. he time base of the display can be adjusted to allow for varying degrees of temporal resolution, as dictated by clinical application. M-mode ultrasound is interpreted by assessing motion patterns of speciic relectors and determining anatomic relationships from characteristic patterns of motion. Currently, the major application of M-mode display is evaluation of embryonic and fetal heart rates, as well as in echocardiography, the rapid motion of cardiac valves and of cardiac chamber and vessel walls. M-mode imaging may play a future role in measurement of subtle changes in vessel wall elasticity accompanying atherogenesis. he mainstay of imaging with ultrasound is provided by real-time, gray-scale, B-mode display, in which variations in display intensity or brightness are used to indicate relected signals

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FIG. 1.13 B-Mode Imaging. A two-dimensional (2-D), real-time image is built by ultrasound pulses sent down a series of successive scan lines. Each scan line adds to the image, building a 2-D representation of echoes from the object being scanned. In real-time imaging, an entire image is created 15 to 60 times per second.

of difering amplitude. To generate a 2-D image, multiple ultrasound pulses are sent down a series of successive scan lines (Fig. 1.13), building a 2-D representation of echoes arising from the object being scanned. When an ultrasound image is displayed on a black background, signals of greatest intensity appear as white; absence of signal is shown as black; and signals of intermediate intensity appear as shades of gray. If the ultrasound beam is moved with respect to the object being examined and the position of the relected signal is stored, the brightest portions of the resulting 2-D image indicate structures relecting more of the transmitted sound energy back to the transducer. In most modern instruments, digital memory is used to store values that correspond to the echo intensities originating from corresponding positions in the patient. At least 28, or 256, shades of gray are possible for each pixel, in accord with the amplitude of the echo being represented. he image stored in memory in this manner can then be sent to a monitor for display. Because B-mode display relates the strength of a backscattered signal to a brightness level on the display device, it is important that the operator understand how the amplitude information in the ultrasound signal is translated into a brightness scale in the image display. Each ultrasound manufacturer ofers several options

for the way the dynamic range of the target is compressed for display, as well as the transfer function that assigns a given signal amplitude to a shade of gray. Although these technical details vary among machines, the way the operator uses them may greatly afect the clinical value of the inal image. In general, it is desirable to display as wide a dynamic range as possible, to identify subtle diferences in tissue echogenicity (see Fig. 1.11). Real-time ultrasound produces the impression of motion by generating a series of individual 2-D images at rates of 15 to 60 frames per second. Real-time, 2-D, B-mode ultrasound is the major method for ultrasound imaging throughout the body and is the most common form of B-mode display. Real-time ultrasound permits assessment of both anatomy and motion. When images are acquired and displayed at rates of several times per second, the efect is dynamic, and because the image relects the state and motion of the organ at the time it is examined, the information is regarded as being shown in real time. In cardiac applications the terms 2-D echocardiography and 2-D echo are used to describe real-time, B-mode imaging; in most other applications the term real-time ultrasound is used. Transducers used for real-time imaging may be classiied by the method used to steer the beam in rapidly generating each

CHAPTER 1

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B

Physics of Ultrasound

11

C

FIG. 1.14 Beam Steering. (A) Linear array. In a linear array transducer, individual elements or groups of elements are ired in sequence. This generates a series of parallel ultrasound beams, each perpendicular to the transducer face. As these beams move across the transducer face, they generate the lines of sight that combine to form the inal image. Depending on the number of transducer elements and the sequence in which they are ired, focusing at selected depths from the surface can be achieved Small high-frequency linear arrays are well-suited for small parts scanning. (B) Curved array. A variant of the linear array, the curved array uses tranducer elements arranged in an arc, producing a pie-shaped image. These transducers are well-suited for abdominal, pelvic, and fetal examinations. (C) Phased array. A phased array transducer produces a sector ield of view by iring multiple transducer elements in precise sequence to generate interference of acoustic wavefronts that steer the beam. The ultrasound beam that results generates a series of lines of sight at varying angles from one side of the transducer to the other, producing a sector image format. These transducers require a small contact area compared to most linear and curved arrays and are useful for scanning in areas where access is limited.

individual image, keeping in mind that as many as 30 to 60 complete images must be generated per second for real-time applications. Beam steering may be done through mechanical rotation or oscillation of the transducer or by electronic means (Fig. 1.14). Electronic beam steering is used in linear array and phased array transducers and permits a variety of image display formats. Most electronically steered transducers currently in use also provide electronic focusing that is adjustable for depth. Mechanical beam steering may use single-element transducers with a ixed focus or may use annular arrays of elements with electronically controlled focusing. For real-time imaging, transducers using mechanical or electronic beam steering generate displays in a rectangular or pie-shaped format. For obstetric, small parts, and peripheral vascular examinations, linear array transducers with a rectangular image format are oten used. he rectangular image display has the advantage of a larger ield of view near the surface but requires a large surface area for transducer contact. Sector scanners with either mechanical or electronic steering require only a small surface area for contact and are better suited for examinations in which access is limited.

transducer in a linear or circular motion. Mechanical sector scanners using one or more single-element transducers do not allow variable focusing. his problem is overcome by using annular array transducers. Although important in the early days of realtime imaging, mechanical sector scanners with ixed-focus, single-element transducers are not presently in common use.

Mechanical Sector Scanners

Linear Arrays Linear array transducers are used for small parts, vascular, and obstetric applications because the rectangular image format produced by these transducers is well suited for these applications.

Early ultrasound scanners used transducers consisting of a single piezoelectric element. To generate real-time images with these transducers, mechanical devices were required to move the

Arrays Current technology uses a transducer composed of multiple elements, usually produced by precise slicing of a piece of piezoelectric material into numerous small units, each with its own electrodes. Such transducer arrays may be formed in a variety of conigurations. Typically, these are linear, curved, phased, or annular arrays. High-density 2-D arrays have also been developed. By precise timing of the iring of combinations of elements in these arrays, interference of the wavefronts generated by the individual elements can be exploited to change the direction of the ultrasound beam, and this can be used to provide a steerable beam for the generation of real-time images in a linear or sector format.

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In these transducers, individual elements are arranged in a linear fashion. By iring the transducer elements in sequence, either individually or in groups, a series of parallel pulses is generated, each forming a line of sight perpendicular to the transducer face. hese individual lines of sight combine to form the image ield of view (see Fig. 1.14A). Depending on the number of transducer elements and the sequence in which they are ired, focusing at selected depths from the surface can be achieved.

Curved Arrays Linear arrays that have been shaped into convex curves produce an image that combines a relatively large surface ield of view with a sector display format (see Fig. 1.14B). Curved array transducers are used for a variety of applications, the larger versions serving for general abdominal, obstetric, and transabdominal pelvic scanning. Small, high-frequency, curved array scanners are oten used in transvaginal and transrectal probes and for pediatric imaging. Phased Arrays In contrast to mechanical sector scanners, phased array scanners have no moving parts. A sector ield of view is produced by multiple transducer elements ired in precise sequence under electronic control. By controlling the time and sequence at which the individual transducer elements are ired, the resulting ultrasound wave can be steered in diferent directions as well as focused at diferent depths (see Fig. 1.14C). By rapidly steering the beam to generate a series of lines of sight at varying angles from one side of the transducer to the other, a sector image format is produced. his allows the fabrication of transducers of relatively small size but with large ields of view at depth. hese transducers are particularly useful for neonatal head ultrasound, as well as for intercostal scanning, to evaluate the heart, liver, or spleen, and for examinations in other areas where access is limited. Two-Dimensional Arrays Transducer arrays can be formed either by slicing a rectangular piece of transducer material perpendicular to its long axis to produce a number of small rectangular elements or by creating a series of concentric elements nested within one another in a circular piece of piezoelectric material to produce an annular array. he use of multiple elements permits precise focusing. A particular advantage of 2-D array construction is that the beam can be focused in both the elevation plane and the lateral plane, and a uniform and highly focused beam can be produced (Fig. 1.15). hese arrays improve spatial resolution and contrast, reduce clutter, and are well suited for the collection of data from volumes of tissue for use in 3-D processing and display. Unlike linear 2-D arrays, in which delays in the iring of the individual elements may be used to steer the beam, annular arrays do not permit beam steering and, to be used for real-time imaging, must be steered mechanically.

Transducer Selection Practical considerations in the selection of the optimal transducer for a given application include not only the requirements for

FIG. 1.15 Two-Dimensional Array. High-density, two-dimensional (2-D) arrays consist of a 2-D matrix of transducer elements, permitting acquisition of data from a volume rather than a single plane of tissue. Precise electronic control of individual elements permits adjustable focusing on both azimuth and elevation planes.

spatial resolution, but also the distance of the target object from the transducer because penetration of ultrasound diminishes as frequency increases. In general, the highest ultrasound frequency permitting penetration to the depth of interest should be selected. For supericial vessels and organs, such as the thyroid, breast, or testicle, lying within 1 to 3 cm of the surface, imaging frequencies of 7.5 to 15 MHz are typically used. hese high frequencies are also ideal for intraoperative applications. If the region to be scanned is very supericial, such that the probe does not allow for focusing at the area of interest, a standof pad can be utilized. For evaluation of deeper structures in the abdomen or pelvis more than 12 to 15 cm from the surface, frequencies as low as 2.25 to 3.5 MHz may be required. When maximal resolution is needed, a high-frequency transducer with excellent lateral and elevation resolution at the depth of interest is required.

IMAGE DISPLAY AND STORAGE With real-time ultrasound, user feedback is immediate and is provided by video display. he brightness and contrast of the image on this display are determined by the ambient lighting in the examination room, the brightness and contrast settings of the video monitor, the system gain setting, and the TGC adjustment. he factor most afecting image quality in many ultrasound departments is probably improper adjustment of the video display, with a lack of appreciation of the relationship between the video display settings and the appearance of hard copy or images viewed on a workstation. Because of the importance of the real-time video display in providing feedback to the user, it is essential that the display and the lighting conditions under which it is viewed are standardized and matched to the display used for interpretation. Interpretation of images and archival storage of images may be in the form of transparencies printed on ilm by optical or laser cameras and printers, videotape, or digital picture

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Physics of Ultrasound

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C

FIG. 1.16 Tissue Harmonics. As sound is propagated through tissue, the high-pressure component of the wave travels more rapidly than the rarefactional component, producing distortion of the wave and generating higher-frequency components (harmonics). (A) The acoustic ield of the primary frequency is represented in blue. (B) The second harmonic (twice the primary frequency) is represented in red. (C) Using a broad-bandwidth transducer, the receiver can be tuned to generate an image from the harmonic frequency rather than the primary frequency. As a result, near ield clutter is reduced since the harmonic only develops at depth in the tissue and the beam proile is improved, leading to better spatial resolution.

archiving and communications system (PACS). Increasingly, digital storage is being used for archiving of ultrasound images.

SPECIAL IMAGING MODES Tissue Harmonic Imaging Variation of the propagation velocity of sound in fat and other tissues near the transducer results in a phase aberration that distorts the ultrasound ield, producing noise and clutter in the ultrasound image. Tissue harmonic imaging provides an approach for reducing the efects of phase aberrations.6 Nonlinear propagation of ultrasound through tissue is associated with the more rapid propagation of the high-pressure component of the ultrasound pressure wave than its negative (rarefactional) component. his results in increasing distortion of the acoustic pulse as it travels within the tissue and causes the generation of multiples, or harmonics, of the transmitted frequency (Fig. 1.16). Tissue harmonic imaging takes advantage of the generation, at depth, of these harmonics. Because the generation of harmonics requires interaction of the transmitted ield with the propagating tissue, harmonic generation is not present near the transducer/ skin interface, and it only becomes important some distance from the transducer. In most cases the near and far ields of the image are afected less by harmonics than by intermediate locations. Using broad-bandwidth transducers and signal iltration or coded pulses, the harmonic signals relected from tissue

interfaces can be selectively displayed. Because most imaging artifacts are caused by the interaction of the ultrasound beam with supericial structures or by aberrations at the edges of the beam proile, these artifacts are eliminated using harmonic imaging because the artifact-producing signals do not consist of suicient energy to generate harmonic frequencies and therefore are iltered out during image formation. Images generated using tissue harmonics oten exhibit reduced noise and clutter (Fig. 1.17). Because harmonic beams are narrower than the originally transmitted beams, spatial resolution is improved and side lobes are reduced.

Spatial Compounding An important source of image degradation and loss of contrast is ultrasound speckle. Speckle results from the constructive and destructive interaction of the acoustic ields generated by the scattering of ultrasound from small tissue relectors. his interference pattern gives ultrasound images their characteristic grainy appearance (see Fig. 1.6), reducing contrast (Fig. 1.18) and making the identiication of subtle features more diicult. By summing images from diferent scanning angles through spatial compounding (Fig. 1.19), signiicant improvement in the contrast-to-noise ratio can be achieved (Fig. 1.20). his is because speckle is random, and the generation of an image by compounding will reduce speckle noise because only the signal is reinforced. In addition, spatial compounding may reduce artifacts that result when an ultrasound beam strikes a specular relector at an angle

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FIG. 1.17 Tissue Harmonic Imaging. (A) Conventional image and (B) tissue harmonic image of gallbladder of patient with acute cholecystitis. Note the reduction of noise and clutter in the tissue harmonic image. Because harmonic beams do not interact with supericial structures and are narrower than the originally transmitted beam, spatial resolution is improved and clutter and side lobes are reduced. (With permission from Merritt CR. Technology update. Radiol Clin North Am. 2001;39:385-397.7)

FIG. 1.18 Effect of Speckle on Contrast. (A) Speckle noise partially obscures the simulated lesion. (B) The speckle has been reduced, increasing contrast resolution between the lesion and the background. (With permission from Merritt CR. Technology update. Radiol Clin North Am. 2001;39:385-397.7)

A

B

A

FIG. 1.19 Spatial Compounding. (A) Conventional imaging is limited to a ixed angle of incidence of ultrasound scan lines to tissue interfaces, resulting in poor deinition of specular relectors that are not perpendicular to the beam. (B) Spatial compounding combines images obtained by insonating the target from multiple angles. In addition to improving detection of interfaces, compounding reduces speckle noise because only the signal is reinforced; speckle is random and not reinforced. This improves contrast.

B

A

B

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Physics of Ultrasound

15

B

FIG. 1.20 Spatial Compounding. (A) Conventional image and (B) compound image of the thyroid. Note the reduced speckle as well as better deinition of regions (arrows) such as supericial tissue as well as small cysts and calciications.

greater or less than 90 degrees. In conventional real-time imaging, each scan line used to generate the image strikes the target at a constant, ixed angle. As a result, strong relectors that are not perpendicular to the ultrasound beam scatter sound in directions that prevent their clear detection and display. his in turn results in poor margin deinition and less distinct boundaries for cysts and other masses. Compounding has been found to reduce these artifacts. Limitations of compounding are diminished visibility of shadowing and enhancement; however, these are ofset by the ability to evaluate lesions, both with and without compounding, preserving shadowing and enhancement when these features are important to diagnosis.7

Three-Dimensional Ultrasound Dedicated 3-D scanners used for fetal (Fig. 1.21), gynecologic, and cardiac scanning may employ hardware-based image registration, high-density 2-D arrays, or sotware registration of scan planes as a tissue volume is acquired. 3-D imaging permits volume

data to be viewed in multiple imaging planes and allows accurate measurement of lesion volume.

Ultrasound Elastography Palpation is an efective method for detection of tissue abnormality based on detection of changes in tissue stifness or elasticity and may provide the earliest indication of disease, even when conventional imaging studies are normal. Ultrasound elastography provides a noninvasive method for evaluation of tissue stifness.8 Tissue contrast in conventional ultrasound imaging is based on the bulk modulus determined by the molecular composition of tissue, whereas elastography relects shear properties that are determined by a higher level of tissue organization, the strain modulus. his higher level of tissue organization is most likely to be altered by disease. he dynamic range of the strain modulus is several orders of magnitude greater than the bulk modulus, permitting contrast resolution far exceeding conventional ultrasound imaging.9 Elastography therefore ofers the potential for a

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PART I

Physics Key Points of Ultrasound Elastography Ultrasound imaging is based on tissue bulk modulus, relecting interactions at the molecular level. Changes in tissue stiffness based on the tissue shear modulus are important indications of disease. Ultrasound elastography provides relatative and quantitative assessment of tissue stiffness. Ultrasound elastography is based on tissue organization (strain modulus). Strain elastography provides an indication of relative tissue stiffness. Shear wave elastography provides a quantitative estimate of the tissue stiffness (strain modulus).

FIG. 1.21 Three-Dimensional Ultrasound Image, 24-Week Fetus. Three-dimensional ultrasound permits collection and review of data obtained from a volume of tissue in multiple imaging planes, as well as a rendering of surface features.

high degree of both sensitivity and speciicity in diferentiating normal and abnormal tissues.8,10,11 Tissue stifness or elasticity is expressed by Young modulus— the ratio of compression pressure (stress) and the resulting deformation (strain) E=σ ε where E is Young modulus expressed in Pa (pascals), σ is the stress, expressed in Newtons, and ε is displacement expressed in m2. Ultrasound-based elastography permits study of the elastic behavior of tissue through two general approaches (Fig. 1.22): strain elastography and shear wave elastography.

Strain Elastography Strain elastography involves measurement of longitudinal tissue displacement before and ater compression, usually by manual manipulation of the ultrasound transducer (see Fig. 1.22A). Speckle tracking using radiofrequency backscatter or Doppler is then used to evaluate tissue motion. Strain elastography cannot determine the Young modulus because the compression pressure (stress) cannot be measured directly. Instead, strain ratios are estimated by comparing lesion strain to surrounding normal tissues and displayed in the image in diferent shades of gray or through color maps (Fig. 1.23). Strain elastography provides an indication of relative stifness of an area of interest compared to its surroundings.

Shear Wave Elastography Longitudinal tissue compression results in the generation of transverse shear waves12,13 (see Fig. 1.22B). In shear wave elastography, shear waves are generated by repetitive compression produced by high-intensity pulses from the ultrasound transducer (see Fig. 1.22B). In contrast to longitudinal compressional waves that propagate very quickly in the human body (≈1540 m/sec), shear waves propagate slowly (≈1-50 m/sec). Shear waves are tracked with high frame rate images to determine their velocity. he propagation velocity of shear waves is directly proportional to Young modulus and provides a quantitative estimate of tissue stifness14,15 (Fig. 1.24).

IMAGE QUALITY he key determinants of the quality of an ultrasound image are its spatial, contrast, and temporal resolution, as well as freedom from certain artifacts.

Spatial Resolution he ability to diferentiate two closely situated objects as distinct structures is determined by the spatial resolution of the ultrasound device. Spatial resolution must be considered in three planes, with diferent determinants of resolution for each. Simplest is the resolution along the axis of the ultrasound beam, or axial resolution. With pulsed wave ultrasound, the transducer introduces a series of brief bursts of sound into the body. Each ultrasound pulse typically consists of two or three cycles of sound. he pulse length is the product of the wavelength and the number of cycles in the pulse. Axial resolution, the maximum resolution along the beam axis, is determined by the pulse length (Fig. 1.25). Because ultrasound frequency and wavelength are inversely related, the pulse length decreases as the imaging frequency increases. Because the pulse length determines the maximum resolution along the axis of the ultrasound beam, higher transducer frequencies provide higher image resolution. For example, a transducer operating at 5 MHz produces sound with a wavelength of 0.308 mm. If each pulse consists of three cycles of sound, the pulse length is slightly less than 1 mm, and this becomes the maximum resolution along the beam

CHAPTER 1

x

precompression

17

x’

y x=y

Physics of Ultrasound

y’ x’ < y’ compression

A

shear waves

B

FIG. 1.22 Elastography. (A) Strain elastography (SE), and (B) shear wave elastography (SWE). Strain elastograms are images of tissue stiffness generated by analysis of speckle displacements before and after mechanical compression of tissue. The precompression frame is compared to a frame obtained after compression. In this example, the lesion is compressed much less than the surrounding tissue, indicating relative stiffness. SE is not quantitative and indicates only the relative hardness or softness of lesions compared to their surroundings. In SWE (B) high-intensity compression pulses from the transducer are focused on an area of interest, resulting in the generation of low-frequency shear waves. Speckle displacement resulting from shear (transverse) waves is tracked with multiple imaging frames in order to estimate shear wave velocity. Shear wave velocity is directly related to Young modulus, permitting a quantitative estimate of tissue stiffness.

A

B

FIG. 1.23 Strain Elastograms. The upper frames (A) show in vivo images of swine liver containing a lesion produced by the injection of a small volume of absolute ethanol. In the precompression image (left) the lesion located within the circle is invisible. The elastogram (right) clearly delineates the lesion as an area of increased stiffness compared to the surrounding tissue. The lower frames (B) show a gray-scale image (left) and strain elastogram (right) of a mixed solid and cystic thyroid nodule. In the elastogram the color map displays relative stiffness with softer areas appearing as shades of red, orange, and yellow, and stiffer areas as dark blue. The nodule is heterogeneous with the relatively noncompressible cystic portions differentiated from more compressible surrounding tissue. (Courtesy of P. O’Kane, Thomas Jefferson University.)

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A - Normal liver v = 1.29 ± -.10 m/s

B - Cirrhotic liver v = 4.41 ± -.17 m/s

FIG. 1.24 Shear Wave Elastograms of (A) Normal and (B) Cirrhotic Liver. Shear wave velocities measured in liver tissue samples by shear wave elastography indicates a velocity of 1.29 ± 0.10 m/sec in the normal liver compared to a velocity of 4.41 ± 0.17 m/sec in the cirrhotic liver. Increased shear wave velocity is associated with increased tissue stiffness due to hepatic ibrosis. (Courtesy of P. O’Kane, Thomas Jefferson University.)

FIG. 1.25 Axial Resolution. Axial resolution is the resolution along (A) the beam axis and is determined by (B) the pulse length. The pulse length is the product of the wavelength (which decreases with increasing frequency) and the number of waves (usually two to three). Because the pulse length determines axial resolution, higher transducer frequencies provide higher image resolution. In (B) for example, a transducer operating at 5 MHz produces sound with a wavelength of 0.31 mm. If each pulse consists of three cycles of sound, the pulse length is slightly less than 1 mm, and objects A and B, which are 0.5 mm apart, cannot be resolved as separate structures. If the transducer frequency is increased to 15 MHz, the pulse length is less than 0.3 mm, permitting A and B to be identiied as separate structures.

A

B

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19

FIG. 1.26 Lateral and Elevation Resolution. Resolution in the planes perpendicular to the beam axis is an important determinant of image quality. Lateral resolution (L) is resolution in the plane perpendicular to the beam and parallel to the transducer and is determined by the width of the ultrasound beam. Lateral resolution is controlled by focusing the beam, usually by electronic phasing to alter the beam width at a selected depth of interest. Azimuth or elevation resolution (E) is determined by the slice thickness in the plane perpendicular to the beam and the transducer. Elevation resolution is controlled by the construction of the transducer. Both lateral resolution and elevation resolution are less than the axial resolution.

axis. If the transducer frequency is increased to 15 MHz, the pulse length is less than 0.4 mm, permitting resolution of smaller details. In addition to axial resolution, resolution in the planes perpendicular to the beam axis must also be considered. Lateral resolution refers to resolution in the plane perpendicular to the beam and parallel to the transducer and is determined by the width of the ultrasound beam. Azimuth resolution, or elevation resolution, refers to the slice thickness in the plane perpendicular to the beam and to the transducer (Fig. 1.26). he width and thickness of the ultrasound beam are important determinants of image quality. Excessive beam width and thickness limit the ability to delineate small features and may obscure shadowing and enhancement from small structures, such as breast microcalciications and small thyroid cysts. he width and thickness of the ultrasound beam determine lateral resolution and elevation resolution, respectively. Lateral and elevation resolutions are signiicantly poorer than the axial resolution of the beam. Lateral resolution is controlled by focusing the beam, usually by electronic phasing, to alter the beam width at a selected depth of interest. Elevation resolution is determined by the construction of the transducer and generally cannot be controlled by the user.

IMAGING PITFALLS In ultrasound, perhaps more than in any other imaging method, the quality of the information obtained is determined by the user’s ability to recognize and avoid artifacts and pitfalls. Many imaging artifacts are induced by errors in scanning technique or improper use of the instrument and therefore are preventable. Artifacts may cause misdiagnosis or may obscure important indings. Understanding artifacts is essential for correct interpretation of ultrasound examinations.

Many artifacts suggest the presence of structures not actually present. hese include reverberation, refraction, and side lobes. Reverberation artifacts arise when the ultrasound signal relects repeatedly between highly relective interfaces that are usually, but not always, near the transducer (Fig. 1.27). Reverberations may also give the false impression of solid structures in areas where only luid is present. Certain types of reverberation may be helpful because they allow the identiication of a speciic type of relector, such as a surgical clip. Reverberation artifacts can usually be reduced or eliminated by changing the scanning angle or transducer placement to avoid the parallel interfaces that contribute to the artifact. Refraction causes bending of the sound beam so that targets not along the axis of the transducer are insonated. heir relections are then detected and displayed in the image. his may cause structures to appear in the image that actually lie outside the volume the investigator assumes is being examined (see Fig. 1.7). Similarly, side lobes may produce confusing echoes that arise from sound beams that lie outside the main ultrasound beam (Fig. 1.28). hese side lobe artifacts are of clinical importance because they may create the impression of structures or debris in luid-illed structures (Fig. 1.29). Side lobes may also result in errors of measurement by reducing lateral resolution. As with most other artifacts, repositioning the transducer and its focal zone or using a diferent transducer will usually allow the diferentiation of artifactual from true echoes. Artifacts may also remove real echoes from the display or obscure information, and important pathologic features may be missed. Shadowing results when there is a marked reduction in the intensity of ultrasound deep to a strong relector or attenuator. Shadowing causes partial or complete loss of information due to attenuation of the sound by supericial structures. Another common cause of loss of image information is improper adjustment of system gain and TGC settings. Many low-level echoes

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FIG. 1.27 Reverberation Artifact. Reverberation artifacts arise when the ultrasound signal relects repeatedly between highly relective interfaces near the transducer, resulting in delayed echo return to the transducer. This appears in the image as a series of regularly spaced echoes at increasing depth. The echo at depth 1 is produced by simple relection from a strong interface. Echoes at levels 2, 3, and 4 are produced by multiple relections between this interface and the surface (simulated image).

FIG. 1.29 Side Lobe Artifact. Transverse image of the gallbladder reveals a bright internal echo (A) that suggests a band or septum within the gallbladder. This is a side lobe artifact related to the presence of a strong out-of-plane relector (B) medial to the gallbladder. The low-level echoes in the dependent portion of the gallbladder (C) are also artifactual and are caused by the same phenomenon. Side lobe and slice thickness artifacts are of clinical importance because they may create the impression of debris in luid-illed structures.

FIG. 1.28 Side Lobes. Although most of the energy generated by a transducer is emitted in a beam along the central axis of the transducer (A), some energy is also emitted at the periphery of the primary beam (B and C). These are called side lobes and are lower in intensity than the primary beam. Side lobes may interact with strong relectors that lie outside of the scan plane and produce artifacts that are displayed in the ultrasound image (see also Fig. 1.29).

are near the noise levels of the equipment, and considerable skill and experience are needed to adjust instrument settings to display the maximum information with the minimum noise. Poor scanning angles, inadequate penetration, and poor resolution may also result in loss of information. Careless selection of transducer frequency and lack of attention to the focal characteristics of

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Physics of Ultrasound

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B

FIG. 1.30 Multipath Artifact. (A) Mirror image of the uterus is created by relection of sound from an interface produced by gas in the rectum. (B) Echoes relected from the wall of an ovarian cyst create complex echo paths that delay return of echoes to the transducer. In both examples, the longer path of the relected sound results in the display of echoes at a greater depth than they should normally appear. In (A) this results in an artifactual image of the uterus appearing in the location of the rectum. In (B) the effect is more subtle and more likely to cause misdiagnosis because the artifact suggests a mural nodule in what is actually a simple ovarian cyst.

the beam will cause loss of clinically important information from deep, low-amplitude relectors and small targets. Ultrasound artifacts may alter the size, shape, and position of structures. For example, a multipath artifact is created when the path of the returning echo is not the one expected, resulting in display of the echo at an improper location in the image (Fig. 1.30).

Shadowing and Enhancement Although most artifacts degrade the ultrasound image and impede interpretation, two artifacts of clinical value are shadowing and enhancement. Again, shadowing results when an object (e.g., calculus) attenuates sound more rapidly than surrounding tissues. Enhancement occurs when an object (e.g., cyst) attenuates less than surrounding tissues. Failure of TGC applied to normal tissue to compensate properly for the attenuation of more highly attenuating (shadowing) or poorly attenuating (enhancing) structures produces the artifact (Fig. 1.31). Because attenuation increases with frequency, the efects of shadowing and enhancement are greater at higher than at lower frequencies. he conspicuity of shadowing and enhancement is reduced by excessive beam width, improper focal zone placement, and use of spatial compounding.

DOPPLER SONOGRAPHY Conventional B-mode ultrasound imaging uses pulse-echo transmission, detection, and display techniques. Brief pulses of ultrasound energy emitted by the transducer are relected from acoustic interfaces within the body. Precise timing allows determination of the depth from which the echo originates. When pulsed wave ultrasound is relected from an interface, the backscattered (relected) signal contains amplitude, phase, and frequency information (Fig. 1.32). his information permits inference of the position, nature, and motion of the interface relecting the pulse. B-mode ultrasound imaging uses only the amplitude information in the backscattered signal to generate the image, with diferences in the strength of relectors displayed in the image in varying shades of gray. Rapidly moving targets, such as red cells in the bloodstream, produce echoes of low

amplitude that are not usually displayed, resulting in a relatively anechoic pattern within the lumens of large vessels. Although gray-scale display relies on the amplitude of the backscattered ultrasound signal, additional information is present in the returning echoes that can be used to evaluate the motion of moving targets.16 When high-frequency sound impinges on a stationary interface, the relected ultrasound has essentially the same frequency or wavelength as the transmitted sound. If the relecting interface is moving with respect to the sound beam emitted from the transducer, however, there is a change in the frequency of the sound scattered by the moving object (Fig. 1.33). his change in frequency is directly proportional to the velocity of the relecting interface relative to the transducer and is a result of the Doppler efect. he relationship of the returning ultrasound frequency to the velocity of the relector is described by the Doppler equation, as follows: ∆F = (FR − FT ) = 2 ⋅ FT ⋅ v c he Doppler frequency shit is ΔF; FR is the frequency of sound relected from the moving target; FT is the frequency of sound emitted from the transducer; v is the velocity of the target toward the transducer; and c is the velocity of sound in the medium. he Doppler frequency shit (ΔF) applies only if the target is moving directly toward or away from the transducer (Fig. 1.34A). In most clinical settings the direction of the ultrasound beam is seldom directly toward or away from the direction of low, and the ultrasound beam usually approaches the moving target at an angle designated as the Doppler angle (Fig. 1.34B). In this case, ΔF is reduced in proportion to the cosine of this angle, as follows: ∆F = (FR − FT ) = 2 ⋅ FT ⋅ v ⋅ cos θ c where θ is the angle between the axis of low and the incident ultrasound beam. If the Doppler angle can be measured, estimation of low velocity is possible. Accurate estimation of target velocity requires precise measurement of both the Doppler frequency shit and the angle of insonation to the direction of

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–0 dB

Physics

Uncorrected

–0 dB

Gain compensated

–10 dB

–25 dB

+10 dB

+10–25 = –15 db

–20 dB

–30 dB

+20 dB

+10–35 = –15 db

B

A –30 dB –0 dB

–10 + 10 dB

–40 dB Gain compensated

+10–3 = +7 dB

C –20 + 20 dB

+30–5 = –15 dB

+30 dB

+20–13 = +7 dB

FIG. 1.31 Shadowing and Enhancement. (A) Uncorrected image of a shadowing breast mass shows that the mass attenuates 25 dB, 15 dB more than the surrounding normal tissue, which attenuates only 10 dB. (B) Application of appropriate time gain compensation (TGC) results in proper display of the normal breast tissue. However, because of the increased attenuation of the mass, a shadow results. (C) Similarly, the cyst attenuates 7 dB less than the normal tissue, and TGC correction for normal tissue results in overampliication of the signals deep to the cyst, producing enhancement of these tissues.

target movement. As the Doppler angle (θ) approaches 90 degrees, the cosine of θ approaches 0. At an angle of 90 degrees, there is no relative movement of the target toward or away from the transducer, and no Doppler frequency shit is detected (Fig. 1.35). Because the cosine of the Doppler angle changes rapidly for angles more than 60 degrees, accurate angle correction requires that Doppler measurements be made at angles of less than 60 degrees. Above 60 degrees, relatively small changes in the Doppler angle are associated with large changes in cosθ, and therefore a small error in estimation of the Doppler angle may result in a large error in the estimation of velocity. hese considerations are important in using both duplex and color Doppler instruments. Optimal imaging of the vessel wall is obtained when

the axis of the transducer is perpendicular to the wall, whereas maximal Doppler frequency diferences are obtained when the transducer axis and the direction of low are at a relatively small angle. In peripheral vascular applications, it is highly desirable that measured Doppler frequencies be corrected for the Doppler angle to provide velocity measurement. his allows comparison of data from systems using diferent Doppler frequencies and eliminates error in interpretation of frequency data obtained at diferent Doppler angles. For abdominal applications, angle-corrected velocity measurements are encouraged, although qualitative assessments of low are oten made using only the Doppler frequency shit data.

Physics of Ultrasound

CHAPTER 1

FT

FIG. 1.32 Backscattered Information. The backscattered ultrasound signal contains amplitude, phase, and frequency information. Signals B and C differ in amplitude but have the same frequency. Amplitude differences are used to generate B-mode images. Signals A and B differ in frequency but have similar amplitudes. Such frequency differences are the basis of Doppler ultrasound.

23

FR

v ∆F = (FR − FT) = 2 • FT • v c

A A

Stationary target: (FR − FT) = 0

B

Target motion toward transducer: (FR − FT) > 0 FT

FR

θ

C

Target motion away from transducer: (FR − FT) < 0

FIG. 1.33 Doppler Effect. (A) Stationary target. If the relecting interface is stationary, the backscattered ultrasound has the same frequency or wavelength as the transmitted sound, and there is no difference in the transmitted frequency (FT) and the relected frequency (FR). (B) and (C) Moving targets. If the relecting interface is moving with respect to the sound beam emitted from the transducer, there is a change in the frequency of the sound scattered by the moving object. When the interface moves toward the transducer (B), the difference in relected and transmitted frequencies is greater than zero. When the target is moving away from the transducer (C), this difference is less than zero. The Doppler equation is used to relate this change in frequency to the velocity of the moving object.

Doppler Signal Processing and Display Several options exist for the processing of ΔF, the Doppler frequency shit, to provide useful information regarding the direction and velocity of blood. Doppler frequency shits encountered clinically are in the audible range. his audible signal may be analyzed by ear and, with training, the operator can identify many low characteristics. More oten, the Doppler shit data are displayed in graphic form as a time-varying plot of the frequency

v

B

∆F = (FR − FT) = 2 • FT • v • cos θ c

FIG. 1.34 Doppler Equations. The Doppler equation describes the relationship of the Doppler frequency shift to target velocity. (A) In its simplest form, it is assumed that the direction of the ultrasound beam is parallel to the direction of movement of the target. This situation is unusual in clinical practice. More often, the ultrasound impinges on the vessel at angle θ. (B) In this case the Doppler frequency shift detected is reduced in proportion to the cosine of θ. ΔF, Frequency shift; FR, relected frequency; FT, transmitted frequency; v, velocity.

spectrum of the returning signal. A fast Fourier transformation is used to perform the frequency analysis. he resulting Doppler frequency spectrum displays the following (Fig. 1.36): • Variation with time of the Doppler frequencies present in the volume sampled

24

PART I

θ = 60° cos θ = 0.5 ∆F = 0.5

Physics θ = 90° cos θ = 0.0 ∆F = 0.0

θ = 0° cos θ = 1.0 ∆F = 1.0

amplitude of each frequency component is displayed in gray scale as part of the spectrum. he presence of a large number of diferent frequencies at a given point in the cardiac cycle results in spectral broadening. In color Doppler imaging systems, a representation of the Doppler frequency shit is displayed as a feature of the image itself (see Fig. 1.36). In addition to the detection of Doppler frequency shit data from each pixel in the image, these systems may also provide range-gated pulsed wave Doppler with spectral analysis for display of Doppler data.

Doppler Instrumentation

FIG. 1.35 Effect of Doppler Angle on Frequency Shift. At an angle of 60 degrees, the detected frequency shift (ΔF) detected by the transducer is only 50% of the shift detected at an angle of 0 degrees. At 90 degrees, there is no relative movement of the target toward or away from the transducer, and no frequency shift is detected. The detected Doppler frequency shift is reduced in proportion to the cosine of the Doppler angle. Because the cosine of the angle changes rapidly at angles above 60 degrees, the use of Doppler angles of less than 60 degrees is recommended in making velocity estimates.

B

A

FIG. 1.36 Doppler Display. (A) Doppler frequency spectrum waveform shows changes in low velocity and direction by vertical delections of the waveform above and below the baseline. The width of the spectral waveform (spectral broadening) is determined by the range of frequencies present at any instant in time (arrow). A brightness (gray) scale is used to indicate the amplitude of each frequency component. (B) Color Doppler imaging. Amplitude data from stationary targets provide the basis for the B-mode image. Signal phase provides information about the presence and direction of motion, and changes in frequency relate to the velocity of the target. Backscattered signals from red blood cells are displayed in color as a function of their motion toward or away from the transducer, and the degree of the saturation of the color is used to indicate the frequency shift from moving red cells.

• he envelope of the spectrum, representing the maximum frequencies present at any given point in time • he width of the spectrum at any point, indicating the range of frequencies present he amplitude of the Doppler signal is related to the number of targets moving at a given velocity. In many instruments the

In contrast to A-mode, M-mode, and B-mode gray-scale ultrasonography, which display the information from tissue interfaces, Doppler ultrasound instruments are optimized to display low information. he simplest Doppler devices use continuous wave (CW) Doppler rather than pulsed wave ultrasound, using two transducers that transmit and receive ultrasound continuously. he transmit and receive beams overlap in a sensitive volume at some distance from the transducer face (Fig. 1.37A). Although direction of low can be determined with CW Doppler, these devices do not allow discrimination of motion coming from various depths, and the source of the signal being detected is diicult, if not impossible, to ascertain with certainty. Inexpensive and portable, CW Doppler instruments are used primarily at the bedside or intraoperatively to conirm the presence of low in supericial vessels. Because of the limitations of CW systems, most applications use range-gated, pulsed wave Doppler. Rather than a continuous wave of ultrasound emission, pulsed wave Doppler devices emit brief pulses of ultrasound energy (see Fig. 1.37B). Using pulses of sound permits use of the time interval between the transmission of a pulse and the return of the echo as a means of determining the depth from which the Doppler shit arises. he principles are similar to the echo-ranging principles used for imaging (see Fig. 1.4). In a pulsed wave Doppler system the sensitive volume from which low data are sampled can be controlled in terms of shape, depth, and position. When pulsed wave Doppler is combined with a 2-D, real-time, B-mode imager in the form of a duplex scanner, the position of the Doppler sample can be precisely controlled and monitored. In color Doppler imaging (Fig. 1.38A), frequency shit information determined from Doppler measurements is displayed as a feature of the image itself.17 Stationary or slowly moving targets provide the basis for the B-mode image. Signal phase provides information about the presence and direction of motion, and changes in echo signal frequency relate to the velocity of the target. Backscattered signals from red blood cells are displayed in color as a function of their motion toward or away from the transducer, and the degree of the saturation of the color is used to indicate the relative frequency shit produced by the moving red cells. Color Doppler low imaging (CDFI) expands conventional duplex sonography by providing additional capabilities. he use of color saturation to display variations in Doppler shit frequency allows an estimation of relative velocity from the image alone, provided that variations in the Doppler angle are noted. he

CHAPTER 1

A

Physics of Ultrasound

25

B

FIG. 1.37 Continuous Wave and Pulsed Wave Doppler. (A) Continuous wave (CW) Doppler uses separate transmit and receive crystals that continuously transmit and receive ultrasound. Although able to detect the presence and direction of low, CW devices are unable to distinguish signals arising from vessels at different depths (green-shaded area). (B) Using the principle of ultrasound ranging (see Fig. 1.4), pulsed wave Doppler permits the sampling of low data from selected depths by processing only the signals that return to the transducer after precisely timed intervals. The operator is able to control the position of the sample volume and, in duplex systems, to view the location from which the Doppler data are obtained.

Limitations of Color Doppler Flow Imaging

Advantages of Power Doppler

Angle dependence Aliasing Inability to display entire Doppler spectrum in the image Artifacts caused by noise

No aliasing Much less angle dependence Noise: a homogeneous background color Increased sensitivity for low detection

display of low throughout the image ield allows the position and orientation of the vessel of interest to be observed at all times. he display of spatial information with respect to velocity is ideal for display of small, localized areas of turbulence within a vessel, which provide clues to stenosis or irregularity of the vessel wall caused by atheroma, trauma, or other disease. Flow within the vessel is observed at all points, and stenotic jets and focal areas of turbulence are displayed that might be overlooked with duplex instrumentation. he contrast of low within the vessel lumen permits visualization of small vessels that are not visible when using conventional imagers and enhances the visibility of wall irregularity. CDFI aids in determination of the direction of low and measurement of the Doppler angle.

Power Doppler An alternative to the display of frequency information with color Doppler imaging is to use a color map that displays the integrated power of the Doppler signal instead of its mean frequency shit18 (see Fig. 1.38B). Because frequency shit data are not displayed, there is no aliasing. he image does not provide information related to low direction or velocity, and power Doppler imaging is much less angle dependent than frequency-based color Doppler display. In contrast to color Doppler, where noise may appear in the image as any color, power Doppler permits noise to be assigned to a homogeneous background color that does not greatly interfere with the image. his results in a signiicant increase in the usable

dynamic range of the scanner, permitting higher efective gain settings and increased sensitivity for low detection (Fig. 1.39).

Interpretation of the Doppler Spectrum Doppler data components that must be evaluated both in spectral display and in color Doppler imaging include the Doppler shit frequency and amplitude, the Doppler angle, the spatial distribution of frequencies across the vessel, and the temporal variation of the signal. Because the Doppler signal itself has no anatomic signiicance, the examiner must interpret the Doppler signal and then determine its relevance in the context of the image. he detection of a Doppler frequency shit indicates movement of the target, which in most applications is related to the presence of low. he sign of the frequency shit (positive or negative) indicates the direction of low relative to the transducer. Vessel stenosis is typically associated with large Doppler frequency shits in both systole and diastole at the site of greatest narrowing, with turbulent low in poststenotic regions. In peripheral vessels, analysis of the Doppler changes allows accurate prediction of the degree of vessel narrowing. Information related to the resistance to low in the distal vascular tree can be obtained by analysis of changes of blood velocity with time, as shown in the Doppler spectral display. Doppler imaging can provide information about blood low in both large and small vessels. Small vessel impedance is relected in the Doppler spectral waveform of aferent vessels.

26

Physics

PART I

A

B

FIG. 1.38 Color Flow and Power Doppler. (A) Color low Doppler imaging uses a color map to display information based on the detection of frequency shifts from moving targets. Noise in this form of display appears across the entire frequency spectrum and limits sensitivity. (B) Power Doppler uses a color map to show the distribution of the power or amplitude of the Doppler signal. Flow direction and velocity information are not provided, but noise is reduced, allowing higher gain settings and improved sensitivity for low detection.

A

B FIG. 1.39 Frequency and Power Mode Color Mapping. (A) Conventional color Doppler uses the color map to show differences in low direction and Doppler frequency shift. Because noise appears over the entire frequency spectrum, gain levels are limited to those that do not introduce excessive noise. (B) Power Doppler color map, in contrast, indicates the amplitude of the Doppler signal. Because most noise is of low amplitude, it is possible to map this to colors near the background. This permits the use of high gain settings that offer signiicant improvements over conventional color Doppler in low detection.

CHAPTER 1

Physics of Ultrasound

27

FIG. 1.40 Impedance. High-resistance waveform in brachial artery (A), produced by inlating forearm blood pressure cuff to a pressure above the systolic blood pressure. As a result of high peripheral resistance, there is low systolic amplitude and reversed diastolic low. Low-resistance waveform in peripheral vascular bed (B), caused by vasodilation stimulated by the prior ischemia. Immediately after release of 3 minutes of occluding pressure, the Doppler waveform showed increased amplitude and rapid antegrade low throughout diastole.

Fig. 1.40 provides a graphic example of the changes in the Doppler spectral waveform resulting from physiologic changes in the resistance of the vascular bed supplied by a normal brachial artery. A blood pressure cuf has been inlated to above systolic pressure to occlude the distal branches supplied by the brachial artery. his occlusion causes reduced systolic amplitude and cessation of diastolic low, resulting in a waveform diferent than that found in the normal resting state. During the period of ischemia induced by pressure cuf occlusion of the forearm vessels, vasodilation has occurred. Immediately ater release of the occluding pressure the Doppler waveform relects a low-resistance peripheral vascular bed with increased systolic amplitude and rapid low throughout diastole, typical for vasodilation. Doppler indices include the systolic-to-diastolic ratio (S/D ratio), resistive index (RI), and pulsatility index (PI) (Fig. 1.41). hese compare blood low in systole and diastole, show resistance to low in the peripheral vascular bed, and help evaluate the perfusion of tumors, renal transplants, the placenta, and other organs. With Doppler ultrasound, it is therefore possible to identify vessels, determine the direction of blood low, evaluate narrowing or occlusion, and characterize blood low to organs and tumors. Analysis of the Doppler shit frequency with time can be used to infer both proximal stenosis and changes in distal vascular impedance. Most work using pulsed wave Doppler imaging has emphasized the detection of stenosis, thrombosis, and low disturbances in major peripheral arteries and veins. In these applications, measurement of peak systolic and end diastolic

FIG. 1.41 Doppler Indices. Doppler low indices used to characterize peripheral resistance are based on the peak systolic frequency or velocity (A), the minimum or end diastolic frequency or velocity (B), and the mean frequency or velocity (M). The most frequently used indices are the systolic-to-diastolic ratio (A/B); resistive index [(A-B)/A]; and pulsatility index [(A-B)/M]. In calculation of the pulsatility index, the minimum diastolic velocity or frequency is used; calculation of the systolic-to-diastolic ratio and resistive index use the end diastolic value.

frequency or velocity, analysis of the Doppler spectrum, and calculation of certain frequency or velocity ratios have been the basis of analysis. Changes in the spectral waveform measured by indices comparing low in systole and diastole indicate the resistance of the vascular bed supplied by the vessel and the changes resulting from a variety of pathologic conditions.

28

PART I

Physics

Changes in Doppler indices from normal may help in the early identiication of rejection of transplanted organs, parenchymal dysfunction, and malignancy. Although useful, these measurements are inluenced not only by the resistance to low in peripheral vessels, but also by heart rate, blood pressure, vessel wall length and elasticity, extrinsic organ compression, and other factors.

Interpretation of Color Doppler Although the graphic presentation of color Doppler imaging suggests that interpretation is made easier, the complexity of the color Doppler image actually makes this a more demanding image to evaluate than the simple Doppler spectrum. Nevertheless, color Doppler imaging has important advantages over pulsed wave duplex Doppler imaging, in which low data are obtained only from a small portion of the area being imaged. To be conident that a conventional Doppler study has achieved reasonable sensitivity and speciicity in detection of low disturbances, a methodical search and sampling of multiple sites within the ield of interest must be performed. In contrast, CDFI devices permit simultaneous sampling of multiple sites and are less susceptible to this error. Although color Doppler can indicate the presence of blood low, misinterpretation of color Doppler images may result in important errors. Each color pixel displays a representation of the Doppler frequency shit detected at that point. he frequency shit displayed is not the peak frequency present at sampling but rather a weighted mean frequency that attempts to account for the range of frequencies and their relative amplitudes at sampling. Manufacturers use diferent methods to derive the weighted mean frequency displayed in their systems. In addition, the pulse repetition frequency (PRF) and the color map selected to display

A

the detected range of frequencies afect the color displayed. he color assigned to each Doppler pixel is determined by the Doppler frequency shit (which in turn is determined by target velocity and Doppler angle), the PRF, and the color map selected for display; therefore the interpretation of a color Doppler image must consider each of these variables. Although most manufacturers provide on-screen indications suggesting a relationship between the color displayed and low velocity, this is misleading because color Doppler does not show velocity and only indicates the weighted mean frequency shit measured in the vessel; without correction for the efect of the Doppler angle, velocity cannot be estimated (Fig. 1.42). Because the frequency shit at a given point is a function of velocity and the Doppler angle, depending on the frequency shit present in a given pixel and the PRF, any velocity may be represented by any color, and under certain circumstances, low-velocity low may not be shown at all. As with spectral Doppler, aliasing is determined by PRF. With color Doppler, aliasing causes frequencies greater than twice the PRF to “wrap around” and to be displayed in the opposite colors of the color map. Inexperienced users tend to associate color Doppler aliasing with elevated velocity, but even low velocities may show marked aliasing if PRF is suiciently low. As PRF is increased, aliasing of high Doppler frequency shits is reduced; however, low-frequency shits may be eliminated from the display, resulting in diagnostic error (Fig. 1.43).

Other Technical Considerations Although many problems and artifacts associated with B-mode imaging (e.g., shadowing) are encountered with Doppler sonography, the detection and display of frequency information related to moving targets present additional technical considerations. It is important to understand the source of these artifacts and

B

FIG. 1.42 Color Doppler. Each color pixel in a color Doppler image represents the Doppler frequency shift at that point, and it cannot be used to estimate velocity. Even though the points A and B have similar color values and therefore similar Doppler frequencies, the velocity at A is much higher than at B because of the large Doppler angle at A compared to B. The velocity represented by a given Doppler frequency increases in proportion to the Doppler angle.

CHAPTER 1

A (PRF = 700 Hz)

Physics of Ultrasound

B (PRF = 4500 Hz)

FIG. 1.43 Pulse Repetition Frequency (PRF). Depending on the color map selected, velocity of the target, Doppler velocity may appear as any color with color Doppler. (A) and (B) are sonograms of identical vessels. (A) PRF is 700 Hz, of the higher Doppler frequency shifts in the carotid artery but permits the identiication of relatively slow low in the 4500 Hz, eliminating aliasing in the artery but also suppressing the display of the low Doppler frequencies in the internal

their inluence on the interpretation of the low measurements obtained in clinical practice.

Doppler Frequency A primary objective of the Doppler examination is the accurate measurement of characteristics of low within a vascular structure. he moving red blood cells that serve as the primary source of the Doppler signal act as point scatterers of ultrasound rather than specular relectors. his interaction results in the intensity of the scattered sound varying in proportion to the fourth power of the frequency, which is important in selecting the Doppler frequency for a given examination. As the transducer frequency increases, Doppler sensitivity improves, but attenuation by tissue also increases, resulting in diminished penetration. Careful balancing of the requirements for sensitivity and penetration is an important responsibility of the operator during a Doppler examination. Because many abdominal vessels lie several centimeters beneath the surface, Doppler frequencies in the range of 3 to 3.5 MHz are usually required to permit adequate penetration. Wall Filters Doppler instruments detect motion not only from blood low but also from adjacent structures. To eliminate these low-frequency signals from the display, most instruments use high pass ilters, or “wall” ilters, which remove signals that fall below a given frequency limit. Although efective in eliminating low-frequency noise, these ilters may also remove signals from low-velocity blood low (Fig. 1.44). In certain clinical situations the measurement of these slower low velocities is of clinical importance, and the improper selection of the wall ilter may result in serious errors of interpretation. For example, low-velocity venous low may not be detected if an improper ilter is used, and low-velocity diastolic low in certain arteries may also be eliminated from the display, resulting in errors in the calculation of Doppler indices, such as the systolic-to-diastolic ratio or resistive index. In general, the ilter should be kept at the lowest practical level, usually 50 to 100 Hz. Spectral Broadening Spectral broadening refers to the presence of a large range of low velocities at a given point in the pulse cycle and, by indicating

29

angle, and PRF, a given which results in aliasing jugular vein. (B) PRF is jugular vein.

Major Sources of Doppler Imaging Artifacts DOPPLER FREQUENCY Higher frequencies lead to more tissue attenuation Wall ilters remove signals from low-velocity blood low INCREASE IN SPECTRAL BROADENING Excessive system gain or changes in dynamic range of the gray-scale display Excessively large sample volume Sample volume too near the vessel wall INCREASE IN ALIASING Decrease in pulse repetition frequency (PRF) Decrease in Doppler angle Higher Doppler frequency transducer DOPPLER ANGLE Relatively inaccurate above 60 degrees SAMPLE VOLUME SIZE Large sample volumes increase vessel wall noise

turbulence, is an important criterion of high-grade vessel narrowing. Excessive system gain or changes in the dynamic range of the gray-scale display of the Doppler spectrum may suggest spectral broadening; opposite settings may mask broadening of the Doppler spectrum, causing diagnostic inaccuracy. Spectral broadening may also be produced by the selection of an excessively large sample volume or by the placement of the sample volume too near the vessel wall, where slower velocities are present (Fig. 1.45).

Aliasing Aliasing is an artifact arising from ambiguity in the measurement of high Doppler frequency shits. To ensure that samples originate from only a selected depth when using a pulsed wave Doppler system, it is necessary to wait for the echo from the area of interest before transmitting the next pulse. his limits the rate with which pulses can be generated, a lower PRF being required for greater depth. he PRF also determines the maximum depth from which unambiguous data can be obtained. If PRF is less than twice the maximum frequency shit produced by movement

30

PART I

Physics

A

B

FIG. 1.44 Wall Filters. Wall ilters are used to eliminate low-frequency noise from the Doppler display, but high wall ilter settings may result in interpretation errors. Here the effect on the display of low-velocity low is shown with wall ilter settings of (A) 100 Hz and (B) 400 Hz. In general, wall ilters should be kept at the lowest practical level, usually in the range of 50 to 100 Hz.

of the target (Nyquist limit), aliasing results (Fig. 1.46). When PRF is less than twice the frequency shit being detected, lower frequency shits than are actually present are displayed. Because of the need for lower PRFs to reach deep vessels, signals from deep abdominal arteries are prone to aliasing if high velocities are present. In practice, aliasing is usually readily recognized. Aliasing can be reduced by increasing the PRF, by increasing the Doppler angle (thereby decreasing the frequency shit), or by using a lower-frequency Doppler transducer.

Doppler Angle When making Doppler measurement of velocity, it is necessary to correct for the Doppler angle. he accuracy of a velocity estimate obtained with Doppler is only as great as the accuracy of the measurement of the Doppler angle. his is particularly true as the Doppler angle exceeds 60 degrees. In general, the Doppler angle is best kept at 60 degrees or less because small changes in the Doppler angle above 60 degrees result in substantial changes in the calculated velocity. herefore measurement inaccuracies result in much greater errors in velocity estimates than do similar errors at lower Doppler angles. Angle correction is not required for the measurement of Doppler indices such as the resistive index, because these measurements are based only on the relationship of the systolic and diastolic amplitudes. Sample Volume Size With pulsed wave Doppler systems, the length of the Doppler sample volume can be controlled by the operator, and the width is determined by the beam proile. Analysis of Doppler signals requires that the sample volume be adjusted to exclude as much of the unwanted clutter as possible from near the vessel walls.

Doppler Gain As with imaging, proper gain settings are essential to achieving accurate and reproducible Doppler measurements. Excessive Doppler gain results in noise appearing at all frequencies and may result in overestimation of velocity. Conversely, insuicient gain may result in underestimation of peak velocity (Fig. 1.47). A consistent approach to setting Doppler gain should be used. Ater placing the sample volume in the vessel, the Doppler gain should be increased to a level where noise is visible in the image, then gradually reduced to the point at which the noise irst disappears completely.

OPERATING MODES: CLINICAL IMPLICATIONS Ultrasound devices may operate in several modes, including real-time, color Doppler, spectral Doppler, and M-mode imaging. Imaging is produced in a scanned mode of operation. In scanned modes, pulses of ultrasound from the transducer are directed down lines of sight that are moved or steered in sequence to generate an image. his means that the number of ultrasound pulses arriving at a given point in the patient over a given interval is relatively small, and relatively little energy is deposited at any given location. In contrast, spectral Doppler imaging is an unscanned mode of operation in which multiple ultrasound pulses are sent in repetition along a line to collect the Doppler data. In this mode the beam is stationary, resulting in considerably greater potential for heating than in imaging modes. For imaging, PRFs are usually a few thousand hertz with very short pulses. Longer pulse durations are used with Doppler than with other imaging

CHAPTER 1

Physics of Ultrasound

31

With current devices operating in imaging modes, concerns about bioefects are minimal because intensities suicient to produce measurable heating are seldom used. With Doppler ultrasound, the potential for thermal efects is greater. Preliminary measurements on commercially available instruments suggest that at least some of these instruments are capable of producing temperature rises of greater than 1°C at sot tissue/bone interfaces, if the focal zone of the transducer is held stationary. Care is therefore warranted when Doppler measurements are obtained at or near sot tissue/bone interfaces, as in the second and third trimester of pregnancy. hese applications require thoughtful application of the principle of ALARA (as low as reasonably achievable). Under ALARA the user should use the lowest possible acoustic exposure to obtain the necessary diagnostic information.

Bioeffects and User Concerns

FIG. 1.45 Spectral Broadening. The range of velocities detected at a given time in the pulse cycle is relected in the Doppler spectrum as spectral broadening. (A) Normal spectrum. Spectral broadening may arise from turbulent low in association with vessel stenosis. (B) and (C) Artifactual spectral broadening. This may be produced by improper positioning of the sample volume near the vessel wall, use of (B) an excessively large sample volume, or (C) an excessive system gain.

modes. In addition, to avoid aliasing and other artifacts with Doppler imaging, it is oten necessary to use higher PRFs than with other imaging applications. Longer pulse duration and higher PRF result in higher duty factors for Doppler modes of operation and increase the amount of energy introduced in scanning. Color Doppler, although a scanned mode, produces exposure conditions between those of real-time and Doppler imaging because color Doppler devices tend to send more pulses down each scan line and may use longer pulse durations than imaging devices. Clearly, every user needs to be aware that switching from an imaging to a Doppler mode changes the exposure conditions and the potential for biologic efects (bioefects).

Although users of ultrasound need to be aware of bioefects concerns, another key factor to consider in the safe use of ultrasound is the user. he knowledge and skill of the user are major determinants of the risk-to-beneit implications of the use of ultrasound in a speciic clinical situation. For example, an unrealistic emphasis on risks may discourage an appropriate use of ultrasound, resulting in harm to the patient by preventing the acquisition of useful information or by subjecting the patient to another, more hazardous examination. he skill and experience of the individual performing and interpreting the examination are likely to have a major impact on the overall beneit of the examination. In view of the rapid growth of ultrasound and its proliferation into the hands of minimally trained clinicians, many more patients are likely to be harmed by misdiagnosis resulting from improper indications, poor examination technique, and errors in interpretation than from bioefects. Misdiagnosis (e.g., of ectopic pregnancy) and failure to diagnose a clinically important anomaly are real dangers, and poorly trained users may be the greatest current hazard of diagnostic ultrasound. Understanding bioefects is essential for the prudent use of diagnostic ultrasound and is important in ensuring that the excellent risk-to-beneit performance of diagnostic ultrasound is preserved. All users of ultrasound should be prudent, understanding as fully as possible the potential risks and obvious beneits of ultrasound examinations, as well as those of alternate diagnostic methods. With this information, operators can monitor exposure conditions and implement the principle of ALARA to keep patient (and in obstetric imaging, the fetal) exposure as low as possible while fulilling diagnostic objectives.

THERAPEUTIC APPLICATIONS: HIGHINTENSITY FOCUSED ULTRASOUND Although the primary medical application of ultrasound has been for diagnosis, therapeutic applications are developing rapidly, particularly the use of high-intensity focused ultrasound (HIFU). HIFU is based on three important capabilities of ultrasound: (1) focusing the ultrasound beam to produce highly localized energy deposition, (2) controlling the location and size of the focal zone, and (3) using intensities suicient to destroy tissue at the focal

32

Physics

PART I

A

C

B

D

FIG. 1.46 Aliasing. Pulse repetition frequency (PRF) determines the sampling rate of a given Doppler frequency. (A) If PRF (arrows) is suficient, the sampled waveform (orange curve) will accurately estimate the frequency being sampled (yellow curve). (B) If PRF is less than half the frequency being measured, undersampling will result in a lower frequency shift being displayed (orange curve). (C) In a clinical setting, aliasing appears in the spectral display as a “wraparound” of the higher frequencies to display below the baseline. (D) In color Doppler display, aliasing results in a wraparound of the frequency color map from one low direction to the opposite direction, passing through a transition of unsaturated color. The velocity throughout the vessel is constant, but aliasing appears only in portions of the vessel because of the effect of the Doppler angle on the Doppler frequency shift. As the angle increases, the Doppler frequency shift decreases, and aliasing is no longer seen.

zone. his has led to an interest in HIFU as a means of destroying noninvasive tumor and controlling bleeding and cardiac conduction anomalies. HIFU exploits thermal (heating of tissues) and mechanical (cavitation) bioefect mechanisms. As ultrasound passes through tissue, attenuation occurs through scattering and absorption. Scattering of ultrasound results in the return of some of the transmitted energy to the transducer, where it is detected and used to produce an image, or Doppler display. he remaining energy is transmitted to the molecules in the acoustic ield and produces heating. At the spatial peak temporal average (SPTA), intensities of 50 to 500 mW/cm2 used for imaging and Doppler, heating is minimal, and no observable bioefects related to tissue heating in humans have yet been documented with clinical devices. With higher intensities, however, tissue heating suicient to destroy tissue may be achieved. Using HIFU at 1 to 3 MHz, focal peak intensities of 5000 to 20,000 W/cm2 may be achieved. his energy can be delivered to a small point several millimeters in

size, producing rapid temperature elevation and resulting in tissue coagulation, with little damage to adjacent tissues (Fig. 1.48). he destruction of tissue is a function of the temperature reached and the duration of the temperature elevation. In general, elevation of tissue to a temperature of 60°C for 1 second is suicient to produce coagulation necrosis. Because of its ability to produce highly localized tissue destruction, HIFU has been investigated as a tool for noninvasive or minimally invasive treatment of bleeding sites, uterine ibroids, and tumors in the prostate, liver, and breast.19,20 As with diagnostic ultrasound, HIFU is limited by the presence of gas or bone interposed between the transducer and the target tissue. he relection of high-energy ultrasound from strong interfaces produced by bowel gas, aerated lung, or bone may result in tissue heating along the relected path of the sound, producing unintended tissue damage. Major challenges with HIFU include image guidance and accurate monitoring of therapy as it is being delivered. Magnetic

CHAPTER 1

Physics of Ultrasound

33

resonance imaging (MRI) provides a means of monitoring temperature elevation during treatment, which is not possible with ultrasound. Guidance of therapy may be done with ultrasound or MRI, with ultrasound guidance having the advantage of veriication of the acoustic window and sound path for the delivery of HIFU. A

Excess gain PSV = 75 cm/sec

B

Proper gain PSV = 60 cm/sec

C

Insufficent gain PSV = 50 cm/sec

FIG. 1.47 Doppler Gain. Accurate estimation of velocity requires proper Doppler gain adjustment. Excessive gain will cause an overestimation of peak velocity (A), and insuficient gain will result in underestimation of velocity (C). To adjust gain properly, the sample volume and Doppler angle are irst set at the sample site. The gain is turned up until noise appears in the background (A), then is gradually reduced just to the point where the background noise disappears from the image (B). PSV, Peak systolic velocity.

FIG. 1.48 High-Intensity Focused Ultrasound (HIFU). Local tissue destruction by heating may be achieved using HIFU delivered with focal peak intensities of several thousand W/cm2. Tissue destruction can be conined to a small area a few millimeters in size without injury to adjacent tissues. HIFU is a promising tool for minimally invasive treatment of bleeding sites, uterine ibroids, and tumors in the prostate, liver, and breast.

REFERENCES 1. Medical diagnostic ultrasound instrumentation and clinical interpretation. Report of the Ultrasonography Task Force. Council on Scientiic Afairs. JAMA. 1991;265(9):1155-1159. 2. Chivers RC, Parry RJ. Ultrasonic velocity and attenuation in mammalian tissues. J Acoust Soc Am. 1978;63(3):940-953. 3. Goss SA, Johnston RL, Dunn F. Comprehensive compilation of empirical ultrasonic properties of mammalian tissues. J Acoust Soc Am. 1978;64(2):423-457. 4. Merritt CR, Kremkau FW, Hobbins JC. Diagnostic ultrasound: bioefects and safety. Ultrasound Obstet Gynecol. 1992;2(5):366-374. 5. Curie J, Curie P. Développement par compression de l’électricité polaire dans les cristaux hémièdres à faces inclinées (Development, via compression, of electric polarization in hemihedral crystals with inclined faces). Bull Soc Minerol Fr. 1880;3:90-93. 6. Krishan S, Li PC, O’Donnell M. Adaptive compensation of phase and magnitude aberrations. IEEE Trans Ultrasonics Fer Freq Control. 1996;43. 7. Merritt CR. Technology update. Radiol Clin North Am. 2001;39(3):385-397. 8. Wells PN, Liang HD. Medical ultrasound: imaging of sot tissue strain and elasticity. J R Soc Interface. 2011;8(64):1521-1549. 9. Krouskop TA, Wheeler TM, Kallel F, et al. Elastic moduli of breast and prostate tissues under compression. Ultrason Imaging. 1998;20(4):260-274. 10. Ophir J, Cespedes I, Ponnekanti H, et al. Elastography: a quantitative method for imaging the elasticity of biological tissues. Ultrason Imaging. 1991; 13(2):111-134. 11. Shiina T, Nightingale KR, Palmeri ML, et al. WFUMB guidelines and recommendations for clinical use of ultrasound elastography: Part 1: basic principles and terminology. Ultrasound Med Biol. 2015;41(5):1126-1147. 12. Madsen EL, Sathof HJ, Zagzebski JA. Ultrasonic shear wave properties of sot tissues and tissuelike materials. J Acoust Soc Am. 1983;74(5):1346-1355. 13. Sarvazyan AP, Rudenko OV, Swanson SD, et al. Shear wave elasticity imaging: a new ultrasonic technology of medical diagnostics. Ultrasound Med Biol. 1998;24(9):1419-1435. 14. Ferraioli G, Parekh P, Levitov AB, Filice C. Shear wave elastography for evaluation of liver ibrosis. J Ultrasound Med. 2014;33(2):197-203. 15. Yoneda M, Suzuki K, Kato S, et al. Nonalcoholic fatty liver disease: US-based acoustic radiation force impulse elastography. Radiology. 2010;256(2):640-647. 16. Merritt CR. Doppler US: the basics. Radiographics. 1991;11(1):109-119. 17. Merritt CR. Doppler color low imaging. J Clin Ultrasound. 1987;15(9):591-597. 18. Rubin JM, Bude RO, Carson PL, et al. Power Doppler US: a potentially useful alternative to mean frequency-based color Doppler US. Radiology. 1994; 190(3):853-856. 19. Dubinsky TJ, Cuevas C, Dighe MK, et al. High-intensity focused ultrasound: current potential and oncologic applications. AJR Am J Roentgenol. 2008; 190(1):191-199. 20. Kennedy JE, Ter Haar GR, Cranston D. High intensity focused ultrasound: surgery of the future? Br J Radiol. 2003;76(909):590-599.

CHAPTER

2

Biologic Effects and Safety J. Brian Fowlkes and Christy K. Holland

SUMMARY OF KEY POINTS • Clinical ultrasound has been found to be an effective imaging modality with an excellent safety proile when used appropriately. • Ultrasound can produce physical effects, which should be understood as part of the beneit-versus-risk assessment as with any medical procedure. • The thermal index (TI) and mechanical index (MI) provide feedback to the user and should be minimized while

obtaining the requisite medical beneit from the ultrasound examination. • Ultrasound exposures during clinical, research, and educational examinations should be as low as reasonably achievable (ALARA). • Users of ultrasound should be appropriately trained and familiar with the equipment operation and controls that affect ultrasound exposure.

CHAPTER OUTLINE REGULATION OF ULTRASOUND OUTPUT PHYSICAL EFFECTS OF SOUND THERMAL EFFECTS Ultrasound Produces Heat Factors Controlling Tissue Heating Spatial Focusing Temporal Considerations Tissue Type Bone Heating Soft Tissue Heating Hyperthermia and Ultrasound Safety Thermal Index Homogeneous Tissue Model (Soft Tissue)

Tissue Model With Bone at the Focus (Fetal Applications) Tissue Model With Bone at the Surface (Transcranial Applications) Estimate of Thermal Effects Summary Statement on Thermal Effects EFFECTS OF ACOUSTIC CAVITATION Potential Sources for Bioeffects Sonochemistry Evidence of Cavitation From Lithotripters Bioeffects in Lung and Intestine Ultrasound Contrast Agents

U

ltrasound has provided a wealth of knowledge in diagnostic medicine and has greatly afected medical practice, particularly in obstetrics. Millions of sonographic examinations are performed each year, and ultrasound remains one of the fastest growing imaging modalities because of its low cost, real-time interactions, portability, and apparent lack of biologic efects (bioefects). No casual relationship has been established between clinical applications of diagnostic ultrasound and bioefects on the patient or operator.

REGULATION OF ULTRASOUND OUTPUT he U.S. Food and Drug Administration (FDA) regulates the maximum output of ultrasound devices to an established level.

34

Considerations for Increasing Acoustic Output Mechanical Index Summary Statement on Gas Body Bioeffects OUTPUT DISPLAY STANDARD GENERAL AIUM SAFETY STATEMENTS EPIDEMIOLOGY CONTROLLING ULTRASOUND OUTPUT ULTRASOUND ENTERTAINMENT VIDEOS

he marketing approval process requires devices to be equivalent in eicacy and output to those produced before 1976. his historic regulation of sonography has provided a safety margin for ultrasound while allowing clinically useful performance. he mechanism has restricted ultrasound exposure to levels that apparently produce few, if any, obvious bioefects based on the epidemiologic evidence, although animal studies have shown some evidence for biologic efects. In an efort to increase the eicacy of diagnostic ultrasound, the maximum acoustic output for some applications has increased through an additional FDA market approval process termed “510K Track 3.” he vast majority of ultrasound systems currently in use were approved through this process. he Track 3 process provides the potential for better imaging performance and, as discussed later, requires that additional information be reported

CHAPTER 2 to the operator regarding the relative potential for bioefects. herefore informed decision making is important concerning the possible adverse efects of ultrasound in relation to the desired diagnostic information. Current FDA regulations that limit the maximum output are still in place, but in the future, systems might allow sonographers and physicians the discretion to increase acoustic output beyond a level that might induce a biologic response. Although the choices made during sonographic examinations may not be equivalent to the risk-versus-beneit decisions associated with imaging modalities using ionizing radiation, the operator will be increasingly responsible for determining the diagnostically required amount of ultrasound exposure. hus the operator should know the potential bioefects associated with ultrasound exposure. Patients also need to be reassured about the safety of a diagnostic ultrasound scan. he scientiic community has identiied some potential bioefects from sonography, and although no causal relation has been established, it does not mean that no efects exist. herefore it is important to understand the interaction of ultrasound with biologic systems.

PHYSICAL EFFECTS OF SOUND he physical efects of sound can be divided into two principal groups: thermal and nonthermal. Most medical professionals recognize the thermal efects of elevated temperature on tissue, and the efects caused by ultrasound are similar to those of any localized heat source. With ultrasound, the heating mainly results from the absorption of the sound ield as it propagates through tissue. However, “nonthermal” sources can generate heat as well. Many nonthermal mechanisms for bioefects exist. Acoustic ields can apply radiation forces (not ionizing radiation) on the structures within the body at both the macroscopic and the microscopic levels, resulting in exerted pressure and torque. he temporal average pressure in an acoustic ield is diferent from the hydrostatic pressure of the luid, and any object in the ield is subject to this change in pressure. he efect is typically considered smaller than other efects because it relies on less signiicant factors in the formulation of the acoustic ield. Acoustic ields can also cause motion of luids. Such acoustically induced low is called streaming. Acoustic cavitation is the action of acoustic ields within a luid to generate bubbles and cause volume pulsation or even collapse in response to the acoustic ield. he result can be heat generation and associated free radical formation, microstreaming of luid around the bubble, radiation forces generated by the scattered acoustic ield from the bubble, and mechanical actions from bubble collapse. he interaction of acoustic ields with bubbles or “gas bodies” (as they are generally called) has been a signiicant area of bioefects research for many years.

THERMAL EFFECTS Ultrasound Produces Heat As ultrasound propagates through the body, energy is lost through attenuation. Attenuation causes loss of penetration and the

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35

inability to image deeper tissues. Attenuation is the result of two processes, scattering and absorption. Scattering of the ultrasound results from the redirection of the acoustic energy by tissue encountered during propagation. With diagnostic ultrasound, some of the acoustic energy transmitted into the tissue is scattered back in the direction of the transducer, termed backscatter, which allows a signal to be detected and images to be made. Energy also is lost along the propagation path of the ultrasound by absorption. Absorption loss occurs substantially through the conversion of the ultrasound energy into heat. his heating provides a mechanism for ultrasound-induced bioefects.

Factors Controlling Tissue Heating he rate of temperature increase in tissues exposed to ultrasound depends on several factors, including spatial focusing, ultrasound frequency, exposure duration, and tissue type.

Spatial Focusing Ultrasound systems use multiple techniques to concentrate or focus ultrasound energy and improve the quality of measured signals. he analogy for light is that of a magnifying glass. he glass collects all the light striking its surface and concentrates it into a small region. In sonography and acoustics in general, the term intensity is used to describe the spatial distribution of ultrasonic power (energy per unit time), where intensity = power/ area and the area refers to the cross-sectional area of the ultrasound beam. Another common beam dimension is the beam width at a speciied location of the ield. If the same ultrasonic power is concentrated into a smaller area, the intensity will increase. Focusing occurs on both transmission of the ultrasound and when receiving the backscattered signals used to form the image. he transmit focusing is of importance in terms of potential biologic efects because this phenomenon controls the applied energy to the tissue. here are ultrasound imaging systems that use plane wave transmission or limited transmit focusing, which may reduce the local intensity, but all ultrasound systems must still operate under the FDA limits. Focusing in an ultrasound system can be used to improve the spatial resolution of the images. he side efect is an increased potential for bioefects caused by heating and cavitation. In general, the greatest heating potential is between the scanhead and the focus, but the exact position depends on the focal distance, tissue properties, and heat generated within the scanhead itself. Returning to the magnifying glass analogy, most children learn that the secret to incineration is a steady hand. Movement distributes the power of the light beam over a larger area, thereby reducing its intensity. he same is true in ultrasound imaging. hus imaging systems that scan a beam through tissue reduce the spatial average intensity. Spectral Doppler and M-mode ultrasound imaging maintain the ultrasound beam in a stationary position (both considered unscanned modes) and therefore provide no opportunity to distribute the ultrasonic power spatially, whereas color low Doppler, power mode Doppler, and B-mode (also called gray-scale) ultrasound imaging require that the beam be moved to new locations (scanned modes) at a rate suicient to produce the real-time nature of these imaging modes.

Physics

PART I

TISSUE ATTENUATION

p+ Attenuation (dB/cm-MHz)

25

p–

TP

15 10 5

PA TA

Sk in t In ilag fa nt e sk ul l Sk ul l

ni o flu tic id Bl oo d Br ai n Li ve M r us cl e Fa Te t nd on

0

Am

Instantaneous intensity

Pulse length (temporal duration)

20

ar

Pressure

Pulse repetition period

C

36

Tissue Type Time

FIG. 2.1 Pressure and Intensity Parameters Measured in Medical Ultrasound. The variables are deined as follows: p+, peak positive pressure in waveform; p−, peak rarefactional pressure in waveform; PA, pulse average; TA, temporal average; TP, temporal peak.

Temporal Considerations he ultrasound power is the temporal rate at which ultrasound energy is produced. herefore controlling how ultrasound is produced in time seems a reasonable method for limiting its efects. Ultrasound can be produced in bursts rather than continuously. Ultrasound imaging systems operate on the principle of pulseecho, in which a burst of ultrasound is emitted, followed by a quiescent period listening for echoes to return. his pulsed wave ultrasound may be swept through the image plane numerous times during an imaging sequence. On the other hand, ultrasound may be transmitted in a continuous wave (CW) mode, in which the ultrasound transmission is not interrupted. he temporal peak intensity refers to the largest intensity at any time during ultrasound exposure (Fig. 2.1). he pulse average intensity is the average value over the duration of the ultrasound pulse. he temporal average intensity is the average over the entire pulse repetition period (elapsed time between onset of ultrasound bursts). he duty factor is deined as the fraction of time the ultrasound ield is “on.” With signiicant time “of ” between pulses (small duty factor), the temporal average value will be signiicantly smaller. For example, a duty factor of 10% will reduce the temporal average intensity by a factor of 10 compared with the pulse average. he time-averaged quantities are the variables most related to the potential for thermal bioefects. Combining temporal and spatial information results in common terms such as the spatial peak, temporal average intensity (ISPTA) and spatial average, temporal average intensity (ISATA). he overall duration, or dwell time, of the ultrasound exposure to a particular tissue is important because longer exposure of

FIG. 2.2 Tissue Attenuation. Values for types of human tissue at body temperature. (Data from Duck FA, Starritt HC, Anderson SP. A survey of the acoustic output of ultrasonic Doppler equipment. Clin Phys Physiol Meas. 1987;8[1]:39-49.47)

the tissue may increase the risk of bioefects. he motion of the scanhead during an examination reduces the dwell time within a particular region of the body and can minimize the potential for bioefects of ultrasound. herefore performing an eicient scan, spending only the time required for diagnosis, is a simple way to reduce exposure.

Tissue Type Numerous physical and biologic parameters control heating of tissues. Absorption is normally the dominant contributor to attenuation in sot tissue. he attenuation coeicient is the attenuation per unit length of sound travel and is usually given in decibels per centimeters-megahertz (dB/cm-MHz). he attenuation typically increases with increasing ultrasound frequency. he attenuation ranges from a negligible amount for luids (e.g., amniotic luid, blood, urine) to the highest value for bone, with some variation among diferent sot tissue types (Fig. 2.2). Another important factor is the body’s ability to cool tissue through blood perfusion. Well-perfused tissue will more efectively regulate its temperature by carrying away the excess heat produced by ultrasound. he exception is when heat is deposited too rapidly, as in therapeutic thermal ablation.1 Bone and sot tissue are two speciic areas of interest based on the diferences in heating phenomena. Bone has high attenuation of incident acoustic energy. In examinations during pregnancy, calciied bone is typically subjected to ultrasound, as in measurement of the biparietal diameter (BPD) of the skull. Fetal bone contains increasing degrees of mineralization as gestation progresses, thereby increasing risk of localized heating. Special heating situations relevant to obstetric ultrasound examinations may also occur in sot tissue, where overlying structures provide little attenuation of the ield, such as the luid-illed amniotic sac.

CHAPTER 2 8

37

TABLE 2.1 Fetal Femur Temperature Incrementsa at 1 W/cm2

7 Temperature increment (°C)

Biologic Effects and Safety

6

Gestational Age (days)

5

Diameter (mm)

Temperature Increments (°C)

0.5 1.2 3.3

0.10 0.69 2.92

59 78 108

4 3 a

Temperature increments in human fetal femur exposed for 20 seconds were found to be approximately proportional to incident intensity. With permission from Drewniak JL, Carnes KI, Dunn F. In vitro ultrasonic heating of fetal bone. J Acoust Soc Am. 1989;86(4):1254-1258.4

2 1 0 0.0

0.5

1.0

1.5

Exposure time (minutes)

Pressure

+

Shocked Normal

|

FIG. 2.3 Heating of Mouse Skull in a Focused Sound Field. For these experiments, frequency was 3.6 MHz, and temporal average focal intensity was 1.5 W/cm2. Solid circles, Young (6 mo) mice (n = 4); vertical bars, two standard errors in height; top curves, theoretical estimation of the temperature increases by Nyborg.3 (With permission from Carstensen EL, Child SZ, Norton S, Nyborg W. Ultrasonic heating of the skull. J Acoust Soc Am. 1990;87[3]: 1310-1317.2)

Bone Heating he absorption of ultrasound at the bone surface allows for rapid deposition of energy from the ield into a limited volume of tissue. he result can be a signiicant temperature rise. For example, Carstensen and colleagues2 combined an analytic approach and experimental measurements of the temperature rise in mouse skull exposed to CW ultrasound to estimate the temperature increments in bone exposures. Because bone has a large absorption coeicient, the incident ultrasonic energy is assumed to be absorbed in a thin planar sheet at the bone surface. he temperature rise of mouse skull has been studied in a 3.6-MHz focused beam with a beam width of 2.75 mm (Fig. 2.3). he temporal average intensity in the focal region was 1.5 W/cm.2 One of two models (upper curve in Fig. 2.3) in common use3 predicts values for the temperature rise about 20% greater than that actually measured in this experiment.2 hus the theoretical model is conservative in nature. Similarly for the fetal femur, Drewniak and colleagues4 indicated that the size and calciication state of the bone contributed to the ex vivo heating of bone (Table 2.1). To put this in perspective and to illustrate the operator’s role in controlling potential heating, consider the following scenario. By reducing the output power of an ultrasound scanner by 10 dB, the predicted temperature rise would be reduced by a factor of 10, making the increase of 3°C seen by these researchers (see Table 2.1) virtually nonexistent. his strongly suggests the use of maximum receive gain and reduction in output power during ultrasound examinations (see section on considerations for controlling ultrasound output). In fetal examinations an attempt should be made to maximize receive gain because this comes at no cost

Time FIG. 2.4 Effect of Finite Amplitude Distortion on a Propagating Ultrasound Pulse. Note the increasing steepness in the pulse, which contains higher frequency components.

to the patient in terms of exposure. Distinctions are oten made between bone positioned deep to the skin at the focal plane of the transducer and bone near the skin surface, as when considering transcranial applications. his distinction is discussed later with regard to the thermal index (TI).

Soft Tissue Heating Two clinical situations for ultrasound exposure in sot tissue are particularly relevant to obstetric and gynecologic applications. First, a common scenario involves scanning through a full bladder. he urine is a luid with a relatively low ultrasound attenuation coeicient. he reduced attenuation allows larger acoustic amplitudes to be applied deeper within the body. Second, the propagating wave may experience inite amplitude distortion, resulting in energy being shited by a nonlinear process from lower to higher frequencies. he result is a shockwave—a gradual wave steepening results in a waveform composed of higher frequency components (Fig. 2.4). Attenuation increases with increasing frequency; therefore the absorption of a large portion of the energy in such a wave occurs over a much shorter distance, concentrating the energy deposition in the irst tissue encountered, which may include the fetus.

PART I

Physics

Ultrasound imaging systems include speciic modalities that rely on nonlinear efects. In tissue harmonic imaging, or native harmonic imaging, the image is created using the backscatter of harmonic components induced by nonlinear propagation of the ultrasound ield. his has distinct advantages in terms of reducing image artifacts and improving lateral resolution in particular. In these nonlinear imaging modes the acoustic output must be suiciently high to produce the efect. he acoustic power currently used is still within the FDA limits, but improvements in image quality using such modes may create the need to modify or relax the regulatory restrictions. Similarly, in elasticity or shear wave imaging, the acoustic pressure may need to be increased to provide suicient acoustic radiation force for imaging tissue stifness. his detail will be discussed in the section on considerations for increasing acoustic output. Transvaginal ultrasound is important to note because of the proximity of the transducer to sensitive tissues such as the ovaries. As discussed later, temperature increases near the transducer may provide a heat source at sites other than the focus of the transducer. In addition, the transducer face itself may be a signiicant heat source because of ineiciencies in its conversion of electric to acoustic energy. Such factors must be considered in the estimation of potential thermal efects in transvaginal ultrasound and other endocavitary applications.

Hyperthermia and Ultrasound Safety Knowledge of the bioefects of ultrasound heating is in part based on the experience available from other, more common forms of hyperthermia, which serve as a basis for safety criteria. Extensive data exist on the efects of short-term and extended temperature increases, or hyperthermia. Teratogenic efects from hyperthermia have been demonstrated in birds, all the common laboratory animals, farm animals, and nonhuman primates.5 he wide range of observed bioefects, from subcellular chemical alterations to gross congenital abnormalities and fetal death, is an indication of the efectiveness or universality of hyperthermic conditions for perturbing living systems.6 he National Council on Radiation Protection and Measurements (NCRP) Scientiic Committee on Biological Efects of Ultrasound compiled a comprehensive list of the lowest reported thermal exposures producing teratogenic efects.7,8 Examination of these data indicated a lower boundary for observed thermally induced bioefects. Questions remain, however, about the relevance of this analysis of hyperthermia to the application of diagnostic ultrasound.9 Ater a careful literature review, O’Brien and colleagues10 suggested a more detailed consideration of thermal efects with regard to short-duration exposures. Fig. 2.5 shows the recommended approach to addressing the combination of temperature and duration of exposure. Note that the tolerance of shorter durations and higher temperatures suggests a substantial safety margin for diagnostic ultrasound. Regardless, it is beneicial to provide feedback to the ultrasound operator as to the relative potential for a temperature rise in a given acoustic ield under conditions associated with a particular examination. his will allow an informed decision as to the exposure needed to obtain diagnostically relevant information.

58 55 Temperature (°C)

38

52 49 46 43 40 37 0.1

1

10

100

1000

Time (s) FIG. 2.5 Conservative Boundary Curve for Nonfetal Bioeffects Caused by a Thermal Mechanism. Note the increase in temperature tolerance associated with shorter durations of exposures, a modiication to the earlier American Institute of Ultrasound in Medicine (AIUM) Conclusions Regarding Heat statement (March 26, 1997). The AIUM approved a revised thermal statement on April 6, 2009. For a complete description of the origins of this curve, see O’Brien and colleagues.10 (With permission from O’Brien Jr WD, Deng CX, Harris GR, et al. The risk of exposure to diagnostic ultrasound in postnatal subjects: thermal effects. J Ultrasound Med. 2008;27[4]:517-535.10)

Thermal Index Based on analysis of hyperthermia data, the NCRP proposed a general statement concerning the safety of ultrasound examinations in which no temperature rise greater than 1°C is expected. In an afebrile patient within this limit, the NCRP concluded that there was no basis for expecting an adverse efect. In cases where the temperature rise might be greater, the operator should weigh the beneit against the potential risk. To assist in this decision, given the range of diferent imaging conditions seen in practice, a thermal index (TI) was approved as part of the Standard for Real-Time Display of hermal and Mechanical Acoustical Output Indices on Diagnostic Ultrasound Equipment of the American Institute of Ultrasound in Medicine (AIUM).11 his standard provides the operator with an indication of the relative potential risk of heating tissue, with calculations based on the imaging conditions and an on-screen display showing the TI. his standard was subsequently adopted as an international standard through the International Electrotechnical Commission (IEC).12

The Thermal Index To more easily inform the physician of the operating conditions that could, in some cases, lead to a temperature elevation of 1°C, a thermal index is deined as TI =

W0 Wdeg

where Wdeg is the ultrasonic source power (in watts) calculated as capable of producing a 1°C temperature elevation under speciic conditions. W0 is the ultrasonic source power (in watts) being used during the current exam. Reproduced with permission of American Institute of Ultrasound in Medicine (AIUM).

CHAPTER 2 he NCRP ultrasound committee introduced the TI concept.8 he purpose of the TI is to provide an indication of the relative potential for increasing tissue temperature, but it is not meant to provide the actual temperature rise. he NCRP recommended two tissue models to aid in the calculation of the ultrasound power that could raise the temperature in tissue by 1°C: (1) a homogeneous model in which the attenuation coeicient is uniform throughout the region of interest, and (2) a ixedattenuation model in which the minimum attenuation along the path from transducer to a distant anatomic structure is independent of the distance because of a low-attenuation luid path (e.g., amniotic luid).8,13,14 Because of concern for the patient, it was recommended that “reasonable worst case” assumptions be made with respect to estimation of temperature elevations in vivo. he FDA, AIUM, and National Electrical Manufacturers Association (NEMA) adopted the TI as part of the output display standard. hey advocate estimating the efect of attenuation in the body by reducing the acoustic power/output of the scanner (W0) by a derating factor equal to 0.3 dB/cm-MHz for the sot tissue model.11 he AIUM hermal Index Working Group considered three tissue models: (1) the homogeneous tissue or sot tissue model, (2) a tissue model with bone at the focus, and (3) a tissue model with bone at the surface, or transcranial model.11 he TI takes on three diferent forms for these tissue models.

Homogeneous Tissue Model (Soft Tissue) he assumption of homogeneity helps simplify the determination of the efects of acoustic propagation and attenuation, as well as the heat transfer characteristics of the tissue. Providing one of the most common applications for ultrasound imaging, this model applies to situations where bone is not present and can generally be used for fetal examinations during the irst trimester (low calciication in bone). In the estimation of potential heating, many assumptions and compromises had to be made to calculate a single quantity that would guide the operator. Calculations of the temperature rise along the axis of a focused beam for a simple, spherically curved, single-element transducer result in two thermal peaks. he irst is in the near ield (between the transducer and the focus), and the second appears close to the focal region.15,16 he irst thermal peak occurs in a region with low ultrasound intensity and wide beam width. When the beam width is large, cooling will occur mainly because of perfusion. In the near ield the magnitude of the local intensity is the chief determinant of the degree of heating. he second thermal peak occurs at the location of high intensity and narrow beam width at or near the focal plane. Here the cooling is dominated by conduction, and the total acoustic power is the chief determinant of the degree of heating. Given the thermal “twin peaks” dilemma, the AIUM hermal Index Working Group compromised in creating a TI that included contributions from both heating domains.11 heir rationale was based on the need to minimize the acoustic measurement load for manufacturers of ultrasound systems. In addition, adjustments had to be made to compensate for efects of the large range of potential apertures. he result is a complicated series of calculations and measurements that must be performed, and to the

Biologic Effects and Safety

39

credit of the many manufacturers, there has been considerable efort in implementing a display standard to provide user feedback. Diferent approaches to these calculations were considered,10 but changes will require that the currently accepted implementation be reexamined and approved for use by the FDA and considered by the IEC.

Tissue Model With Bone at the Focus (Fetal Applications) Applications of ultrasound in which the acoustic beam travels through sot tissue for a ixed distance and impinges on bone occur most oten in obstetric scanning during the second and third trimesters. Carson and colleagues13 recorded sonographic measurements of the maternal abdominal wall thickness in various stages of pregnancy. Based on their results, the NCRP recommended that the attenuation coeicients for the irst, second, and third trimesters be 1.0, 0.75, and 0.5 dB/MHz, respectively.7 hese values represent “worst case” estimates. In addition, Siddiqi and colleagues17 determined the average tissue attenuation coeficient for transabdominal insoniication (exposure to ultrasound waves) in a patient population of nonpregnant, healthy volunteers was 2.98 dB/MHz. his value represents an average measured value and is much diferent from the worst-case estimates previously listed. his leads to considerable debate on how such parameters should be included in an index. In addition, bone is a complex, hard connective tissue with a calciied collagenous intercellular structure. Its absorption coeicient for longitudinal waves is a factor of 10 greater than that for most sot tissues (see Fig. 2.2). Shear waves are also created in bone as sound waves strike bone at oblique incidence. he absorption coeicients for shear waves are even greater than those for longitudinal waves.18-20 Based on the data of Carstensen and colleagues2 described earlier, the NCRP proposed a thermal model for bone heating. Using this model, the Bone hermal Index (TIB) is estimated for conditions in which the focus of the beam is at or near bone. Again, assumptions and compromises had to be made to develop a functional TI for the case of bone exposure, as follows: • For unscanned mode transducers (operating in a ixed position) with bone in the focal region, the location of the maximum temperature increase is at the surface of the bone. herefore the TIB is calculated at the distance along the beam from the transducer where it is maximized, a worst-case assumption. • For scanned modes, the Sot Tissue hermal Index (TIS) is used because the temperature increase at the surface is either greater than or approximately equal to the temperature increase with bone in the focus. Tissue Model With Bone at the Surface (Transcranial Applications) For adult cranial applications, the same model as that with bone at the focus is used to estimate the temperature distribution in situ. However, because the bone is located at the surface, immediately ater the acoustic beam enters the body, attenuation of the acoustic power output is not included.11 In this situation the equivalent beam diameter at the surface is used to calculate the

40

PART I

Physics

acoustic power and derive the Cranial Bone hermal Index (TIC).

Estimate of Thermal Effects Ultrasound users should keep in mind several points when referring to the TI as a means of estimating the potential for thermal efects. First, the TI is not synonymous with temperature rise. A TI equal to 1 does not mean the temperature will rise 1°C. An increased potential for thermal efects can be expected as TI increases. Second, a high TI does not mean that bioefects are occurring, but only that the potential exists. he thermal models employed for TI calculation may not consider factors that may reduce the actual temperature rise. However, TI should be monitored during examinations and minimized when possible. Finally, there is no consideration in the TI for the duration of the scan, so minimizing the overall examination time will reduce the potential for efects. here have been proposals suggesting the inclusion of such a dwell time efect,21 but these have not been adopted.

Summary Statement on Thermal Effects he AIUM statement concerning thermal efects of ultrasound includes several conclusions that can be summarized as follows22: • Adult examinations resulting in a temperature rise of up to 2°C are not expected to cause bioefects. (Many ultrasound examinations fall within these parameters.) • A signiicant number of factors control heat production by diagnostic ultrasound. • Ossiied bone is a particularly important concern for ultrasound exposure.

• A labeling standard now provides information concerning potential heating in sot tissue and bone. • Even though an FDA limit exists for fetal exposures, predicted temperature rises can exceed 2°C. • hermal indices are expected to track temperature increases better than any single ultrasonic ield parameter.

EFFECTS OF ACOUSTIC CAVITATION Potential Sources for Bioeffects Knowledge concerning the interaction of ultrasound with gas bodies (which many term “cavitation”) has signiicantly increased over time, although it is not as extensive as that for ultrasound thermal efects and other sources of hyperthermia. Acoustic cavitation inception is demarcated by a speciic threshold value: the minimum acoustic pressure necessary to initiate the growth of a cavity in a luid during the rarefaction phase of the cycle. Several parameters afect this threshold, including initial bubble or cavitation nucleus size, acoustic pulse characteristics (e.g., center frequency, pulse repetition frequency [PRF], pulse duration), ambient hydrostatic pressure, and host luid parameters (e.g., density, viscosity, compressibility, heat conductivity, surface tension). Inertial cavitation refers to bubbles that undergo large variations from their equilibrium sizes in a few acoustic cycles. Speciically during contraction, the surrounding luid inertia controls the bubble motion.23 Large acoustic pressures are necessary to generate inertial cavitation, and the collapse of these cavities is oten violent.

The AIUM Statement on Mammalian Biological Effects of Heat24 APPROVED MARCH 25, 2015 1. An excessive temperature increase can result in toxic effects in mammalian systems. The biological effects observed depend on many factors, such as the exposure duration, the type of tissue exposed, its cellular proliferation rate, and its potential for regeneration. Age and stage of development are important factors when considering fetal and neonatal safety. Temperature increases of several degrees Celsius above the normal core range can occur naturally. The probability of an adverse biological effect increases with both the duration and the magnitude of the temperature rise.

2. In general, adult tissues are more tolerant of temperature increases than fetal and neonatal tissues. Therefore, higher temperatures and/or longer exposure durations would be required for thermal damage. The considerable data available on the thermal sensitivity of adult tissues support the following inferences10: a. For exposure durations up to 50 hours, there have been no signiicant adverse biological effects observed due to temperature increases less than or equal to 1.5°C above normal.25 b. For temperature increases between 1.5°C and 6°C above normal, there have been no signiicant adverse biological effects observed due to temperature increases less than or equal to 6 − [log10(t/60)]/0.6 where t is the exposure duration in seconds. For

example, for temperature increases of 4°C and 6°C, the corresponding limits for the exposure durations t are 16 minutes and 1 minute, respectively. c. For temperature increases greater than 6°C above normal, there have been no signiicant adverse biological effects observed due to temperature increases less than or equal to 6 − [log10(t/60)]/0.3 where t is the exposure duration in seconds. For example, for temperature increases of 9.6°C and 6.0°C, the corresponding limits for the exposure durations t are 5 and 60 seconds, respectively. d. For exposure durations less than 5 seconds, there have been no signiicant, adverse biological effects observed due to temperature increases less than or equal to 9 − [log10(t/60)]/0.3 where t is the exposure duration in seconds. For example, for temperature increases of 18.3°C, 14.9°C, and 12.6°C, the corresponding limits for the exposure durations t are 0.1, 1, and 5 seconds, respectively. 3. Acoustic output from diagnostic ultrasound devices is suficient to cause temperature elevations in fetal tissue. Although fewer data are available for fetal tissues, the following conclusions are justiied10,26: a. In general, temperature elevations become progressively greater from B-mode to color Doppler to spectral Doppler applications.

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The AIUM Statement on Mammalian Biological Effects of Heat24—cont’d b. For identical exposure conditions, the potential for thermal bioeffects increases with the dwell time during examination. c. For identical exposure conditions, the temperature rise near bone is signiicantly greater than in soft tissues, and it increases with ossiication development throughout gestation. For this reason, conditions in which an acoustic beam impinges on ossifying fetal bone deserve special attention due to its close proximity to other developing tissues. d. The current U.S. Food and Drug Administration regulatory limit for the derated spatial-peak temporalaverage intensity (ISPTA.3) is 720 mW/cm2. For this exposure, the theoretical estimate of the maximum temperature increase in the conceptus may exceed 1.5°C. e. Although an adverse fetal outcome is possible at any time during gestation, most severe and detectable effects of thermal exposure in animals have been observed during the period of organogenesis. For this reason, exposures during the irst trimester should be restricted to the lowest outputs consistent with obtaining the necessary diagnostic information. f. Ultrasound exposures that elevate fetal temperature by 4°C above normal for 5 minutes or more have the potential to induce severe developmental defects. Thermally induced congenital anomalies have been observed in a large variety of animal species. In current clinical practice, using commercially available equipment, it is unlikely that such thermal exposure would occur at a speciic fetal anatomic site provided that the thermal index (TI) is less than 2.0 and the dwell time on that site does not exceed 4 minutes. g. Transducer self-heating is a signiicant component of the temperature rise of tissues close to the transducer. This may be of signiicance in transvaginal

scanning, but no data for the fetal temperature rise are available. 4. The temperature increase during exposure of tissues to diagnostic ultrasound ields is dependent on: (1) output characteristics of the acoustic source, such as frequency, source dimensions, scan rate, output power, pulse repetition frequency, pulse duration, transducer selfheating, exposure time, and wave shape; and (2) tissue properties, such as attenuation, absorption, speed of sound, acoustic impedance, perfusion, thermal conductivity, thermal diffusivity, anatomic structure, and the nonlinearity parameter. 5. Calculations of the maximum temperature increase resulting from ultrasound exposure are not exact because of the uncertainties and approximations associated with the thermal, acoustic, and structural characteristics of the tissues involved. However, experimental evidence shows that calculations are generally capable of predicting measured values within a factor of 2. Thus, such calculations are used to obtain safety guidelines for clinical exposures in which direct temperature measurements are not feasible. These guidelines, called thermal indices,a provide a real-time display of the relative probability that a diagnostic system could induce thermal injury in the exposed subject. Under most clinically relevant conditions, the soft tissue thermal index (TIS) and the bone thermal index (TIB) either overestimate or closely approximate the best available estimate of the maximum temperature increase (ΔTmax). For example, if TIS = 2, then ΔTmax ≤ 2°C; actual temperature increases are also dependent on dwell time.

However, in some applications, such as fetal examinations in which the ultrasound beam passes through a layer of relatively unattenuating liquid, such as urine or amniotic luid, the TI can underestimate ΔTmax by up to a factor of 2.27,28

a

The thermal indices are the nondimensional ratios of attenuated acoustic power at a speciic point to the attenuated acoustic power required to raise the temperature at that point in a speciic tissue model by 1°C.29 AIUM, American Institute of Ultrasound in Medicine. Reproduced with permission from American Institute of Ultrasound in Medicine (AIUM). Statement on mammalian biological effects of heat. Laurel, MD: AIUM; 2015. Available from: http://www.aium.org/oficialStatements/17. Updated March 25, 2015. Cited October 7, 2016.24

he efect of preexisting cavitation nuclei may be one of the principal controlling factors in mechanical efects that result in biologic efects. he body is such an excellent ilter that these nucleation sites may be found only in small numbers and at selected sites. For example, if water is iltered down to 2 µm, the cavitation threshold doubles.30 heoretically, the tensile strength of water that is devoid of cavitation nuclei is about 100 megapascals (MPa).31 Various models have been suggested to explain bubble formation in animals,32,33 and these models have been used extensively in cavitation threshold determination. One model is used in the prediction of SCUBA diving tables and may also have applicability

to patients.34 It remains to be seen how well such models will predict the nucleation of bubbles from diagnostic ultrasound in the body. Fig. 2.6 shows a 1-MHz therapeutic ultrasound unit generating bubbles in gas-saturated water. he particular medium and ultrasound parameters were chosen to optimize the conditions for cavitation. Using CW ultrasound and many preexisting gas pockets in the water set the stage for the production of cavitation. Even though these acoustic pulses are longer than those typically used in diagnostic ultrasound, cavitation efects have also been observed with diagnostic pulses in luids.35 Ultrasound contrast agents composed

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FIG. 2.6 Acoustic Cavitation Bubbles. This cavitation activity is being generated in water using a common therapeutic ultrasound device. (Courtesy of National Center for Physical Acoustics, University of Mississippi.)

FIG. 2.8 Collapsing Bubble Near a Boundary. When cavitation is produced near boundaries, a liquid jet may form through the center of a bubble and strike the boundary surface. (Courtesy of Lawrence A. Crum.)

a therapeutic ultrasound device; the setup is backlighted (in red) to show the bubbles and experimental apparatus. he chemiluminescence emissions are the blue bands seen through the middle of the liquid sample holder. he light emitted is suicient to be seen by simply adapting one’s eyes to darkness. Electron spin resonance can also be used with molecules that trap free radicals to detect cavitation activity capable of free radical production.38 A number of other chemical detection schemes are presently employed to detect cavitation from diagnostic devices in vitro.

Evidence of Cavitation From Lithotripters

FIG. 2.7 Chemical Reaction Induced by Cavitation Producing Visible Light. The reaction is the result of free radical production. (Courtesy of National Center for Physical Acoustics, University of Mississippi.)

of stabilized gas bubbles should provide a source of cavitation nuclei, as discussed later in the section on ultrasound contrast agents.

Sonochemistry Free radical generation and detection provide a means to observe cavitation and to gauge its strength and potential for damage. he sonochemistry of free radicals is the result of very high temperatures and pressures within the rapidly collapsing bubble. hese conditions can even generate light, or sonoluminescence.36 With the addition of the correct compounds, chemical luminescence can also be used for free radical detection and can be generated with short pulses similar to those used in diagnostic ultrasound.37 Fig. 2.7 shows chemiluminescence generated by

It is possible to generate bubbles in vivo using short pulses with high amplitudes of extracorporeal shockwave lithotripsy (ESWL). he peak positive pressure for lithotripsy pulses can be as high as 50 MPa, with a rarefactional pressure of about 20 MPa. Finite amplitude distortion causes high frequencies to appear in high-amplitude ultrasound ields. Although ESWL pulses have signiicant energy at high frequencies because of inite amplitude distortion, a large portion of the energy is actually in the 100-kHz range, much lower than frequencies in diagnostic scanners. he lower frequency makes cavitation more likely. Aymé and Carstensen39 showed that the higher frequency components in nonlinearly distorted pulses contributed little to the killing of Drosophila larvae. Interestingly, evidence indicates that collapsing bubbles play a role in stone disruption.40-42 A bubble collapsing near a surface may form a liquid jet through its center, which strikes the surface (Fig. 2.8). Placing a sheet of aluminum foil at the focus of a lithotripter generates small pinholes.40 he impact is even suicient to pit solid brass and aluminum plates. At very high acoustic amplitudes, tissue can be disrupted and even emulsiied using ultrasound in a process termed “histotripsy.”43-45 Peak rarefactional pressures used in this form of therapeutic ultrasound can be as high as 25 to

CHAPTER 2 30 MPa, at which point gas bubbles form spontaneously in a very consistent controlled fashion that allows for therapeutic applications. Clearly, lithotripsy and histotripsy difer greatly from diagnostic ultrasound in the acoustic power generated and are not comparable in the bioefects produced. However, some diagnostic devices produce peak rarefactional pressures greater than 3 MPa, which is in the lower range of lithotripter outputs.46-48 Lung damage and surface petechiae have been noted as side efects of ESWL in clinical cases.49 Inertial cavitation was suspected as the cause, prompting several researchers to study the efects of diagnostic ultrasound exposure on the lung parenchyma.50,51

Bioeffects in Lung and Intestine Lung tissue and intestinal tissue are key locations for examining for bioefects of diagnostic ultrasound.50 he presence of air in the alveolar spaces constitutes a signiicant source of gas bodies. Child and colleagues51 measured threshold pressures for hemorrhage in mouse lung exposed to 1- to 4-MHz short-pulse diagnostic ultrasound (i.e., 10- and 1-µm pulse durations). he threshold of damage in murine lung at these frequencies was 1.4 MPa. Pathologic features of this damage included extravasation of blood cells into the alveolar spaces.52 he authors hypothesized that cavitation, originating from gas-illed alveoli, was responsible for the damage. heir data provided the irst direct evidence that clinically relevant, pulsed ultrasound exposures produce deleterious efects in mammalian tissue in the absence of signiicant heating. Hemorrhagic foci induced by 4-MHz pulsed Doppler ultrasound have also been reported in the monkey.53 Damage in the monkey lung was of a signiicantly lesser degree than that in the mouse. In these studies it was impossible to show categorically that bubbles induced these efects because the cavitation-induced bubbles were not observed. hresholds for petechial hemorrhage in the lung caused by ultrasound have been measured in mouse, rat, rabbit and pig.54-56 Direct mechanical stresses associated with propagation of ultrasound in the lung were believed to contribute to the damage observed.50,57 hresholds for hemorrhage in the murine intestine exposed to pulsed ultrasound have also been determined.58 Kramer and colleagues59 assessed cardiopulmonary function in rats exposed to pulsed ultrasound well above the acoustic output threshold of damage, at a mechanical index (MI) of 9.7. Measurements of cardiopulmonary function included arterial blood pressure, heart rate, respiratory rate, and arterial blood gases (Pco2 and Po2). If only one side of the rat lung was exposed, the cardiopulmonary measurements did not change signiicantly between baseline and postexposure values because of the functional respiratory reserve in the unexposed lobes. However, when both sides of the lung had signiicant ultrasound-induced lesions, the rats were unable to maintain systemic arterial pressure or resting levels of arterial Po2. Further studies are required to determine the relevance of these indings to humans. In general, tissues containing air (or stabilized gas) are more susceptible to damage than are

Biologic Effects and Safety

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tissues without gas. Also, no conirmed reports of petechial hemorrhage below an MI of 0.4 have been noted in animal studies. As recently as 2012, this threshold in lungs was conirmed in a small animal model.60 However, it should be noted that the mechanism for pulmonary efects might not follow the functional frequency dependence embedded in the MI.61

Ultrasound Contrast Agents he apparent absence of cavitation in many locations in the body can result from the lack of available cavitation nuclei. Based on evidence in the lung and intestine in mammalian models described earlier, the presence of gas bodies clearly reduces the requisite acoustic ield for producing bioefects. Many ultrasound contrast agents are composed of stabilized gas bubbles, so they could provide readily available nuclei for potential cavitation activity. his makes the investigation of bioefects in the presence of ultrasound contrast agents an important area of research.62-64 Studies have also shown that ultrasound exposure in the presence of contrast agents produces small vascular petechiae and endothelial damage in mammalian systems.65-70 Acoustic emissions from activated microbubbles correlate with the degree of vascular damage.67,68 As a result, the AIUM has a safety statement on the bioefects of diagnostic ultrasound with gas body contrast agents. his bioefect may occur, but the issue remains whether it constitutes a signiicant physiologic risk. he safety statement is designed to make sonographers and physicians aware of the potential for bioefects in the presence of gas contrast agents and allow them to make an informed decision based on a risk-versus-beneit assessment. Some research also indicates the production of premature ventricular contractions (PVCs) during cardiac scanning in the presence of ultrasound contrast agents. At least one human study indicated an increase in PVCs only when ultrasound imaging was performed with a contrast agent, and not with ultrasound imaging alone or during injection of the agent without imaging.71 Another study72 revealed that oscillating microbubbles afect stretch activation channels73,74 in cardiac cells, which generates membrane depolarization and triggers action potentials and thus PVCs. he importance of this bioeffect is also being debated because there is a naturally occurring rate of PVCs, and a small increase may not be considered clinically important, particularly if the patient beneits from using the agent. Additional consideration might be given to patients with speciic conditions in whom additional PVCs should be avoided. he consequences of the ultrasound contrast agent bioefects reported thus far require more study. Although the potential exists for a bioefect, its scale and inluence on human physiology remain unclear. Contrast agents have demonstrated eicacy for speciic indications, facilitating patient management.75 In addition, clinical trials and marketing follow-up of many patients receiving ultrasound and contrast agents have reported few efects. Several publications provide evidence conirming the safety of ultrasound contrast agent use.76-79

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The AIUM Statement on Mammalian Biological Effects in Tissues With Gas Body Contrast Agents80 APPROVED MARCH 25, 2015 Presently available ultrasound contrast agents consist of suspensions of gas bodies (stabilized gaseous microbubbles). The gas bodies have the correct size for strong echogenicity with diagnostic ultrasound and also for passage through the microcirculation. Commercial agents undergo rigorous clinical testing for safety and eficacy before Food and Drug Administration approval is granted, and they have been in clinical use in the United States since 1994. Detailed information on the composition and use of these agents is included in the package inserts. In the United States, contrast agents have been approved for opaciication of the left ventricular chamber and delineation of the left ventricular endocardial border. Outside the United States, additional approved indications include imaging lesions of the breast and liver, portal vein, and extracranial carotid and peripheral arteries. Many other diagnostic applications are under development or clinical testing. Contrast agents carry some potential for nonthermal bioeffects when ultrasound interacts with the gas bodies. The mechanism for such effects is related to the physical phenomenon of acoustic cavitation. Several published reports describe adverse bioeffects in mammalian tissue in vivo resulting from exposure to diagnostic ultrasound with gas body contrast agents in the circulation. Induction of premature ventricular contractions by triggered contrast echocardiography in humans has been reported for a noncommercial agent and in laboratory animals for commercial agents. Microvascular leakage, killing of cardiomyocytes, and glomerular capillary hemorrhage, among other bioeffects, have been reported in animal studies. Two medical ultrasound societies have examined this potential risk of bioeffects in diagnostic ultrasound with contrast agents and provide extensive reviews of the topic: the World Federation for

Ultrasound in Medicine and Biology Contrast Agent Safety Symposium81 and the American Institute of Ultrasound in Medicine 2005 Bioeffects Consensus Conference.62 More recently, the British Medical Ultrasound Society issued a detailed assessment of methods for the safe use of diagnostic ultrasound, including use of contrast agents.82 Based on a review of these reports and recent literature, the Bioeffects Committee has issued the following statement. STATEMENT ON MAMMALIAN BIOLOGICAL EFFECTS OF DIAGNOSTIC ULTRASOUND WITH GAS BODY CONTRAST AGENTS Induction of premature ventricular contractions, microvascular leakage with petechiae, glomerular capillary hemorrhage, local cell killing, and other effects in mammalian tissue in vivo have been reported and independently conirmed for diagnostic ultrasound exposure with a mechanical index (MI) above about 0.4 and a gas body contrast agent present in the circulation. Although the medical signiicance of such microscale bioeffects is uncertain, minimizing the potential for such effects represents prudent use of diagnostic ultrasound. In general, for imaging with contrast agents at an MI above 0.4, practitioners should use the minimal agent dose, MI, and examination time consistent with eficacious acquisition of diagnostic information. In addition, the echocardiogram should be monitored during high-MI contrast cardiac-gated perfusion echocardiography, particularly in patients with a history of myocardial infarction or unstable cardiovascular disease. Furthermore, physicians and sonographers should follow all guidance provided in the package inserts of these drugs, including precautions, warnings, and contraindications.

AIUM, American Institute of Ultrasound in Medicine. Reproduced with permission from American Institute of Ultrasound in Medicine (AIUM). Statement on mammalian biological effects in tissues with gas body contrast agents. Laurel, MD: AIUM; 2015. Available from: http://www.aium.org/oficialStatements/25. Approved March 25, 2015. Cited October 7, 2016.80

Considerations for Increasing Acoustic Output Situations arise where increasing acoustic output in ultrasound imaging could provide improved performance, particularly at signiicant depths. he desire to increase acoustic output was the original impetus for the development of the FDA 510K Track 3 mechanism in situations in which imaging was challenging for deep tissue structures, particularly in obstetrics. Modes such as tissue harmonic imaging and elasticity and shear wave imaging may also beneit from similar considerations. A working group of the Output Standards Subcommittee of the AIUM Technical Standards Committee examined on the potential beneits and risks of conditionally increased acoustic pressure. he resulting white paper83 provides a rationale for a three-tiered approach for conditionally increased acoustic output that follows the model employed for elevated output in magnetic resonance imaging, and concludes with summary

recommendations to facilitate clinical studies monitored by an institutional review board to investigate the beneits of an increased acoustic output in speciic tissues. One of the fundamental assumptions in the MI calculation is the presence of a preexisting gas body. Based on theoretical predictions and experimentally reported cavitation thresholds for tissues that do not contain preexisting gas bodies, the working group found this assumption to be overly conservative and concluded that exceeding the recommended maximum MI given in the FDA guidance could be warranted without concern for increased risk of cavitation in these tissues. In the future, the ultrasound research community will need examine how much improvement in diagnostic ultrasound imaging might be achieved with increased acoustic output.

Mechanical Index Calculations for cavitation prediction have yielded a trade-of between peak rarefactional pressure and frequency.84 his

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10 MI=2 5

Threshold pressure (MPa)

MI=1 190 W

cm–2

2

1 MI=0.3 10 W cm–2 5

2

0.1 5

1

2

5

10

Frequency (MHz) Adult mouse lung (10 µs) Adult mouse lung (1 µs) Neonatal mouse lung (10 µs) Fruit fly larvae (10 µs) Elodea leaves (5 µs) FIG. 2.9 Threshold for Bioeffects From Pulsed Ultrasound Scan Using Low Temporal Average Intensity. Data shown are the threshold for effects measured in peak rarefactional pressures (p− in Fig. 2.1) as a function of ultrasound frequency used in the exposure. Pulse durations are shown in parentheses in the key below the graph. Also shown for reference purposes are the values for the mechanical index (MI) and the local spatial peak, pulse average intensity (ISPPA). (With permission from American Institute of Ultrasound in Medicine. Consensus Report on Potential Bioeffects of Diagnostic Ultrasound. J Ultrasound Med. 2008;27:503-515.22)

predicted trade-of assumes short-pulse (a few acoustic cycles) and low–duty cycle ultrasound (0.7 cm) is associated with severe portal hypertension (portohepatic gradient >10 mm Hg)82 (Fig. 4.31C and D). • Paraumbilical vein: Runs in the falciform ligament and connects the let portal vein to the systemic epigastric veins

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near the umbilicus (Cruveilhier-Baumgarten syndrome)86 (Fig. 4.31A). Some studies suggest that, if the hepatofugal low in the patent paraumbilical vein exceeds the hepatopetal low in the portal vein, patients may be protected from developing esophageal varices.87,88 • Splenorenal and gastrorenal: Tortuous veins may be seen in the region of the splenic and let renal hilus (Fig. 4.31E and F), which represent collaterals between the splenic, coronary, and short gastric veins and the let adrenal or renal veins. • Intestinal: Regions in which the gastrointestinal tract becomes retroperitoneal so that the veins of the ascending and descending colon, duodenum, pancreas, and liver may anastomose with the renal, phrenic, and lumbar veins (systemic tributaries). • Hemorrhoidal: he perianal region where the superior rectal veins, which extend from the inferior mesenteric vein, anastomose with the systemic middle and inferior rectal veins. Duplex Doppler sonography provides additional information regarding direction of portal low. False results may occur, however, when sampling is obtained from periportal collaterals in patients with portal vein thrombosis or hepatofugal portal low.89 Normal portal venous low rates vary in the same individual, increasing postprandially and during inspiration75,90 and decreasing ater exercise or in the upright position.91 An increase of less than 20% in the diameter of the portal vein with deep inspiration indicates portal hypertension with 81% sensitivity and 100% speciicity.92 he normal portal vein demonstrates an undulating hepatopetal (toward the liver) low. Mean portal venous low velocity is 15 to 18 cm/sec and varies with respiration and cardiac pulsation. As portal hypertension develops, the low in the portal vein loses its undulatory pattern and becomes monophasic. As the severity of portal hypertension increases, low becomes biphasic and inally hepatofugal (away from the liver). Intrahepatic arterial-portal venous shunting may also be seen. Chronic liver disease is also associated with increased splanchnic blood low. Evidence suggests that portal hypertension is partly caused by the hyperdynamic low state of cirrhosis. Zwiebel et al.93 found that blood low was increased in the superior mesenteric arteries and splenic arteries of patients with cirrhosis and splenomegaly, compared with normal controls. Of interest, in patients with cirrhosis and normal-sized livers, splanchnic blood low was not increased. Patients with isolated splenomegaly and normal livers were not included in this study. he limitations of Doppler sonography in the evaluation of portal hypertension include the inability to determine vascular pressures and low rates accurately. Patients with portal hypertension are oten ill, with contracted livers, abundant ascites, and loating bowel, all of which create a technical challenge. In a comparison of duplex Doppler sonography with magnetic resonance angiography, MRI imaging was superior in the assessment of patency of the portal vein and surgical shunts, as well as in detection of varices.94 However, when technically adequate, the Doppler study was accurate in the assessment of normal portal anatomy and low direction. Duplex Doppler sonography has

the added advantages of decreased cost and portability of the equipment and therefore should be used as the initial screening method for portal hypertension.

Portal Vein Thrombosis Portal vein thrombosis has been associated with malignancy, including HCC, metastatic liver disease, carcinoma of the pancreas, and primary leiomyosarcoma of the portal vein,95 as well as with chronic pancreatitis, hepatitis, septicemia, trauma, splenectomy, portacaval shunts, hypercoagulable states such as pregnancy and in neonates, omphalitis, umbilical vein catheterization, and acute dehydration.96 Sonographic indings of portal vein thrombosis include echogenic thrombus within the lumen of the vein, portal vein collaterals, expansion of the caliber of the vein, and cavernous transformation96 (Figs. 4.32 and 4.33). Cavernous transformation of the portal vein refers to numerous wormlike vessels at the porta hepatis, which represent periportal collateral circulation.97 his pattern is observed in long-standing thrombosis, requiring up to 12 months to occur, and thus is more likely to develop with benign disease.98 Acute thrombus may appear relatively anechoic and thus may be overlooked unless Doppler ultrasound interrogation is performed. Malignant thrombosis of the portal vein has a high association with HCC and is oten expansive, as is malignant occlusion from other primary or secondary disease (Fig. 4.32A and B and Fig. 4.34). Doppler sonography is useful in distinguishing between benign and malignant portal vein thrombi in patients with cirrhosis. Both bland and malignant thrombi may demonstrate venous blood low. Pulsatile (arterial) low, however, has been found to be 95% speciic for the diagnosis of malignant portal vein thrombosis (see Fig. 4.32). he sensitivity was only 62% because many malignant thrombi are hypovascular.99

Budd-Chiari Syndrome he Budd-Chiari syndrome is a relatively rare disorder characterized by occlusion of the lumens of the hepatic veins with or without occlusion of the IVC lumen. he degree of occlusion and presence of collateral circulation predict the clinical course. Some patients die in the acute phase of liver failure. Causes of Budd-Chiari syndrome include coagulation abnormalities such as polycythemia rubra vera, chronic leukemia, and paroxysmal nocturnal hemoglobinuria; trauma; tumor extension from primary HCC, renal carcinoma, and adrenocortical carcinoma; pregnancy; congenital abnormalities; and obstructing membranes. he classic patient in North America is a young adult woman taking oral contraceptives who presents with an acute onset of ascites, right upper quadrant pain, hepatomegaly, and, to a lesser extent, splenomegaly. In some cases, no causal factor is found. he syndrome is more common in other geographic areas, including India, South Africa, and Asia. Sonographic evaluation of the patient with Budd-Chiari syndrome includes gray-scale and Doppler features.100-111 Ascites is invariably seen. he liver is typically large and bulbous in the acute phase (Fig. 4.35A). Hemorrhagic infarction may produce signiicant altered regional echogenicity. As infarcted areas become more ibrotic, echogenicity increases.109 he caudate lobe is oten

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FIG. 4.32 Portal Vein Thrombosis: Benign and Malignant. Malignant thrombus: transverse views of (A) the vein at the porta hepatis and (B) left ascending left portal vein. Both are distended with occlusive thrombus. Benign thrombus: (C) transverse and (D) sagittal images of simple, bland nonocclusive thrombus in the left portal vein at the porta hepatis.

A

B

FIG. 4.33 Cavernous Transformation of Portal Vein. (A) Gray-scale image. (B) Color Doppler image. Numerous periportal collateral vessels are present.

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FIG. 4.34 Metastasis to the Portal Vein From Colon Cancer. (A) Sagittal view of the main portal vein at the porta hepatis and (B) subcostal oblique sonogram of the left ascending branch of the portal vein show the portal vein is distended and highly echogenic (arrows). There is also evidence of cavernous transformation, an uncommon accompaniment of malignant portal vein occlusion.

A

B

FIG. 4.35 Acute Budd-Chiari Syndrome. (A) Transverse view of liver shows a large, bulbous caudate lobe. (B) Sagittal view of right hepatic vein shows echoes within the vein lumen consistent with thrombosis, with absence of the vessel toward the inferior vena cava. Doppler ultrasound showed no low in this vessel.

spared in Budd-Chiari syndrome because the emissary veins drain directly into the IVC at a lower level than the involved main hepatic veins. Increased blood low through the caudate lobe leads to relative caudate enlargement. Real-time scanning allows the radiologist to evaluate the IVC and hepatic veins noninvasively. Sonographic features include evidence of the hepatic vein occlusion (Fig. 4.35B and Fig. 4.36) and the development of abnormal intrahepatic collaterals (Fig. 4.37). he extent of hepatic venous involvement in Budd-Chiari

syndrome includes partial or complete inability to see the hepatic veins, stenosis with proximal dilation, intraluminal echogenicity, thickened walls, thrombosis (Figs. 4.38 and 4.39), and extensive intrahepatic collaterals107,108 (see Fig. 4.37). Membranous “webs” may be identiied as echogenic or focal obliterations of the lumen.107 Real-time ultrasonography, however, underestimates the presence of thrombosis and webs and may be inconclusive in a cirrhotic patient with hepatic veins that are diicult to image.108 Intrahepatic collaterals, on gray-scale images, show as

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B

FIG. 4.36 Budd-Chiari Syndrome. Abnormal hepatic vein appearance in three patients on transverse images of intrahepatic inferior vena cava. (A) Right hepatic vein is not seen at all. Middle and left hepatic veins show tight strictures just proximal to the inferior vena cava. (B) Right hepatic vein is seen as a thrombosed cord. Middle hepatic vein does not reach the inferior vena cava. Left hepatic vein is not seen. (C) Only a single hepatic vein, the middle hepatic vein, can be seen as a thrombosed cord.

FIG. 4.37 Budd-Chiari Syndrome. Abnormal intrahepatic collaterals on gray-scale sonograms in two patients. Both images show vessels with abnormal locations and increased tortuosity compared with the normal intrahepatic vasculature.

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FIG. 4.38 Budd-Chiari Syndrome. (A) Gray-scale transverse image of hepatic venous conluence shows complete absence of the right hepatic vein with obliteration of the lumen of a common trunk for the middle and left hepatic veins. (B) Color Doppler image shows that blood low in the middle hepatic vein (blue) is normally directed toward the inferior vena cava. As the trunk is obliterated, all the blood is lowing out of the left hepatic vein (red), which is abnormal. Other images showed anastomoses of the left hepatic vein with surface collaterals. (C) Color Doppler image shows an anomalous left hepatic vein with low to the inferior vena cava (normal direction) and aliasing from a long stricture. (D) Spectral Doppler waveform of the anomalous left hepatic vein shows a very high abnormal velocity of approximately 140 cm/sec, conirming the tight stricture.

tubular vascular structures in an abnormal location and typically are seen extending from a hepatic vein to the liver surface, where they anastomose with systemic capsular vessels. Duplex Doppler ultrasound and color Doppler low imaging (CDFI) can help determine both the presence and the direction of hepatic venous low in the evaluation of patients with suspected Budd-Chiari syndrome. he middle and let hepatic veins are best scanned in the transverse plane at the level of the xiphoid process. he right hepatic vein is best evaluated from a right intercostal approach.105 he intricate pathways of blood low out of the liver in the patient with Budd-Chiari syndrome can be mapped with documentation of hepatic venous occlusions,

hepatic-systemic collaterals, hepatic venous–portal venous collaterals, and increased caliber of anomalous or accessory hepatic veins. he normal blood low in the IVC and hepatic veins is phasic in response to both the cardiac and respiratory cycles.100 In Budd-Chiari syndrome, low in the IVC, hepatic veins, or both, changes from phasic to absent, reversed, turbulent, or continuous.104,112 Continuous low has been called the pseudoportal Doppler signal and appears to relect either partial IVC obstruction or extrinsic IVC compression.103 he portal blood low also may be afected and is characteristically either slowed or reversed.104

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The Liver

103

IVC

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RHV

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D

FIG. 4.39 Budd-Chiari Syndrome With Extensive Inferior Vena Cava Thrombosis. (A) Sagittal image of the inferior vena cava (IVC) shows that it is distended with echogenic thrombus. (B) Middle hepatic vein as a thrombosed cord. (C) Gray-scale image of right hepatic vein (RHV) and (D) color Doppler image show that anomalous right hepatic vein is distended with thrombus. There is low in the vein proximal to the thrombus.

he use of Doppler in the patient with suspected Budd-Chiari syndrome lends strong supportive evidence to the gray-scale impression of missing, compressed, or otherwise abnormal hepatic veins and IVC.102,112 Associated reversal of low in the portal vein and epigastric collaterals is also optimally assessed with this technique.112 Hepatic veno-occlusive disease causes progressive occlusion of the small hepatic venules. he disease is endemic in Jamaica, secondary to alkaloid toxicity from bush tea. In North America, most cases are iatrogenic, secondary to hepatic irradiation and chemotherapy used in bone marrow transplantation.101 Patients with hepatic veno-occlusive disease are clinically indistinguishable from those with Budd-Chiari syndrome. Duplex Doppler

sonography demonstrates normal caliber, patency, and phasic forward (toward the heart) low of the main hepatic veins and IVC.101 Flow in the portal vein, however, may be abnormal, showing either reversed or “to and fro” low.101,113 In addition, the diagnosis of hepatic veno-occlusive disease may be suggested in a patient with decreased portal blood low (compared with baseline measurement before ablative therapy).101

Portal Vein Aneurysm Aneurysms of the portal vein are rare. heir origin is either congenital or acquired secondary to portal hypertension. Portal vein aneurysms have been described proximally at the junction of the superior mesenteric and splenic veins and distally involving

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the portal venous radicles. he sonographic appearance is that of a vascular mass connected to the portal system with turbulent low.

Intrahepatic Portosystemic Venous Shunts Intrahepatic arterial-portal istulas are well-recognized complications of large-gauge percutaneous liver biopsy and trauma. Conversely, intrahepatic portohepatic venous shunts are rare. heir cause is controversial and believed to be either congenital or related to portal hypertension.114,115 Patients typically are middle aged and present with hepatic encephalopathy. Anatomically, portohepatic venous shunts are more common in the right lobe. Sonography demonstrates a tortuous tubular vessel or complex vascular channels, which connect a branch of the portal vein to a hepatic vein or the IVC.114-116 he diagnosis is conirmed angiographically.

Aneurysm, Pseudoaneurysm, and Dissection he hepatic artery is the fourth most common site of an intraabdominal aneurysm, following the infrarenal aorta, iliac, and splenic arteries. Eighty percent of patients with a hepatic artery aneurysm experience catastrophic rupture into the peritoneum, biliary tree, gastrointestinal tract, or portal vein.117 Hepatic artery pseudoaneurysm secondary to chronic pancreatitis has been described. he duplex Doppler sonographic examination revealed turbulent arterial low within a sonolucent mass.117 Primary dissection of the hepatic artery is rare and in most cases leads to death before diagnosis.118 Sonography may show the intimal lap with the true and false channels.

Hereditary Hemorrhagic Telangiectasia Hereditary hemorrhagic telangiectasia, or Osler-Weber-Rendu, is an autosomal dominant disorder that causes arteriovenous (AV) malformations in the liver, hepatic ibrosis, and cirrhosis. Patients present with multiple telangiectasias and recurrent

A

episodes of bleeding. Sonographic indings include a large feeding common hepatic artery up to 10 mm, multiple dilated tubular structures representing AV malformations, and large draining hepatic veins secondary to AV shunting.119

Peliosis Hepatis Peliosis hepatis is a rare liver disorder characterized by blood-illed cavities ranging from less than a millimeter to many centimeters in diameter. It can be distinguished from hemangioma by the presence of portal tracts within the ibrous stroma of the blood spaces. he pathogenesis of peliosis hepatis involves rupture of the reticulin ibers that support the sinusoidal walls, secondary to cell injury or nonspeciic hepatocellular necrosis. he diagnosis of peliosis can be made with certainty only by histologic examination. Most cases of peliosis afect the liver, although other solid internal organs and lymph nodes may be involved in the process as well. Although early reports described incidental detection of peliosis hepatis at autopsy in patients with chronic wasting disorders, it has now been seen following renal and liver transplantation, in association with a multitude of drugs, especially anabolic steroids, and with an increased incidence in patients with HIV.119 he HIV association may occur alone or as part of bacillary angiomatosis in the spectrum of opportunistic infections of AIDS.120 Peliosis hepatis has the potential to be aggressive and lethal. he imaging features of peliosis hepatis have been described in single case reports,121-123 although oten without adequate histologic conirmation. Angiographically, the peliotic lesions have been described as accumulations of contrast detected late in the arterial phase and becoming more distinct in the parenchymal phase.124 On sonography, described lesions are nonspeciic and have shown single or multiple masses of heterogeneous echogenicity.119,120,125 Calciications have been reported125 (Fig. 4.40). Peliosis hepatis is diicult to diagnose both clinically and radiologically and must be suspected in a susceptible individual with a liver mass.

B

FIG. 4.40 Peliosis Hepatis. Peliosis hepatis in 34-year-old woman with deteriorating liver function necessitating transplantation. (A) Sagittal right lobe and (B) sagittal left lobe scans show multiple large liver masses with innumerable tiny punctate calciications. (With permission from Muradali D, Wilson SR, Wanless IR, et al. Peliosis hepatis with intrahepatic calciications. J Ultrasound Med. 1996;15[3]:257-260.125)

CHAPTER 4

HEPATIC MASSES Focal liver masses include a variety of malignant and benign neoplasms, as well as masses with developmental, inlammatory, and traumatic causes. In cross-sectional imaging, two basic issues relate to a focal liver lesion: characterization of a known liver lesion (what is it?) and detection (is it there?). he answer to either question requires a focused examination, oten adjusted according to the clinical situation.

Liver Mass Characterization Characterization of a liver mass on conventional sonography is based on the appearance of the mass on gray-scale imaging and vascular information derived from spectral, color, and power Doppler sonography. With excellent spatial and contrast resolution, the gray-scale morphology of a mass allows for the differentiation of cystic and solid masses, and characteristic appearances may suggest the correct diagnosis without further evaluation. Oten, however, deinitive diagnosis is not based on gray-scale information alone, but on vascular information obtained on conventional Doppler ultrasound examination. However, conventional Doppler oten fails in the evaluation of a focal liver mass, particularly in a large patient or on a small or deep liver lesion, or on a mass with inherent weak Doppler signals. Motion artifact is also highly problematic for abdominal Doppler ultrasound studies, and a let lobe liver mass close to the pulsation of the cardiac apex, for example, can limit assessment by conventional Doppler. For these reasons, conventional ultrasound is not regarded highly for characterization of focal liver masses, and a mass detected on ultrasound is historically evaluated further with CECT or MRI for deinitive characterization.

Role of Microbubble Contrast Agents Worldwide, noninvasive diagnosis of focal liver masses is achieved with CECT and MRI based on recognized enhancement patterns in the arterial and portal venous phases. hese noninvasive methods of characterization have become so accurate that excisional and percutaneous biopsy for diagnosis of liver masses is now rarely performed. In recent years, however, CEUS has joined the ranks of CT and MRI in providing similar diagnostic information as well as information unique to CEUS.126 Injection of a microbubble contrast agent to enhance the Doppler signal from blood and imaging with a specialized imaging technique such as pulse inversion sonography allow for preferential detection of the signal from the contrast agent while suppressing the signal from background tissue. Ultrasound contrast agents currently in use are secondgeneration agents comprising tiny bubbles of a perluorocarbon gas contained within a stabilizing shell. Microbubble contrast agents are blood pool agents that do not difuse through the vascular endothelium. his is of potential importance when imaging the liver because comparable contrast agents for CT and MRI may difuse into the interstitium of a tumor. Our personal experience with perluorocarbon microbubble agents is largely based on the use of Deinity (Lantheus Medical Imaging, Billerica, MA) and brief exposure to Optison (GE Healthcare,

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Milwaukee, WI).127,128 We routinely perform CEUS for characterization of incidentally detected liver masses, those found on surveillance scans of patients at risk for HCC, and any focal mass referred by our clinicians found on outside imaging or indeterminate on CT and MRI.129 Microbubble contrast agents for ultrasound are unique in that they interact with the imaging process.127 he major determinant of this interaction is the peak negative pressure of the transmitted ultrasound pulse, relected by the mechanical index (MI). he bubbles show stable, nonlinear oscillation when exposed to an ultrasound ield with a low MI, with the production of harmonics of the transmitted frequency, including the frequency double that of the sound emitted by the transducer, the second harmonic. When the MI is raised suiciently, the bubbles undergo irreversible disruption, with the production of a brief but bright, high-intensity ultrasound signal (see Chapter 3). Liver lesion characterization with microbubble contrast agents is based on lesional vascularity and lesional enhancement in the arterial phase (10-40 sec), portal venous phase (40-90 sec), and late phase (up to 5 minutes). Lesional vascularity assessment depends on continuous imaging of the agents while they are within the vascular pool. We document the presence, number, distribution, and morphology of any lesional vessels. A low MI is essential because it will preserve the contrast agent population without destruction of the bubbles in the imaging ield, allowing for prolonged periods of real-time observation. he morphology of the lesional vessels is discriminatory and facilitates the diagnosis of liver lesions (Fig. 4.41). Lesional enhancement is best determined by comparing the echogenicity of the lesion to the echogenicity of the liver at a similar depth on the same frame and requires knowledge of liver blood low. he liver has a dual blood supply from the hepatic artery and portal vein. he liver derives a larger proportion of its blood from the portal vein, whereas most liver tumors derive their blood supply from the hepatic artery. At the initiation of the injection, the low-MI technique will cause the entire ield of view (FOV) to appear virtually black, regardless of the baseline appearance of the liver and the lesion in question. In fact, a known mass may be invisible at this point. As the microbubbles arrive in the FOV, the discrete vessels in the liver and then those within a liver lesion will be visualized, followed by increasing generalized enhancement as the microvascular volume of liver and lesion ills with the contrast agent. he liver parenchyma will appear more echogenic in the arterial phase than at baseline, and even more enhanced in the portal venous phase, as a relection of its blood low. Vascularity and enhancement patterns of a liver lesion, by comparison, will therefore relect the actual blood low and hemodynamics of the lesion in question, such that a hyperarterialized mass will appear more enhanced against a less enhanced liver on an arterial phase sequence. Conversely, a hypoperfused lesion will appear as a dark or hypoechoic region within the enhanced liver on an arterial phase sequence. Currently, evaluation of lesional enhancement is usually performed with the low-MI technique just described. However, details of vessel morphology and lesional enhancement are even more sensitively assessed using a bubble-tracking technique called maximum-intensity projection (MIP) imaging.130 In this

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A

B

C

D

FIG. 4.41 Early Arterial Phase Vascular Morphology. Shown on real-time dynamic ultrasound, this is contributory to diagnosis of focal liver masses. (A) Stellate vessels are highly suggestive of focal nodular hyperplasia. (B) Peripheral discontinuous nodular enhancement without linear vascularity suggests hemangioma. (C) Rim enhancement has a high association with malignant disease, especially metastases and cholangiocarcinoma. (D) Dysmorphic tortuous vessels are suggestive of malignant tumors, in this case a hepatocellular carcinoma. The illing from the periphery, as here, is common for this diagnosis.

technique, performed either at wash-in of contrast or at the peak of arterial phase enhancement, a brief high-MI exposure will destroy all the bubbles within the FOV. Sequential frames, as the lesion and liver are reperfused, will track the bubble course providing exquisite resolution (Fig. 4.42, Videos 4.5 and 4.6). here are established algorithms for the diagnosis of focal liver masses with CEUS, with similarities to CT and MRI algorithms but also important diferences131-133 (Table 4.3). Diagnosis of benign liver masses, hemangioma, and focal nodular hyperplasia (FNH) is extremely accurate showing characteristic features of enhancement in the arterial phase and sustained enhancement in the portal venous phase (Fig. 4.43),

such that their enhancement equals or exceeds the enhancement of the adjacent liver. Malignant tumors, by comparison, tend to show washout, such that the tumor appears unenhanced in the portal venous phase of enhancement (Fig. 4.44). Exceptions to this general rule include frequent washout of benign hepatic adenoma and delayed or no washout of HCC. Discrimination of benign and malignant liver masses has similar high accuracy.134

Liver Mass Detection Excellent spatial resolution allows small lesions to be well seen on sonography. herefore it is not size but echogenicity that

CHAPTER 4

FIG. 4.42 Normal Liver Vasculature. Temporal maximum-intensity projection image shows accumulated enhancement in 11 seconds after contrast material arrives in liver. Depiction of vessel structure to ifth-order branching is evident. Focal unenhanced region (arrow) is slowly perfusing hemangioma. (With permission from Wilson S, Jang H, Kim T, et al. Real-time temporal maximum-intensity-projection imaging of hepatic lesions with contrast-enhanced sonography. AJR Am J Roentgenol. 2008;190[3]:691-695.130)

determines lesion conspicuity on a sonogram. hat is, a tiny mass of only a few millimeters will be easily seen if it is increased or decreased in echogenicity compared with the adjacent liver parenchyma. Because many metastases are either hypoechoic or hyperechoic relative to the liver, a careful examination should allow for their detection. Nonetheless, many metastatic lesions are of similar echogenicity to the background liver, making their detection diicult or impossible, even if they are of a substantial size. his occurs when the backscatter from the lesion is virtually identical to the backscatter from the liver parenchyma. To combat this inherent problem of lack of contrast between many metastatic liver lesions and the background liver on conventional sonography, contrast-enhanced liver ultrasound is helpful (Fig. 4.45). CEUS increases the backscatter from the liver compared with the liver lesions, thereby improving their detection. his occurs rapidly following the arterial phase of enhancement and generally lasts for several minutes beginning in the portal venous and persisting for the late phase. Of historic interest is the use of the irst-generation contrast agent Levovist (Schering AG, Berlin). Ater clearance of the contrast agent from the vascular pool, the microbubble persisted in the liver, probably within the Kupfer cells on the basis of phagocytosis. A high-MI sweep through the liver produced bright enhancement in the distribution of the bubbles. herefore all normal liver enhances. Liver metastases, lacking Kupfer cells,

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do not enhance and therefore show as black or hypoechoic holes within the enhanced parenchyma135 (Fig. 4.45A and B). In a multicenter study conducted in Europe and Canada, more and smaller lesions were seen than on baseline scan.136 Overall, lesion detection was equivalent to that of CT and MRI. he decibel diference between the lesions and the liver parenchyma is increased many fold because of increased backscatter from contrast agent within the normal liver tissue. Although many results were compelling, these irst-generation contrast agents are no longer marketed. Today, current requirements for improved lesion detection use a similar technique of CEUS with a perluorocarbon contrast agent and low-MI scanning in both the arterial and the portal venous phase. he use of a low-MI imaging technique for lesion detection has advantages in terms of scanning because the microbubble population is preserved and timing is not so critical. Virtually all metastases will be unenhanced relative to the liver in the portal and the late phase and the liver parenchyma will remain optimally enhanced. herefore malignant lesions tend to appear hypoechoic in the portal phase, allowing for improved lesion detection (Fig. 4.45C and D). his observation, that malignant lesions tend to be hypoechoic in the portal venous phase of perluorocarbon liver enhancement, is helpful for both lesion detection and lesion characterization. Enhancement of benign lesions, FNH, and hemangioma generally equals or exceeds liver enhancement in the portal venous phase. Detection of hypervascular liver masses (e.g., HCC, metastases) is also improved by scanning with perluorocarbon agents in the arterial phase. hese lesions will generally show as hyperechoic masses relative to the liver parenchyma in the arterial phase because they are predominantly supplied by hepatic arterial low.

HEPATIC NEOPLASMS Sonographic visualization of a focal liver mass may occur in a variety of clinical scenarios, ranging from incidental detection to identiication in a symptomatic patient or as part of a focused search in a patient at risk for hepatic neoplasm. Hemangiomas, FNH, and adenomas are the benign neoplasms typically encountered in the liver, whereas HCC and metastases account for the majority of malignant tumors. he role of imaging in the evaluation of an identiied focal liver mass is to determine which masses are potentially clinically important, requiring conirmations of their diagnoses, and which masses are likely to be insigniicant and benign, not requiring further evaluation to conirm their nature. On a sonographic study, there is considerable overlap in the appearances of focal liver masses. Once a liver mass is seen, however, the excellent contrast and spatial resolution of state-of-the-art ultrasound equipment have provided guidelines for the initial management of patients, which include recognition of the following features: • A hypoechoic halo identiied around an echogenic or isoechoic liver mass is an ominous sonographic sign necessitating deinitive diagnosis. • A hypoechoic and solid liver mass is highly likely to be signiicant and also requires deinitive diagnosis.

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TABLE 4.3 Schematic of Algorithm for Liver Mass Diagnosis on Contrast-Enhanced Ultrasound

Hemangioma

or

AP Peripheral nodular enhancement Centripetal progression of enhancement PVP Complete or partial fill-in AP Centrifugal hypervascular enhancement Stellate arteries PVP Sustained enhancement Hypoechoic central scar

FNH

AP Diffuse or centripetal hypervascular enhancement Dysmorphic arteries Adenoma

or

AP Rim enhancement Diffuse hypervascular Hypovascular

or

Metastases

or

Arterial phase (AP)

(+) Enhancement

PVP Sustained enhancement Soft wash out

PVP Fast washout

Portal venous phase (PVP)

Soft wash out

(–) enhancement (wash out)

AP, Arterial phase; FNH, focal nodular hyperplasia; PVP, portal venous phase. With permission from Wilson SR, Burns PN. Microbubble-enhanced US in body imaging: what role? Radiology. 2010;257(1):24-39.148

• Multiple solid liver masses may be signiicant and suggest possible metastatic or multifocal malignant liver disease. However, hemangiomas are also frequently multiple. • Clinical history of malignancy, chronic liver disease or hepatitis, and symptoms referable to the liver are requisite information for interpretation of a focal liver lesion.

Benign Hepatic Neoplasms Cavernous Hemangioma Cavernous hemangiomas are the most common benign tumors of the liver, occurring in approximately 4% of the population. hey occur in all age groups but are more common in adults, particularly women, with a female-to-male ratio of approximately 5:1. Histologically, hemangiomas consist of multiple vascular channels that are lined by a single layer of endothelium and

separated and supported by ibrous septa. he vascular spaces may contain thrombi. he vast majority of hemangiomas are small, asymptomatic, and discovered incidentally. Large lesions may, in rare cases, produce symptoms of acute abdominal pain, caused by hemorrhage or thrombosis within the tumor. hrombocytopenia, caused by sequestration and destruction of platelets within a large cavernous hemangioma (Kasabach-Merritt syndrome), occasionally occurs in infants and is rare in adults. Traditional teaching suggests that once identiied in the adult, hemangiomas usually have reached a stable size, rarely changing in appearance or size.137,138 In our practice, however, we have documented substantial growth of some lesions over many years of follow-up. Hemangiomas may enlarge during pregnancy or with the administration of estrogens, suggesting the tumor is hormone dependent.

CHAPTER 4

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B

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FIG. 4.43 Sustained enhancement in the portal venous phase, on contrast-enhanced ultrasound (CEUS) and contrast-enhanced computed tomography (CECT) scan, suggestive of a benign mass. (A) and (C) are arterial phase images on CT and CEUS, respectively, both showing arterial phase hyperenhancement. (B) and (D) are portal venous phase images on CT and CEUS, respectively, both showing sustained enhancement and a nonenhanced scar. This sustained enhancement is concordant on the two scans and suggests a benign tumor. This is a conirmed FNH. See also Video 4.5. (With permission from Wilson S, Greenbaum L, Goldberg B. Contrast-enhanced ultrasound: what is the evidence and what are the obstacles? AJR Am J Roentgenol. 2009;193[1]:55-60.129)

he sonographic appearance of cavernous hemangioma varies. Typically the lesion is small ( 3 cm Internal soft tissue Mural or septal thickening

including symptomatic patients, growth of the cyst on serial studies, tumor greater than 3 cm in diameter, internal sot tissue, and mural or septal thickening. Multiple societies have proposed algorithms to follow incidentally detected pancreatic cysts,155 but there is a great deal of uncertainty in this process,156,157 and future assessment may rely on novel tumor markers and molecular analysis rather than cross-sectional imaging morphology.158 Data from 2015 suggest that pancreatic cysts found incidentally by using CT or MRI may be associated with increased mortality for patients younger than 65 years and an overall increased risk of pancreatic adenocarcinoma.159

Simple Pancreatic Cysts Simple pancreatic cysts are rare in the general population, with a prevalence of 0.2%160 to 1.2%.151 hese low percentages may underestimate true prevalence because imaging161 and autopsy162 studies have recorded a substantially higher prevalence, about 20% and 24.3%, respectively. Our experience suggests that the lower prevalence rates are closer to the actual experience in clinical imaging. Detecting a simple pancreatic cyst should raise suspicion of an inherited disease that has a high prevalence of

cysts, such as autosomal dominant polycystic kidney disease (ADPKD)163 or von Hippel–Lindau (VHL) disease.164 Multiple pancreatic cysts can also occur in individuals with cystic ibrosis.165 Multiple pancreatic cysts are more common in VHL disease than in ADPKD. Prevalence of pancreatic cysts in patients with VHL ranges from 50% to 90%, making pancreatic cysts the most common type of lesion in VHL disease.164 hus multiple simple pancreatic cysts should suggest the diagnosis of VHL (Fig. 7.75). In addition to simple cysts, other pancreatic lesions associated with VHL include serous cystic neoplasm and pancreatic endocrine tumors, with a slightly increased risk of ductal adenocarcinoma.164

Cystic Neoplasms Cystic tumors of the pancreas account for about 10% of cystic pancreatic lesions. Although most solid tumors are ductal adenocarcinomas with a poor prognosis, cystic tumors are usually either benign lesions or low-grade malignancies. Malignant cystic tumors account for about 1% of all pancreatic malignancies.73 Mucinous tumors such as intraductal papillary mucinous neoplasm and mucinous cystic neoplasm are oten malignant. he risk of malignancy is greater in older individuals. Reliable prevalence data are diicult to ind166 but are estimated in Table 7.4.

Serous Cystic Neoplasm Serous cystic neoplasm, previously known as microcystic adenoma, is typically a benign tumor, although a few invasive, malignant examples have been reported.73,166 Serous cystic neoplasm occurs more frequently in women and is most oten found in the pancreatic head.154 hese lesions are composed of myriad tiny cysts, generally too small to be individually resolved sonographically (Fig. 7.76). he multiple relective interfaces caused by the walls of the tiny cysts leads to an echogenic appearance, analogous to that of autosomal recessive polycystic kidney disease. hrough transmission is usual. Larger cysts (1-3 cm in diameter) oten are present at the periphery of the lesion. A radially oriented, ibrous pattern occurs in a minority of patients,149 and a central calciication is oten present (30%50%) (Fig. 7.77). Small lesions (5 cm

10%

90% 100% 50%-60% 100% Nonhyperfunctioning

All tumors VIP, Vasoactive intestinal polypeptide.

SMA SMV

Ao

Stent IVC

FIG. 7.84 Pancreatic Endocrine Tumor, Nonhyperfunctioning. Longitudinal oblique color Doppler sonogram shows 5-cm, hypoechoic malignant tumor large enough to cause bile duct obstruction, requiring stenting. Internal color low is typical with pancreatic endocrine tumors. Ao, Aorta; IVC, interior vena cava; SMA, superior mesenteric artery; SMV, superior mesenteric vein.

Unusual and Rare Neoplasms FIG. 7.83 Insulinoma on Intraoperative Ultrasound. This 10-mm lesion was discovered because of hyperinsulinism. (Courtesy of Dr. Hisham Tchelepi.)

clinically—because of pain,185 mass efect, or, if malignant, invasion and metastasis119 (Fig. 7.84). Incidental detection of smaller, nonhyperfunctioning tumors is becoming more frequent (Fig. 7.85). hese tumors are usually well deined and round or oval. hey generally appear hypoechoic compared to the normal parenchyma. hese tumors may have cystic changes and calciication.187 he larger, nonhyperfunctioning pancreatic endocrine tumors may be diicult to diferentiate from the more common pancreatic ductal adenocarcinoma. Sonographic indings that suggest the diagnosis are (1) prominent internal color low (rare in carcinoma), (2) lack of biliary or pancreatic ductal dilation in a pancreatic head lesion, and (3) lack of progression or metastasis on serial imaging.

On ultrasound, many histologic variants of pancreatic ductal adenocarcinoma are indistinguishable from tumors with the usual histologic features. hese include adenosquamous cell carcinoma, anaplastic carcinoma, and pleomorphic giant cell carcinoma. Acinar cell carcinoma and pleomorphic giant cell carcinoma, although oten indistinguishable from ductal adenocarcinoma, may be larger and may exhibit central necrosis. Primary pancreatic lymphoma is prohibitively rare, although adenopathy or difuse involvement from more generalized disease occurs with some frequency.120 Other rare pancreatic tumors include connective tissue–origin tumors (sarcomas), pancreaticoblastomas, dysontogenetic cysts, and metastases.190,191

Lipoma In contrast to the usual echogenic appearance of fat and fatty lesions, pancreatic lipomas are usually hypoechoic192,193 (Fig. 7.86). Other lipomas may have a mixed appearance, with a variable amount of internal echoes, or they may appear hyperechoic. he cause of hypoechoic fat is not known but may involve the number

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Stomach Pancreas LK

Spleen

A

Pancreas tail

B

C

D

FIG. 7.85 Small, Nonhyperfunctioning Pancreatic Endocrine Tumors. (A) Transverse sonogram shows 9-mm hypoechoic nonhyperfunctioning pancreatic endocrine tumor (arrow) discovered incidentally during an abdominal ultrasound. The pancreatic tail was removed. (B) and (C) In another patient, gray-scale (B) and color Doppler (C) sonograms show 2-cm hypervascular pancreatic endocrine tumor indenting the superior mesenteric artery (arrow). (D) In another patient, intraoperative ultrasound shows a 9-mm lesion (arrows) that was discovered incidentally. Marked dilation of the pancreatic duct is noted and can be a hallmark of serotonin-secreting pancreatic endocrine tumors. Intraoperative ultrasound is considered essential in many institutions for the surgical management of pancreatic endocrine tumors. PD, Pancreatic duct.

L L

A

B

FIG. 7.86 Pancreatic Lipoma. (A) Transverse sonogram of almost anechoic pancreatic lipoma (L). In contrast to the usual echogenic appearance of fat and fatty lesions, pancreatic lipomas are usually hypoechoic. (B) Computed tomography image conirms the fatty nature of the lesion. (Courtesy of Dr. Vinay Duddlewar.)

CHAPTER 7

FIG. 7.87 Lung Carcinoma Metastasis to Pancreas. Longitudinal sonogram shows typical hypoechoic metastasis (arrow). Pancreatic metastases are the most common pancreatic neoplasm in autopsy series but are rarely found clinically because they generally occur late with widespread metastatic disease.

of blood vessels, amount and thickness of connective tissue stroma, number of ibrous septae that separate fat lobules, and amount of water content in the fat.192,194

Metastatic Tumors In autopsy series, metastasis is the most common pancreatic neoplasm, found about four times as oten as pancreatic cancer.191 Clinical discovery of metastasis was rare until the advent of modern imaging.195 Pancreatic metastases are rarely clinically signiicant because they generally occur late in patients with widespread metastatic disease. Primary tumors that most oten metastasize to the pancreas include renal cell carcinoma, breast carcinoma, lung carcinoma (Fig. 7.87), melanoma, colon carcinoma, and stomach carcinoma.120,191,195 With metastasis to the pancreas, there may be a long interval between initial diagnosis of the primary lesion and discovery of the metastasis. his is especially true of renal cell carcinoma and, to a lesser degree, melanoma. Klein et al.195 found that the mean delay between discovery of the primary renal cell carcinoma and metastasis was 10 years; the longest interval was more than 24 years. A classic scenario is the discovery of a hypervascular mass (or masses) in the pancreas of a patient who had a remote, presumably cured renal cell carcinoma (Fig. 7.88). Diferential diagnosis from a hypervascular pancreatic endocrine tumor may be diicult in such cases.

CONTRAST-ENHANCED ULTRASOUND Contrast-enhanced ultrasound (CEUS) shows promise as a technique that will be beneicial in both endoscopic ultrasound and transabdominal ultrasound of the pancreas. Historically, CEUS was best considered an experimental technique.98,196

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FIG. 7.88 Renal Cell Carcinoma Metastasis to Pancreas. Longitudinal color Doppler sonogram shows hypervascular metastasis. Differentiation from a hypervascular pancreatic endocrine tumor may be dificult in these cases.

However, more recent data suggest that CEUS may become much more routine.197-199 Fan states, “CEUS has obvious superiority over conventional US in the general diagnostic accuracy of solid pancreatic lesions and in the diagnostic consistency among doctors. he performances of CEUS are similar to that of CECT in the diagnosis of pancreatic carcinoma and focal pancreatitis.”200 CEUS might be helpful in diagnosing pancreatic necrosis in patients with severe acute pancreatitis.147

Acknowledgment he authors would like to acknowledge Dr. Philip Ralls, the prior author of this chapter. His supreme dedication and passion for quality ultrasound practice and education in all areas was exemplary, and his images and text form the backbone of this updated version. REFERENCES 1. Harisinghani MG, Saini S, Schima W, et al. Simethicone coated cellulose as an oral contrast agent for ultrasound of the upper abdomen. Clin Radiol. 1997;52(3):224-226. 2. Lev-Toaf AS, Langer JE, Rubin DL, et al. Safety and eicacy of a new oral contrast agent for sonography: a phase II trial. AJR Am J Roentgenol. 1999;173(2):431-436. 3. Abu-Yousef MM, El-Zein Y. Improved US visualization of the pancreatic tail with simethicone, water, and patient rotation. Radiology. 2000;217(3):780-785. 4. Mori H, McGrath FP, Malone DE, Stevenson GW. he gastrocolic trunk and its tributaries: CT evaluation. Radiology. 1992;182(3):871-877. 5. Winter 3rd TC. “Proximal” versus “distal” in the pancreas. Radiographics. 2013;33(2):622-623. 6. Glaser J, Stienecker K. Pancreas and aging: a study using ultrasonography. Gerontology. 2000;46(2):93-96. 7. Guerra M, Gutiérrez L, Carrasco R, Arroyo A. Size and echogenicity of the pancreas in Chilean adults: echotomography study in 261 patients]. Rev Med Chil. 1995;123(6):720-726.

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143. Ralls PW, Wren SM, Radin R, et al. Color low sonography in evaluating the resectability of periampullary and pancreatic tumors. J Ultrasound Med. 1997;16(2):131-140. 144. Tomiyama T, Ueno N, Tano S, et al. Assessment of arterial invasion in pancreatic cancer using color Doppler ultrasonography. Am J Gastroenterol. 1996;91(7):1410-1416. 145. Wren SM, Ralls PW, Stain SC, et al. Assessment of resectability of pancreatic head and periampullary tumors by color low Doppler sonography. Arch Surg. 1996;131(8):812-817. 146. Ishida H, Konno K, Hamashima Y, et al. Assessment of resectability of pancreatic carcinoma by color Doppler sonography. Abdom Imaging. 1999;24(3):295-298. 147. Rickes S, Malfertheiner P. Echo-enhanced sonography—an increasingly used procedure for the diferentiation of pancreatic tumors. Dig Dis. 2004;22(1):32-38. 148. Fernández-del Castillo C, Targarona J, hayer SP, et al. Incidental pancreatic cysts: clinicopathologic characteristics and comparison with symptomatic patients. Arch Surg. 2003;138(4):427-434. 149. Edirimanne S, Connor SJ. Incidental pancreatic cystic lesions. World J Surg. 2008;32(9):2028-2037. 150. Sahani DV, Saokar A, Hahn PF, et al. Pancreatic cysts 3 cm or smaller: how aggressive should treatment be? Radiology. 2006;238(3):912-919. 151. Spinelli KS, Fromwiller TE, Daniel RA, et al. Cystic pancreatic neoplasms: observe or operate. Ann Surg. 2004;239(5):651-657. 152. Maker AV, Lee LS, Raut CP, et al. Cytology from pancreatic cysts has marginal utility in surgical decision-making. Ann Surg Oncol. 2008;15(11):3187-3192. 153. Belsley NA, Pitman MB, Lauwers GY, et al. Serous cystadenoma of the pancreas: limitations and pitfalls of endoscopic ultrasound-guided ine-needle aspiration biopsy. Cancer. 2008;114(2):102-110. 154. Megibow AJ. Update in imaging of cystic pancreatic masses for gastroenterologists. Clin Gastroenterol Hepatol. 2008;6(11):1194-1197. 155. Berland LL, Silverman SG, Gore RM, et al. Managing incidental indings on abdominal CT: white paper of the ACR incidental indings committee. J Am Coll Radiol. 2010;7(10):754-773. 156. Johnson PT, Horton KM, Megibow AJ, et al. Common incidental indings on MDCT: survey of radiologist recommendations for patient management. J Am Coll Radiol. 2011;8(11):762-767. 157. Brook OR, Beddy P, Pahade J, et al. Delayed growth in incidental pancreatic cysts: are the Current American College of Radiology recommendations for follow-up appropriate? Radiology. 2015;140972. 158. Freeny PC, Saunders MD. Moving beyond morphology: new insights into the characterization and management of cystic pancreatic lesions. Radiology. 2014;272(2):345-363. 159. Chernyak V, Flusberg M, Haramati LB, et al. Incidental pancreatic cystic lesions: is there a relationship with the development of pancreatic adenocarcinoma and all-cause mortality? Radiology. 2015;274(1):161-169. 160. Ikeda M, Sato T, Morozumi A, et al. Morphologic changes in the pancreas detected by screening ultrasonography in a mass survey, with special reference to main duct dilatation, cyst formation, and calciication. Pancreas. 1994;9(4):508-512. 161. Zhang XM, Mitchell DG, Dohke M, et al. Pancreatic cysts: depiction on single-shot fast spin-echo MR images. Radiology. 2002;223(2):547-553. 162. Kimura W, Nagai H, Kuroda A, et al. Analysis of small cystic lesions of the pancreas. Int J Pancreatol. 1995;18(3):197-206. 163. Chang MY, Ong AC. Autosomal dominant polycystic kidney disease: recent advances in pathogenesis and treatment. Nephron Physiol. 2008;108(1):p1-p7. 164. Leung RS, Biswas SV, Duncan M, Rankin S. Imaging features of von HippelLindau disease. Radiographics. 2008;28(1):65-79. 165. Cahill ME, Parmentier JM, Van Ruyssevelt C, Pauls CH. Pancreatic cystosis in cystic ibrosis. Abdom Imaging. 1997;22(3):313-314. 166. Adsay NV. Cystic neoplasia of the pancreas: pathology and biology. J Gastrointest Surg. 2008;12(3):401-404. 167. Ohashi KM, Maruyama Y. Four cases of mucin-producing cancer of the pancreas: speciic indings in the ampulla of Vater [Japanese]. Prog Dig Endosc. 1982;20:348-351. 168. Zamora C, Sahel J, Cantu DG, et al. Intraductal papillary or mucinous tumors (IPMT) of the pancreas: report of a case series and review of the literature. Am J Gastroenterol. 2001;96(5):1441-1447.

CHAPTER 7 169. Sarr MG, Kendrick ML, Nagorney DM, et al. Cystic neoplasms of the pancreas: benign to malignant epithelial neoplasms. Surg Clin North Am. 2001;81(3):497-509. 170. Lim JH, Lee G, Oh YL. Radiologic spectrum of intraductal papillary mucinous tumor of the pancreas. Radiographics. 2001;21(2):323-337. 171. Suzuki M, Fujita N, Onodera H, et al. Mucinous cystic neoplasm in a young male patient. J Gastroenterol. 2005;40(11):1070-1074. 172. Klimstra DS, Wenig BM, Hefess CS. Solid-pseudopapillary tumor of the pancreas: a typically cystic carcinoma of low malignant potential. Semin Diagn Pathol. 2000;17(1):66-80. 173. Shuja A, Alkimawi KA. Solid pseudopapillary tumor: a rare neoplasm of the pancreas. Gastroenterol Rep (Oxf). 2014;2(2):145-149. 174. Sidden CR, Mortele KJ. Cystic tumors of the pancreas: ultrasound, computed tomography, and magnetic resonance imaging features. Semin Ultrasound CT MR. 2007;28(5):339-356. 175. Buetow PC, Buck JL, Pantongrag-Brown L, et al. Solid and papillary epithelial neoplasm of the pancreas: imaging-pathologic correlation on 56 cases. Radiology. 1996;199(3):707-711. 176. Tucci G, Muzi MG, Nigro C, et al. Dermoid cyst of the pancreas: presentation and management. World J Surg Oncol. 2007;5:85. 177. Demos TC, Posniak HV, Harmath C, et al. Cystic lesions of the pancreas. AJR Am J Roentgenol. 2002;179(6):1375-1388. 178. Koenig TR, Loyer EM, Whitman GJ, et al. Cystic lymphangioma of the pancreas. AJR Am J Roentgenol. 2001;177(5):1090. 179. Cives M, Strosberg J. An update on gastroenteropancreatic neuroendocrine tumors. Oncology (Williston Park). 2014;28(9):749-756, 758. 180. Kloppel G, Heitz PU. Pancreatic endocrine tumors. Pathol Res Pract. 1988;183(2):155-168. 181. Phan GQ, Yeo CJ, Hruban RH, et al. Surgical experience with pancreatic and peripancreatic neuroendocrine tumors: Review of 125 patients. J Gastrointest Surg. 1998;2(5):473-482. 182. Shah S, Mortele KJ. Uncommon solid pancreatic neoplasms: ultrasound, computed tomography, and magnetic resonance imaging features. Semin Ultrasound CT MR. 2007;28(5):357-370. 183. O’Grady HL, Conlon KC. Pancreatic neuroendocrine tumours. Eur J Surg Oncol. 2008;34(3):324-332. 184. Grant CS. Insulinoma. Best Pract Res Clin Gastroenterol. 2005;19(5): 783-798.

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185. Horton KM, Hruban RH, Yeo C, Fishman EK. Multi-detector row CT of pancreatic islet cell tumors. Radiographics. 2006;26(2):453-464. 186. Doppman JL, Chang R, Fraker DL, et al. Localization of insulinomas to regions of the pancreas by intra-arterial stimulation with calcium. Ann Intern Med. 1995;123(4):269-273. 187. Buetow PC, Miller DL, Parrino TV, Buck JL. Islet cell tumors of the pancreas: clinical, radiologic, and pathologic correlation in diagnosis and localization. Radiographics. 1997;17(2):453-472. 188. Kawamoto S, Shi C, Hruban RH, et al. Small serotonin-producing neuroendocrine tumor of the pancreas associated with pancreatic duct obstruction. AJR Am J Roentgenol. 2011;197(3):W482-W488. 189. Shi C, Siegelman SS, Kawamoto S, et al. Pancreatic duct stenosis secondary to small endocrine neoplasms: a manifestation of serotonin production? Radiology. 2010;257(1):107-114. 190. Degen L, Wiesner W, Beglinger C. Cystic and solid lesions of the pancreas. Best Pract Res Clin Gastroenterol. 2008;22(1):91-103. 191. Cubilla AL, Fitzgerald PJ. Cancer of the exocrine pancreas: the pathologic aspects. CA Cancer J Clin. 1985;35(1):2-18. 192. Ryan MF, Hamilton PA, Smith AJ, Khalifa M. Radiologic features of pancreatic lipoma. Can Assoc Radiol J. 2003;54(1):41-44. 193. Barutcu O, Cihangiroglu M, Yildirim T, et al. Fat containing unusual tumor of the pancreas. Eur Radiol. 2002;12(4):770-773. 194. Spencer GM, Rubens DJ, Roach DJ. Hypoechoic fat: a sonographic pitfall. AJR Am J Roentgenol. 1995;164(5):1277-1280. 195. Klein KA, Stephens DH, Welch TJ. CT characteristics of metastatic disease of the pancreas. Radiographics. 1998;18(2):369-378. 196. D’Onofrio M, Zamboni G, Faccioli N, et al. Ultrasonography of the pancreas. 4. Contrast-enhanced imaging. Abdom Imaging. 2007;32(2):171-181. 197. Ardelean M, Sirli R, Sporea I, et al. Contrast enhanced ultrasound in the pathology of the pancreas—a monocentric experience. Med Ultrason. 2014;16(4):325-331. 198. Grossjohann HS. Contrast-enhanced ultrasound for diagnosing, staging and assessment of operability of pancreatic cancer. Dan Med J. 2012;59(12):B4536. 199. D’Onofrio M, Gallotti A, Principe F, Mucelli RP. Contrast-enhanced ultrasound of the pancreas. World J Radiol. 2010;2(3):97-102. 200. Fan Z, Li Y, Yan K, et al. Application of contrast-enhanced ultrasound in the diagnosis of solid pancreatic lesions—a comparison of conventional ultrasound and contrast-enhanced CT. Eur J Radiol. 2013;82(9):1385-1390.

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8

The Gastrointestinal Tract Stephanie R. Wilson

SUMMARY OF KEY POINTS • High-resolution ultrasound allows for excellent depiction of the bowel, including the normal multilayered appearance of the bowel wall and many pathologic features. • Ultrasound is a safe, objective, and accurate method for measuring the severity of inlammatory activity in inlammatory bowel disease, an essential requirement considering the young population most often affected by this chronic and often debilitating disease. • Contrast-enhanced ultrasound is an objective biomarker that may accurately evaluate disease activity in those with bowel wall inlammation. • Elastography measures bowel wall stiffness, increasing in those with chronic disease, helping to differentiate

patients amenable to medical therapy from those requiring surgical intervention. • Transrectal ultrasound (TRUS) is an excellent noninvasive and well-tolerated procedure for staging of rectal tumors. • Transvaginal ultrasound increases accuracy of bowel ultrasound in many women as pathologic features located deep in the pelvis may only be visible with this technique. • Transperineal scan allows for accurate depiction of perianal inlammatory masses without necessity of performing often painful scans with endoanal or endorectal placement of the transducer.

CHAPTER OUTLINE ANATOMY AND SONOGRAPHIC TECHNIQUE The Gut Signature Gut Wall Pathology Imaging Technique Doppler Evaluation of Gut Wall Contrast-Enhanced Ultrasound and Elastography of the Bowel GASTROINTESTINAL TRACT NEOPLASMS Adenocarcinoma Gastrointestinal Stromal Tumors Lymphoma Metastases INFLAMMATORY BOWEL DISEASE: CROHN DISEASE Classic Features Gut Wall Thickening Inlammatory Fat Lymphadenopathy Hyperemia Mucosal Abnormalities Conglomerate Masses

G

COMPLICATIONS Strictures Incomplete Mechanical Bowel Obstruction Localized Perforation Inlammatory Masses Fistula Formation Perianal Inlammatory Disease ACUTE ABDOMEN Right Lower Quadrant Pain Acute Appendicitis Crohn Appendicitis Right-Sided Diverticulitis Acute Typhlitis Mesenteric Adenitis With Terminal Ileitis Right-Sided Segmental Omental Infarction Left Lower Quadrant Pain Acute Diverticulitis OTHER ABNORMALITIES Mechanical Bowel Obstruction Paralytic Ileus

astrointestinal (GI) tract sonography is frequently frustrating and always challenging. Gas content within the gut lumen can make visibility diicult or even impossible; intraluminal luid may mimic cystic masses; and fecal material can create a variety of artifacts and pseudotumors. Nevertheless, normal gut

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Gut Edema Gastrointestinal Tract Infections AIDS Patients Pseudomembranous Colitis Congenital Cysts Ischemic Bowel Disease Pneumatosis Intestinalis Mucocele of Appendix Gastrointestinal Tract Hematoma Peptic Ulcer Bezoars Intraluminal Foreign Bodies Celiac Disease Cystic Fibrosis ENDOSONOGRAPHY Upper Gastrointestinal Tract Rectum: Tumor Staging of Rectal Carcinoma Anal Canal Fecal Incontinence Perianal Inlammatory Disease Acknowledgment

has a reproducible pattern, or gut signature, and a variety of gut diseases create recognizable sonographic abnormalities. herefore ultrasound may play a valuable role in the evaluation of patients in a variety of clinical situations, including suspicion of acute conditions of the GI tract, especially appendicitis and diverticulitis.

CHAPTER 8 Recent years have shown growing interest in the use of ultrasound for surveillance of patients with inlammatory bowel disease. Further, endosonography, performed with high-frequency transducers in the gut lumen, is an increasingly popular technique for assessing the esophagus, stomach, and rectum.

ANATOMY AND SONOGRAPHIC TECHNIQUE The Gut Signature he gut is a continuous hollow tube with four concentric layers (Fig. 8.1). From the lumen outward, these layers are (1) mucosa, which consists of an epithelial lining, loose connective tissue (or lamina propria), and muscularis mucosa; (2) submucosa; (3) muscularis propria, with inner circular and outer longitudinal ibers; and (4) serosa or adventitia. hese histologic layers correspond with the sonographic appearance1-3 (Table 8.1) and are referred to as the gut signature, where up to ive layers may be visualized (Fig. 8.2). he sonographic layers appear alternately echogenic and hypoechoic; the irst, third, and ith layers are echogenic, and the second and fourth layers are hypoechoic. his relationship

TABLE 8.1 Gut Signature: HistologicSonographic Correlation Histology

Sonography

Supericial mucosa/interface (epithelium and lamina propria) Muscularis mucosa Submucosa Muscularis propria (inner circular and outer longitudinal ibers) Serosa/interface

Echogenic Hypoechoic Echogenic Hypoechoic Echogenic

Submucosa Mucosa Epithelium Lamina propria Muscularis mucosa

Muscularis propria FIG. 8.1 Schematic Depiction of the Histologic Layers of the Gut Wall.

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of the histologic layering with the sonographic layering is best remembered by recognition that the muscular components of the gut wall—the muscularis mucosa and the muscularis propria—constitute the hypoechoic layers on sonography. On routine sonograms, the gut signature may vary from a “bull’s-eye” in cross section, with an echogenic central area and a hypoechoic rim, to full depiction of the ive sonographic layers. he quality of the scan and the resolution of the transducer determine the degree of layer diferentiation. Ultrasound is superior to both computed tomography (CT) and magnetic resonance imaging (MRI) for resolution of the gut wall layers. he normal gut wall is uniform and compliant, with an average thickness of 3 mm if distended and 5 mm if not. Other morphologic features that allow recognition of speciic portions of the gut include the gastric rugae (in the stomach), valvulae conniventes (plicae circulares in the small intestines), and haustra (in the colon) (Fig. 8.3). Real-time sonography allows assessment of the content and diameter of the GI lumen and the motility of the gut. Hypersecretion, mechanical obstruction, and ileus are implicated when gut luid is excessive. Peristalsis is normally seen in the small bowel and stomach. Activity may be increased with mechanical obstruction and inlammatory enteritides. Decreased activity is seen with paralytic ileus and in the end stages of mechanical bowel obstruction.

Gut Wall Pathology Evaluation of thickened gut on sonography is far superior to the evaluation of normal gut for two important reasons. hick gut, particularly if associated with abnormality of the perienteric sot tissues, creates a mass efect, which is easily seen on sonography. In addition, thickened gut is frequently relatively gasless, improving its sonographic evaluation. Gut wall pathology creates characteristic sonographic patterns (Fig. 8.4). he most familiar, the target pattern, was irst described by Lutz and Petzoldt4 in 1976 and later by Bluth et al.,5 who referred to the pattern as a “pseudokidney,” noting that a pathologically signiicant lesion was found in more than 90% of patients with this pattern. In both descriptions the hypoechoic external rim corresponds to thickened gut wall, whereas the echogenic center relates to residual gut lumen or mucosal ulceration. Identiication of thickened gut on sonographic examination may be related to a variety of diseases. Diagnostic possibilities are predicted by determining the (1) extent and location of disease, (2) preservation or destruction of wall layering, and (3) concentricity or eccentricity of wall involvement. Benignancy is favored by long segment involvement with concentric thickening and wall layer preservation. he classic benign pathology showing gut wall thickening is Crohn disease. Malignancy is favored by short segment involvement with eccentric disease and wall layer destruction. he classic malignant pathology showing gut wall thickening is adenocarcinoma of the stomach or colon. hese are guidelines rather than rules, because chronically thickened gut in Crohn disease may show layer destruction related to ibrotic and subacute inlammatory change, and iniltrative adenocarcinoma may show some wall layer preservation. Lymphadenopathy and hyperemia of the thickened gut wall

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FIG. 8.2 Gut Signature in a Patient With Mild Gut Thickening Caused by Crohn Disease. The muscle layers are hypoechoic. The submucosa and supericial mucosa layers are hyperechoic. There is a small amount of luid and air in the gut lumen.

may be seen in association with both malignant and benign gut wall thickening. Gut wall masses, as distinguished from thickened gut wall, may be intraluminal, mural, or exophytic, all with or without ulceration. Intraluminal gut masses and mucosal masses have a variable appearance on sonography but are frequently hidden by gas or luminal content. In contrast, gut pathology creating an exophytic mass (without or with mucosal involvement or ulceration) may form masses that are more readily visualized. hese may be diicult to assign to a GI tract origin if typical gut signatures, targets, or pseudokidneys are not seen on sonographic examination. Consequently, intraperitoneal masses of varying morphology, which do not clearly arise from the solid abdominal viscera or the lymph nodes, should be considered to have a potential gut origin.

Imaging Technique Routine sonograms are best performed when the patient has fasted. A real-time survey of the entire abdomen is performed

with a 3.5- to 5-MHz transducer, and any obvious masses or gut signatures are observed. he pelvis is scanned before and ater the bladder is emptied because the full bladder facilitates visualization of pathologic conditions in some patients and displaces abdominal bowel loops in others. A routine gut evaluation should include assessment of all of the small bowel and the colon. In women, transvaginal sonography is invaluable for evaluation of the portions of the gut within the true pelvis, particularly the rectum, sigmoid colon, and, in some patients, the ileum. Further, oral luid and a Fleet enema may improve localization and diagnosis of intraluminal or intramural gastric masses and rectal masses, respectively. Still images in long-axis and cross-sectional views as well as cine sweeps to show pathologic features allow for optimal review. Areas of interest then receive detailed analysis, including compression sonography6 (Fig. 8.5). Although this technique was initially described using high-frequency linear probes, 5- to 9-MHz convex probes and some sector probes work extremely well. he critical factor is a transducer with a short focal zone,

CHAPTER 8

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FIG. 8.3 Gut Recognition. (A) Sagittal and (B) cross-sectional views of the stomach show normal gastric rugae. The collapsed stomach shows variable wall thickness. (C) and (D) Valvulae conniventes (plicae circulares) of the small bowel. These are more easily seen when (C) there is luid in the lumen of the bowel or (D) the valvulae are edematous. (E) and (F) Variations in the appearance of the colonic haustrations in two normal persons.

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FIG. 8.4 Gut Wall Pathology. Schematic of sonographic appearances with sonographic equivalents. Top, Intraluminal mass. Inlammatory pseudopolyp on sonogram. Middle, Pseudokidney sign, with symmetrical wall thickening and wall layer destruction. Carcinoma of the colon on sonogram. Bottom, Exophytic mass. Serosal seed on visceral peritoneum of the gut on sonogram. (With permission from Wilson SR. The bowel wall looks thickened: what does that mean? In: Cooperberg PL, editor. RSNA categorical course syllabus. Chicago: RSNA; 2002. pp. 219-228.1)

allowing optimal resolution of structures close to the skin. Slow, graded pressure is applied. Normal gut will be compressed and gas pockets displaced away from the region of interest. In contrast, thickened abnormal loops of bowel and obstructed noncompressible loops will remain unchanged. Patients with peritoneal irritation or local tenderness will usually tolerate the slow, gentle increase in pressure of compression sonography, whereas they show a marked painful response if rapid, uneven scanning is performed.

Doppler Evaluation of Gut Wall Normal gut shows little signal on conventional color Doppler because interrogation is diicult in a normal and mobile bowel loop. Both neoplasia and inlammatory disease show increased vascularity compared with the normal gut wall (Fig. 8.6), whereas ischemic and edematous gut tends to be relatively hypovascular. he addition of color and spectral Doppler ultrasound evaluation to the study of the gut wall provides supportive evidence that gut wall thickening is caused by either ischemic or inlammatory

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FIG. 8.5 Schematic of Compression Sonography. Left, Normal gut is compressed. Middle, Abnormally thickened gut, or right, an obstructed loop, such as that seen in acute appendicitis, will be noncompressible.

change in the patient with acute abdominal pain. Teefey et al.7 examined 35 patients and found absent or barely visible blood low on color Doppler and absence of arterial signal to be suggestive of ischemia. In contrast, readily detected color Doppler low was consistent with inlammation.

Contrast-Enhanced Ultrasound and Elastography of the Bowel Two exciting new applications of ultrasound of the bowel include contrast-enhanced ultrasound (CEUS) and elastography. he former provides objective repeatable measures of mural blood low, which may change in response to inlammation and neoplasia, and the latter measures bowel wall stifness.9 Although these investigations are still in their infancy, their additional beneit over routine gray-scale ultrasound with Doppler is evident. heir great contribution to the evaluation of those with inlammatory bowel disease will be discussed in that section. CEUS is also useful in the assessment of mass lesions to determine the presence of vascularity analogous to the role of contrast enhancement on CT or MRI scan.

GASTROINTESTINAL TRACT NEOPLASMS he role of sonography in the evaluation of GI tract neoplasms is similar to that of CT. Visualization is limited in cases of early mucosal lesions or with small intramural nodules, whereas tumors growing to produce an exophytic mass, a thickened segment of gut, or a sizable intraluminal mass are more easily detected (Fig. 8.7, Video 8.1). Sonograms are frequently performed early in

the diagnostic workup of patients with GI tract tumors, oten before their initial identiication. Vague abdominal symptomatology, abdominal pain, a palpable abdominal mass, and anemia are common indications for these scans. Appreciation of the typical morphologies associated with GI tract neoplasia may lead to accurate recognition, localization, and even staging of disease, with the opportunity for directing appropriate further investigation, including sonography-guided aspiration biopsy.

Adenocarcinoma Adenocarcinoma is the most common malignant tumor of the GI tract. Grossly, it has variable growth patterns (see Fig. 8.7), including iniltrative, polypoid, fungating, and ulcerated tumors. Most GI tract mucosal cancers are not visualized on sonography. However, large masses, either intraluminal or exophytic, and annular tumors create sonographic abnormalities.10,11 Tumors of variable length may thicken the gut wall in either a concentric symmetrical or an asymmetrical pattern. A target or pseudokidney morphology may be created (see Fig. 8.4). Air in mucosal ulcerations typically produces linear echogenic foci, oten with ring-down artifact, within the bulk of the mass. Tumors are usually, but not invariably, hypoechoic. Annular lesions may produce gut obstruction with dilation, hyperperistalsis, and increased luminal luid of the gut proximal to the tumor site.11 Evidence of direct invasion, regional lymph node enlargement, and liver metastases should be sought. Adenocarcinoma accounts for 80% of all malignant gastric neoplasms, where iniltration may be supericial or transmural, the latter creating a linitis plastica, or “leather bottle,” stomach. Adenocarcinoma occurs much less frequently in the small bowel than in the stomach or large bowel. It accounts for approximately

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FIG. 8.6 Contribution of Doppler to Gut Assessment in Three Patients. (A) and (B) Cross-sectional images of the ileum proximal to an inlammatory stricture in Crohn disease. The lumen is distended with luid. The wall is slightly thick. (B) Color Doppler image shows marked hyperemia of the gut wall as a relection of its inlammation. (C) and (D) Transvaginal views in a young woman with right lower quadrant pain show the appendix as a round, tubular structure adjacent to the ovary. (D) Color Doppler image shows that appendix is hyperemic, consistent with inlammation. (E) and (F) Transverse images of the ascending colon show wall thickening with total layer destruction related to invasive colon carcinoma. Neoplastic tumors of the gut invariably show vascularity as here.

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FIG. 8.7 Adenocarcinoma of the Gut in Three Patients. (A) and (B) Cancer at gastroesophageal junction. (A) Sagittal and (B) transverse sonograms of the upper abdomen show a pseudokidney (arrowheads) adjacent to the left lobe of the liver. (C) and (D) Carcinoma of descending colon. (C) Long-axis image of the colon shows an abrupt transition from normal to thickened bowel. (D) An axial image shows a hypoechoic, circumferential mass with an “apple core” appearance. There is echogenic iniltrated fat and an enlarged hypoechoic lymph node adjacent to the tumor. (E) and (F) Intraluminal villous adenocarcinoma of stomach. (E) Transverse sonogram after luid ingestion shows a relatively well-deined, inhomogeneous, echogenic mass (arrows) within body of stomach. Fluid is in the stomach lumen (S). (F) Conirmatory barium swallow shows the villous tumor (arrows). See also Video 8.1.

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50% of the small bowel tumors found, 90% of them arising in either the proximal jejunum (Fig. 8.8A and B) or the duodenum. Crohn disease is associated with a signiicantly increased incidence of adenocarcinoma that usually develops in the ileum. Small bowel adenocarcinomas are generally annular in gross morphology, frequently with ulceration. Colon carcinoma is very common and accounts for virtually all malignant colorectal neoplasms. Colorectal adenocarcinoma grows with two major gross morphologic patterns: polypoid intraluminal tumors, which are most prevalent in the cecum and ascending colon, and annular constricting lesions (see Fig. 8.7C and D), which are most common in the descending and sigmoid colon. In rare cases, iniltrative tumors similar to those seen in the stomach may occur in the colon (Fig. 8.8C and D).

Gastrointestinal Stromal Tumors Of the mesenchymal tumors afecting the gut, those of smooth muscle origin are the most common and account for about 1% of all GI tract neoplasms. hese gastrointestinal stromal tumors (GISTs) are found most oten in the stomach and the small bowel.

Colonic tumors are the least common and occur most oten in the rectum. Although GISTs may be found as an incidental observation at surgery, sonography, or autopsy, these vascular tumors frequently become very large and may undergo ulceration, degeneration, necrosis, and hemorrhage.12 On sonography, smooth muscle (stromal) tumors typically produce round mass lesions of varying size and echogenicity, oten with central cystic areas13 related to hemorrhage or necrosis (Fig. 8.9). heir gut origin is not always easily determined, but if ulceration is present, pockets of gas in an ulcer crater may suggest their origin. Smooth muscle tumors of gut origin should be considered in the diferential diagnosis of incidentally noted, indeterminate abdominal masses in asymptomatic patients, particularly if they show central cystic or necrotic change (Fig. 8.9E and F). hese tumors are very amenable to sonographicguided aspiration biopsy.

Lymphoma he gut may be involved with lymphoma in two basic forms: as widespread dissemination in stage III or IV lymphoma of any

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FIG. 8.8 Adenocarcinoma of Bowel: Sonographic-CT Correlation. (A) Sonogram and (B) CT scan show large, necrotic, left upper quadrant mass at the ligament of Treitz with enlargement of the perienteric lymph nodes (arrow) in a 60-year-old man who presented with abdominal discomfort and blood loss. (C) and (D) Iniltrative carcinoma of transverse colon in a 42-year-old man who presented to the emergency department with acute abdominal pain. (C) Transverse sonogram of the epigastrium shows a featureless segment of thick gut with total loss of wall layering in the location of the transverse colon. Deep to the gut is a diffuse echogenic mass effect (arrow) suggesting iniltrated or inlamed fat. (D) Conirmatory CT scan. The iniltrated fat is black and streaky on the CT image. Neoplasia was not suspected on the basis of either imaging test or at surgery.

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FIG. 8.9 Gastrointestinal Stromal Tumors (GISTs) in Four Patients. (A) and (B) Exophytic gut mass, a gastric leiomyoma. (A) Transverse sonogram of epigastrium shows the normal gastric gut signature and the focal exophytic mass. (B) After water ingestion, the lumen contains luid that appears hypoechoic. The solid mass is clearly seen. (C) and (D) Gastric leiomyosarcoma. (C) Transverse sonogram after luid ingestion shows a complex, smooth intramural mass (arrows) projecting into the luid-illed stomach lumen (S). (D) Conirmatory barium swallow shows the intramural tumor (arrows). (E) and (F) Two patients with a large, upper abdominal, complex, and necrotic-appearing mass on sonography. Although the gut origin of the masses is not evident on the images, the correct diagnosis of GIST was suggested based on the appearance. The jejunum is the origin of the tumor in (E) and the stomach in (F).

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cell type or, more oten, as primary lymphoma of the GI tract, which is virtually always a non-Hodgkin lymphoma. Primary tumors constitute only 2% to 4% of all GI tract malignant tumors12 but account for 20% of those found in the small bowel. hree predominant growth patterns are observed: nodular or polypoid, carcinoma-like ulcerations, and iniltrating tumor masses that frequently invade the adjacent mesentery and lymph nodes. Small, submucosal nodules may be easily overlooked on sonography. However, many patients have large, easily visible, very hypoechoic, ulcerated masses in the stomach or small bowel14,15 (Fig. 8.10). Long, linear, high-amplitude echoes with ring-down artifacts, indicating gas in the residual lumen or ulcerations, and aneurysmal dilation of the bowel lumen are common observations. his particular pathologic state has been recognized as one of the more frequent presentations of patients with acquired immunodeiciency syndrome (AIDS)–related lymphoma. Regional lymph node enlargement may be visualized, although generalized lymph node abnormality is uncommon.

bowel, and colon are involved. On sonography, small submucosal nodules that tend to ulcerate are rarely seen, whereas large, difusely iniltrative tumors with large ulcerations are common, particularly in the small bowel where they create hypoechoic, well-deined masses that oten have bright, specular echoes with ring-down artifacts in areas of ulceration. Secondary neoplasm afecting the omentum and peritoneum may cause ascites (which may be particulate ascites), tiny or conluent supericial secondary nodules on the gut surface, or extensive omental cakes that virtually engulf the involved gut loops17 (Fig. 8.12). Metastases to the peritoneum most oten arise from primary tumors in the ovary or the gut. A drop metastasis in the pelvic pouch of Douglas shows as a small, solid, peritoneal nodule without obvious origin from the pelvic viscera.

INFLAMMATORY BOWEL DISEASE: CROHN DISEASE

Metastases Malignant melanoma and primary tumors of the lung and breast are the tumors most likely to have secondary involvement of the GI tract16 (Fig. 8.11). In order of frequency, the stomach, small

Inlammatory bowel disease (IBD) comprises Crohn disease and ulcerative colitis. Ulcerative colitis is a mucosal inlammation of the colon and oten shows little in the way of gross morphologic

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FIG. 8.10 Small Bowel Lymphoma in Two Patients. (A) Transverse left sonogram shows a hypoechoic round mass lesion. Central echogenicity with ring-down gas artifact suggests its gut origin. (B) Correlative CT scan shows large, soft tissue mass with corresponding residual gut lumen. (C) Sonogram in AIDs patient shows a focal midabdominal, hypoechoic mass with no wall layer deinition, which is classic for gut lymphoma. The luminal gas appears as central bright echogenicity with dirty shadowing. (D) Correlative CT scan.

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FIG. 8.11 Metastatic Malignant Melanoma to Small Bowel. (A) Transverse paraumbilical sonogram shows well-deined, hypoechoic mass with central irregular echogenicity with gas artifact suggesting gut origin. (B) Conirmatory CT scan.

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FIG. 8.12 Peritoneal Metastases in Two Patients. (A) Transvaginal image shows ascites and visceral peritoneal plaque on the surface of the small bowel loop (arrows) from metastatic ovarian cancer. (B) Transvaginal scan of peritoneal drop metastasis from stomach primary shows grossly particulate ascites. There is a small peritoneal implant in the vesicouterine angle.

change except with acute disease. Further, the involved colon is readily evaluated with colonoscopy and also with all crosssectional imaging, making its assessment relatively straightforward. Crohn disease, by comparison, is a chronic transmural. he peak age of onset is early in life, between the ages of 15 and 40 years, thus afecting patients during their most productive years. he natural course of the disease includes alternating periods of active inlammation and remission with a strong tendency to complicate over time, with the development of penetrating and/ or ibrostenotic lesions. As a result, surgical intervention rates have been high. Historically, Crohn disease was managed according to patient symptomatology. It is recognized, however, that neither inlammatory markers nor symptoms are an accurate relection of the state of the disease. Today, therefore, there is a dramatic shit in approach with an efort to treat to the target

of mucosal healing on endoscopy, including the use of aggressive biologic therapy and the increasing popularity of early introduction of anti–tumor necrosis factor-α (anti-TNFα). hese management changes necessitate frequent monitoring of all patients because repeated endoscopic performance is poorly tolerated, expensive, and not without risk. herefore safe, objective, noninvasive, and accurate methods for measuring the severity of inlammatory activity are vital. Imaging plays a major role in the diagnosis of disease,18 in the detection of recurrence, and in the recognition of complications, which may be associated with a silent clinical course. Surveillance imaging and monitoring response to therapy (which may be both expensive and toxic) is of prime importance. In a meta-analysis comparing diferent modalities for diagnosis of IBD, mean sensitivity estimates for the diagnosis on a per-patient

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basis were high and not signiicantly diferent for ultrasound (89.7%), MRI (93.0%), and CT (84.3%).19 herefore in this era of cost and radiation awareness, ultrasound is rising in importance for imaging of IBD.20 Sonography is our routine evaluation technique for initial disease diagnosis, the detection of recurrence,21 the determination of the extent, complications22 and activity of disease, and in the assessment of response to treatment. Although any portion of the gut may be involved, Crohn disease most commonly afects the terminal ileum and the colon. his transmural, granulomatous inlammatory process afects all layers of the gut wall and also the perienteric sot tissues. Grossly, the gut wall may become very thick and rigid with secondary luminal narrowing. Discrete or continuous ulcers and deep issures are characteristic, frequently leading to istula formation. Mesenteric lymph node enlargement and matting of involved loops are common. he mesentery may be markedly thickened and fatty, creeping over the edges of the gut to the antimesenteric border. he classic features of Crohn disease—wall thickening, inlammatory fat, lymphadenopathy, and hyperemia—relect these gross morphologic changes. Complications of Crohn disease include stricture, incomplete bowel obstruction, perforation, istulas, and inlammatory masses.21

he immediate objectives of a sonogram on a patient with known or suspected IBD, therefore, include documentation of the distribution and the extent of the disease, as well as the disease activity. A global assessment is made on ultrasound grading all of the classic features from 0, not present; through 1, mild; 2, moderate; and 3, showing severe change23 (Table 8.2). Utilization of such a scoring system allows for consistency of performance and reproducibility of results. It also facilitates comparisons for monitoring response to therapy.

Crohn Disease on Sonography CLASSIC FEATURES Gut wall thickening Inlammatory fat Mesenteric lymphadenopathy Hyperemia COMPLICATIONS Strictures Mechanical bowel obstruction Perforation Inlammatory masses Fistulas Appendicitis

TABLE 8.2 Ultrasound Global Assessment Showing Crohn Disease Activity Scores on GrayScale Ultrasound and Color Doppler Imaging Classiication

Gray-Scale Ultrasound Features of Activity Wall thickness (mm) Inlammatory fat

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INACTIVE 8.1

• Absent • Perienteric region resembles normal mesenteric fat

• Masslike • Slightly echogenic • Of less area than the bowel on axial view • Small regions of color without the vessel

• Masslike • More echogenic • Equal area to the bowel on axial view • Medium-length segments of color vessels in the bowel wall

• Masslike • Signiicantly echogenic • Of greater area than the bowel on axial view

• Mild wall thickness • Minimal inlammatory fat • Present but not minimal signal on CDI • Wall layer preservation

• Moderate wall thickness • Moderate inlammatory fat • Moderate signal on CDI • ± Wall layer preservationa

Color Doppler imaging (CDI) Mural blood low

• Absent

Ultrasound global assessment

• No signs of active disease

• Circumferential or continuous depiction of vessels in the bowel wall with or without mesenteric vessels • Moderate to severely thickened bowel wall • Abundant inlammatory fat • Long continuous mural blood vessels on CDI • ± Wall layer preservationa • Spiculation of serosal bordera

Loss of wall layering and serosal spiculation both suggest increasing disease severity. Reproduced with permission from Medellin-Kowalewski A, Wilkens R, Wilson A, et al. Quantitative contrast-enhanced ultrasound parameters in Crohn disease: their role in disease activity determination with ultrasound. AJR Am J Roentgenol. 2016;206(1):64-73.23

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Classic Features Gut Wall Thickening Gut wall thickening is the most frequently observed abnormality in patients with Crohn disease and varies in proportion to disease severity. Its identiication comprises the basis for initial disease detection, for detection of recurrence,24 and for determining the extent of disease. In a meta-analysis on the accuracy of sonography in detecting Crohn disease, Fraquelli et al.25 showed sensitivity and speciicity of 88% and 93%, respectively, when a bowel wall thickness threshold greater than 3 mm was used, and 75% and 97% with a threshold greater than 4 mm. Gut wall thickening in Crohn disease is most frequently concentric and may be marked.26,27 Wall echogenicity varies depending on the degree of inlammatory iniltration and ibrosis. Stratiication with retention of the gut layers is typical (Fig. 8.13A and B; also see Fig. 8.2, Videos 8.2 and 8.3). A target or pseudokidney appearance is possible in acute disease or long-standing ibrotic or subacute inlammatory disease as the gut wall layering is progressively lost (Fig. 8.13C and D). Long-standing and oten burnt-out disease may also show wall thickening with fat deposition in the submucosa, which appears as increased echogenicity of this layer (Fig. 8.13E and F). Actively involved gut typically appears rigid and ixed, with decreased or absent peristalsis (Video 8.4). Involvement of the serosal border of the bowel may result in spiculation of the border of the bowel (Fig. 8.14). Skip areas are frequent. Involved segments vary in length from a few millimeters to many centimeters. Bowel wall thickening may be caused by acute inlammatory change or related to chronic ibrosis and smooth muscle hypertrophy. Inlammatory Fat Mesenteric edema and inlammation of the mesenteric fat are also characteristic of Crohn disease, producing a mass in the mesentery adjacent to the diseased gut that may creep over the border of the abnormal gut or completely engulf it, the so-called creeping fat. Fat creeping onto the margins of the involved gut creates a uniform echogenic halo around the mesenteric border of the gut, with a thyroidlike appearance in cross section (Fig. 8.15). It may become more heterogeneous and even hypoechoic in long-standing disease. Creeping fat is the most common cause of gut loop separation seen on GI contrast studies.21 It is also the most striking and detectable abnormality on sonography of patients with perienteric inlammatory processes. herefore detection of creeping fat should lead to a detailed evaluation of the regional gut. Lymphadenopathy Tender and enlarged mesenteric and perienteric nodes are common features of the active phase of inlammation with Crohn disease (Fig. 8.16). Lymphadenopathy may persist in the inactive phase. he nodes appear as focal hypoechoic masses circumferentially surrounding the gut and in the expected location of the mesenteric attachment. Nodes are frequently quite round, are of moderate size, and typically lose the normal linear echogenic streak from the nodal hilum. Similar to the gut, the lymph nodes show hyperemia as a relection of their inlammation.

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Hyperemia Mesenteric vascularization and neoangiogenesis are recognized components of the inlammatory process, and evaluation of blood low is a useful tool for monitoring inlammatory activity and response to therapy. Disease activity correlates with hyperemia, as seen on color Doppler evaluation28 (Fig. 8.17, Video 8.5). Although subjective, this addition of color Doppler to gray-scale sonography can provide valuable supportive evidence of inlammatory change in the gut and adjacent inlamed fat21 (see Fig. 8.6B, D, and F). However, color Doppler shows blood low in major blood vessels with relatively fast-moving blood and does not show blood low at the perfusion level. To overcome this limitation of activity assessment, there has been increasing interest over recent years in the use of CEUS of the bowel, performed with the injection of microbubble contrast agents. Using ultrasound quantitative techniques, CEUS allows for objective measurement of blood low at the perfusion level as a relection of activity. On observation, we look for transmural enhancement of the bowel wall and also a “comb sign,” relective of blood low within the mesenteric vasculature (Fig. 8.18, Videos 8.6 and 8.7). Generation of time intensity curves allows for measurement of the peak enhancement and the area under the curve. Studies have shown a direct correlation between the level of bowel wall enhancement and active inlammatory disease, as assessed on colonoscopy.29,30 Further, Ripollés et al.29 show that CEUS measurements perform better than wall thickness in prediction of disease severity at colonoscopy. In our own laboratory, we have integrated the objective measurements of blood low on CEUS with the baseline gray-scale assessments of wall thickness and inlammatory fat to improve the objectivity of activity assessments on ultrasound.23 Mucosal Abnormalities Although endoscopy remains the major tool for evaluating mucosal and luminal abnormality, ultrasound may on occasion show luminal polypoid masses, such as inlammatory polyps, and deep ulcerations with pockets of echogenic air projecting within the gut wall. Ultrasound may also show intramural sinus tracts with air dissecting within the layers of the bowel wall (Fig. 8.19), as a complication of both Crohn disease and diverticulitis. Conglomerate Masses Conglomerate masses may be related to clumps of matted bowel, inlamed edematous mesentery, increased fat deposition in the mesentery, or, infrequently, mesenteric lymphadenopathy. Involved loops may demonstrate angulation and ixation resulting from retraction of the thickened ibrotic mesentery.

COMPLICATIONS Strictures Strictures are the most common complication of Crohn disease requiring surgical intervention. hese are due to rigid narrowing of the gut lumen, contributed to by mural inlammation, ibrosis, and smooth muscle hypertrophy. he luminal surfaces of involved

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FIG. 8.13 Gut Wall Thickening in Three Patients With Crohn Disease. (A) Cross-sectional and (B) sagittal views showing the typical thickening in active disease with wall layer retention; arrow, lymph node. (C) Cross-sectional and (D) sagittal views show complete loss of wall layering, as seen with active disease. (E) Sonogram and (F) corresponding CT image of the terminal ileum in a patient with burnt-out disease and fatty deposition in the submucosa, which appears echogenic on the sonogram. See also Videos 8.2 and 8.3. (C and D with permission from Wilson SR. The bowel wall looks thickened: what does that mean? In: Cooperberg PL, editor. RSNA categorical course syllabus. Chicago: RSNA; 2002. pp. 219-228.1)

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FIG. 8.14 Concerning Features for Severe Disease and Complication on Bowel Ultrasound in Two Patients. (A) A long-axis view of the terminal ileum shows bowel wall thickening and abundant surrounding echogenic inlammatory fat. The serosal margin of the bowel shows spiculation. (B) A long-axis view of the terminal ileum shows a hypoechoic bowel with loss of wall layering. There is a ixed acute angulation as well as spiculation of the serosal margin. Both the spiculation and ixed angulation have an association with stricture and perforation.

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FIG. 8.15 Creeping Fat in Two Patients With Crohn Disease. (A) Cross-sectional view of terminal ileum shows a hyperechoic mass effect (arrows) along the medial border of the gut representing creeping fat. (B) Conirmatory CT scan shows both the thick wall of the terminal ileum and the streaky fat (arrows). In another patient, (C) long-axis and (D) cross-sectional images of the sigmoid colon show gut wall thickening and surrounding echogenic inlammatory fat (arrows).

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FIG. 8.16 Lymphadenopathy in Two Patients With Crohn Disease. (A) Transverse image in the right lower quadrant shows a thick terminal ileum in cross section. There is inlamed fat in the location of the mesentery. A mesenteric node (arrow) shows as a small, solid, hypoechoic mass within the fat. (B) Multiple mesenteric nodes of varying size show as hypoechoic soft tissue masses within the mesentery, optimally shown in an oblique plane between the region of the ileocecal valve and the aortic bifurcation.

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FIG. 8.17 Classic Features of Active Crohn Disease. Gray-scale (A, C) and color Doppler (B, D) images of the terminal ileum show moderate wall thickening (7 mm), moderate inlammatory fat, and moderate hyperemia on color Doppler imaging. See also Videos 8.4 and 8.5.

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B FIG. 8.18 Contrast-Enhanced Ultrasound of the Bowel in Crohn Disease, Subjective and Objective. (A) Two images of contrast-enhanced bowel, axial view, show the comblike vessels from vascularization of the mesentery and the transmural enhancement of the bowel wall. The adjacent images on the right are low mean intensity poor detail gray-scale, used for reference. (B) Images are in long axis. A region of interest in the bowel wall and a subsequent objective time intensity curve allow measurement of the peak enhancement and area under the curve. At the bottom is the time intensity curve that allows for quantiication of the enhancement parameters. See also Videos 8.6 and 8.7. (A with permission from Wilson S. Evaluation of the small intestine by ultrasonography. In: Gourtsoyiannis N, editor. Radiologic imaging of the small intestine. Heidelberg: Springer-Verlag; 2002. pp. 73-86.18)

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FIG. 8.19 Intramural Sinus Tract in Active Crohn Disease of the Neoterminal Ileum. (A) and (B) Long-axis views of the terminal ileum show wall thickening and surrounding abundant inlammatory fat. The luminal surfaces are in apposition and are central within the thickened loop. (B) Bright echogenic line running parallel to the serosa, an intramural sinus tract illed with air. (C) and (D) Axial images show two bright echogenic linear streaks suggesting air dissected within the layers of the bowel, deep to the echogenic submucosal layer.

segments of gut most oten appear to be in ixed constant apposition, with the lumen appearing as a linear echogenic central area within a thickened gut loop (Fig. 8.20). his is in contrast to thickened sections, where the luminal diameter may be maintained (Fig. 8.21). Fixed acute angulations are frequent associations with advanced strictures (Video 8.8). Incomplete mechanical obstruction may be inferred if dilated, hyperperistaltic segments are seen proximal to a stricture (Fig. 8.21C and D, Videos 8.9 and 8.10). Peristaltic waves from the obstructed gut, proximal to a narrowed segment, may produce visible movement through the strictured segment. Less oten, involved segments of gut show luminal dilation with sacculation, as well as narrowing, and the retained lumen is of variable caliber. Concretions and bezoars may develop in gut between strictured segments. Parente et al.31 showed that bowel ultrasound is an accurate technique for detecting small bowel strictures, especially in patients with severe disease who are candidates for surgery. Management of strictures in Crohn disease is challenging. Diferentiating between patients who have a predominantly inlammatory versus a mainly ibrotic component of their stricture is imperative to improve selection between medical therapy and surgery. Investigations using only gray-scale ultrasound features are frequently inconclusive. However, bowel ultrasound has been shown to detect ibrosis using a variety of elastographic techniques. Shear wave

elastography uses acoustic radiation force impulse technology to assess elastic properties of tissue through an acoustic ultrasound force that propagates a shear wave through tissue. Measurements of the velocity in meters per second (m/sec) of this shear wave traversing through the tissue are made. Shear wave elastography provides an objective and reproducible quantitative measurement of tissue stifness.32 Early investigations assessing ibrosis in animal models with elastography show some promising results.33 Our recent experience combines both CEUS and point shear wave elastography. Our results suggest CEUS parameters relect inlammation and elastography values relect the chronic features of ibrosis and smooth muscle hypertrophy, improving greatly our contributions to patient management.34

Incomplete Mechanical Bowel Obstruction Obstructive symptoms of bloating abdominal pain and abdominal distention are frequently associated with stricture in IBD. On sonography, distended prestenotic loops of bowel are luid distended and show dysfunctional and excess peristalsis (see Fig. 8.21C and D, Videos 8.9 and 8.10).

Localized Perforation Although free perforation of the bowel is rare in Crohn disease, localized perforation with phlegmonous masses contained within the surrounding perienteric inlammatory fat is common

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FIG. 8.20 Strictures in Three Patients With Crohn Disease. (A) An axial view of the terminal ileum shows wall thickening and surrounding inlammatory fat. (B) The long-axis image shows long segment thickening with luminal apposition. (C) Conirmatory luoroscopic image from a small bowel enema shows the long, tight stricture in the ileum. (D) and (E) Sonograms of the terminal ileum show an abrupt transition in the caliber of the gut (arrow). The gut proximal to the arrow is dilated and luid illed. The distal gut has a stricture, conirmed on (F), the small bowel enema. (G) Short-axis image through the stricture shows the thickened wall and surrounding inlamed fat. (H) Long-axis image of the neoterminal ileum shows a thickened, featureless wall with a caliber alteration (arrows). (I) Conirmatory CT scan.

(Fig. 8.22, Video 8.11). Spiking of the border of acutely inlamed gut is characteristic (see Fig. 8.14). On occasion, an air-containing tract may be identiied, traversing the bowel wall into the perienteric fat. Phlegmonous masses should alert the sonographer to possible underlying localized perforation.

Inlammatory Masses Inlammatory masses involving the ibrofatty mesentery are the most common complication of Crohn disease, although the development of abscesses with drainable pus occurs infrequently. Before the stage of liquefaction, phlegmonous change may be noted as poorly deined, hypoechoic areas without luid content

interdigitating into the surrounding inlamed fat (Figs. 8.23A and B and 8.24A). Abscess formation results in a complex or luid-illed mass (Figs. 8.23G-I and 8.24B). Gas content within an abscess is helpful in suggesting an abscess, but this gas content is also a potential source of sonographic error, particularly if large quantities are present. Abscesses may be intraperitoneal or extraperitoneal or may be in remote locations such as the liver, abdominal wall (Fig. 8.23H and I), and psoas muscles. An excellent application of CEUS is in the characterization of inlammatory masses related to the bowel in a variety of clinical situations. he diferentiation of phlegmonous inlammatory masses, without drainable pus, from those with liquid content

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FIG. 8.21 Bowel Proximal to a Stricture in Three Patients. (A) and (B) Images of the small bowel slightly proximal to a stricture show a luid-distended lumen and moderate mural wall thickening. (C) and (D) Two patients with prestenotic luid-distended bowel and a stricture distal with an obvious transition point. See also Videos 4.9 and and 4.10.

is frequently a challenge.35 he addition of CEUS will quickly and efectively diferentiate these masses as phlegmons are invariably hypervascular, whereas all luid-containing abscesses are completely avascular on CEUS (Fig. 8.25)

Fistula Formation his characteristic penetrating complication of Crohn disease occurs most oten at the proximal end of a thickened, strictured segment of bowel. Although mucosal ulcerations are not well assessed on sonography, deep issures in the gut wall or intramural sinus tracts appear as echogenic linear areas penetrating deeply into the wall beyond the margin of the gut lumen (see Fig. 8.22, Video 8.11). With istula formation, linear bands of varying echogenicity can be seen extending from segments of abnormal gut to the skin (Fig. 8.26C), bladder (Figs. 8.26B and 8.27D), vagina, or other abnormal loops (Video 8.12). If there is gas or movement in the istula during the sonographic study, the istula will usually appear bright or echogenic, with or without ring-down artifact related to air in the tract. Conversely, if the tract is empty or partially closed, the istula may appear as a hypoechoic or hypoechoic tract. Palpation of the abdomen during the examination may produce

movement of luid or air through the istula, assisting in its identiication.

Perianal Inlammatory Disease Perianal inlammation is a frequent and debilitating complication of Crohn disease and its presence at initial diagnosis is a poor prognostic indicator. Highly complex, transsphincteric tracts may extend to involve the deep tissues of the buttocks (Fig. 8.28), perineum, scrotum (men), and labia and vagina (women). Unlike commonly encountered perianal istulas based on the cryptoglandular theory, istulas in Crohn disease have no predilection for the location of the internal openings and are highly complex. In patients of either gender, we have found transperineal scanning to be the most comfortable and oten most informative technique, performed alone or in combination with transrectal ultrasound.36 Further, in women, transvaginal scan contributes greatly to our assessment of rectal and perirectal disease. It is also ideal for showing enterovesical, enterovaginal, and rectovaginal istulas.37 Rectal involvement in Crohn disease is characterized by (1) thickening of the rectal wall with wall layer preservation, (2) inlammation of the perirectal fat, and (3) enlargement of the perirectal lymph nodes.

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FIG. 8.22 Localized Perforation With Phlegmon. Two young women with acute lare of Crohn disease symptoms. (A) and (B) First patient. (A) Cross-sectional and (B) long-axis images of the bowel show wall thickening and a deep hypoechoic mass with ingerlike projections into the surrounding perienteric fat, suggesting phlegmon. Also, on (A), air appears as a bright focus extending beyond the lumen of the bowel into the bowel wall, suggesting localized perforation. (C) and (D) Second patient. (C) Cross-sectional image of the ileum shows a large area of disruption of the bowel wall, an adjacent hypoechoic phlegmon, and an air tract from localized perforation. (D) Long-axis image of loop of ileum shows that the wall is uniformly thickened with layer preservation. The phlegmon is on the margin of the bowel and not shown in the longitudinal view. See also Video 8.11.

ACUTE ABDOMEN Sonography is a valuable imaging tool in patients with speciic suspected acute GI abnormalities such as acute appendicitis or acute diverticulitis.38 However, its contribution to the assessment of patients with possible GI tract disease is less certain. Seibert et al.39 emphasized the value of ultrasound in assessing the patient with a distended and gasless abdomen and detecting ascites, unsuspected masses, and abnormally dilated, luid-illed loops of small bowel. In my experience, sonography has been helpful not only in the gasless abdomen but also in a variety of other situations. he real-time aspect of sonographic study allows for direct patient–sonographer/physician interaction, with conirmation of palpable masses and focal points of tenderness. he doctrine “scan where it hurts” is invaluable and has led sonographers to describe the value of the sonographic equivalent

to clinical examination with such descriptors as a sonographic Murphy sign or sonographic McBurney sign. Similar to the radiographic approach to plain ilm interpretation, a systematic approach is essential in the sonographic assessment of the abdomen in a patient with an acute abdomen of uncertain origin. he abdominal ultrasound evaluation should include visible gas and luid (to determine their luminal or extraluminal location), the perienteric sot tissues, and the GI tract itself. Identiication of gas in a location where it is not usually found is a clue to many important diagnoses. he gas itself may appear as a bright, echogenic focus, but the identiication of the artifacts associated with the gas pockets usually leads to their detection. hese include both ring-down artifact and “dirty” shadowing. Extraluminal gas may be intraperitoneal (Free intraperitoneal

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FIG. 8.23 Inlammatory Masses in Crohn Disease. Top row, Phlegmons (P). (A) Loop of thick sigmoid colon is seen in cross section. Adjacent to the margin is a poorly deined, hypoechoic zone within extensive inlamed fat. (B) Transverse sonogram in the right lower quadrant shows a thick terminal ileum supericially. Within the extensive inlamed fat is a poorly deined, hypoechoic zone representing the phlegmon. (C) Conirmatory CT scan. Middle row, Inlammatory masses, with air but no drainable pus. (D) Transverse image of the right lower quadrant shows abundant inlamed fat. Centrally, there is a small luid collection or abscess (A) with small, echogenic shadowing foci (arrows) caused by air bubbles. (E) Cross-sectional sonogram through the terminal ileum shows gut thickening, echogenic inlamed fat, and a poorly deined, focal hypoechoic area deep to the gut. Bubbles of gas outside the gut are seen as bright, echogenic foci (arrow) on sonography. (F) Conirmatory CT scan. Bottom row, Drainable abscesses. (G) Large, interloop luid collection. (H) Sonogram and (I) conirmatory CT scan show a supericial luid collection with small gas bubbles in the anterior abdominal wall. (B, E, F, H, and I with permission from Sarrazin J, Wilson SR. Manifestations of Crohn disease at US. Radiographics. 1996;16[3]:499-520.21)

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FIG. 8.24 Inlammatory Masses on Sonography. (A) Classic phlegmon with no drainable pus. The mass is hypoechoic and interdigtitates with the surrounding inlammatory fat. There are bright foci of extraluminal air within. (B) Classic abscess—a well-deined mass with uniform low-level echoes within related to the presence of pus.

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FIG. 8.25 Use of Contrast-Enhanced Ultrasound (CEUS) to Distinguish Between Abscess and Phlegmon; Exams in Two Patients. Both examinations include a contrast-enhanced image (left) and low-resolution gray-scale image (right). (A) Hypoechoic mass on baseline is completely avascular on CEUS diagnostic for a luid-containing abscess (A). (B) Hypoechoic mass is uniformly vascular on CEUS, diagnostic for a hypervascular inlammatory mass, a phlegmon. (With permission from Wilson S. Evaluation of the small intestine by ultrasonography. In: Gourtsoyiannis N, editor. Radiologic imaging of the small intestine. Heidelberg: Springer-Verlag; 2002. pp. 73-86.18)

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FIG. 8.26 Fistulas in Patients With Crohn Disease. (A) and (B) Enterovesical istulas. (A) Tract between the abnormal gut (G) and the bladder (B). An air bubble within shows as a bright, echogenic focus (arrow). (B) Hypoechoic tract connects an inlammatory mass (M) to the bladder (B). (C) Enterocutaneous istula. Hypoechoic tract runs from a loop of abnormal gut (G) to the skin surface (arrow). (D) Rectovaginal istula on transvaginal sonogram appears as a bright, air-containing tract (arrow) coursing from the rectum (R) to the vagina (V). See also Video 8.12 for enteroenteric istula.

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FIG. 8.27 Enterovesical Fistula in Crohn Disease. (A) and (B) Cross-sectional images of the terminal ileum show wall thickening and hyperemia. (C) Air in the bladder appears as nondependent bright echoes with dirty shadowing. (D) and (E) Long-axis views of the ileum show the hyperemia and the constant luminal apposition, consistent with stricture. (F) Bladder with the luminal air and an air-containing tract from the bladder to the adjacent bowel. (G) Dilated, luid-illed bowel proximal to the thickening, suggesting incomplete mechanical bowel obstruction. (H) and (I) Coronal CT images conirm the bladder air and an inlammatory mass related to the bladder dome.

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FIG. 8.28 Perianal Inlammatory Crohn Disease. (A) Axial image of the anal canal shows an internal opening (arrow) posteriorly at 6 o’clock. A transsphincteric istula runs to a large, horseshoe-shaped posterior abscess more optimally shown in (B), which also shows deeper collections in the left buttock.

air) or retroperitoneal, and its presence should suggest either hollow viscus perforation or infection with gas-forming organisms40 (Fig. 8.29). Nonluminal gas may be easily overlooked, particularly if the collection is large. Gas in the wall of the GI tract, pneumatosis intestinalis, with or without gas in the portal veins, raises the possibility of ischemic gut. he likelihood of gas artifacts between the abdominal wall and the underlying liver to be related to free intraperitoneal gas was well described by Lee et al.40 In my group’s work, we have found that the peritoneal stripe appears as a bright, continuous, echogenic line, and that air adjacent to the peritoneal stripe produces enhancement of this layer, because the gas has a higher acoustic impedance to sound waves than does the peritoneum itself. Careful peritoneal assessment is best done with a 5-MHz probe or even a 7.5-MHz probe, with the focal zone set at the expected level of the peritoneum. In a clinical situation, enhancement of the peritoneal stripe is a highly speciic but insensitive sign to detect pneumoperitoneum.41 Loculated luid collections can mimic portions of the GI tract. Let upper quadrant and pelvic collections suggestive of the stomach and rectum may be clariied by adding luid orally and rectally. Assessing peristaltic activity and wall morphology also helps in distinguishing luminal from extraluminal collections. Interloop and lank collections are aperistaltic and tend to correspond in contour to the adjacent abdominal wall or intestinal loops, frequently forming acute angles, which are rarely seen with intraluminal luid. he appearance of the perienteric sot tissues is frequently the irst and most obvious clue to abdominal pathology on abdominal sonograms. Inlammation of the perienteric fat shows as a hyperechoic mass efect (see Fig. 8.15), oten without the usual appearance of normal gut and its contained small pockets of gas. Neoplastic iniltration of the perienteric fat is oten

Acute Abdomen: Sonographic Approach GAS Intraluminal Extraluminal Intraperitoneal Retroperitoneal Gut wall Gallbladder/biliary ducts Portal veins FLUID Intraluminal Normal caliber gut Dilated gut Extraluminal Free Loculated MASSES Neoplastic Inlammatory Perienteric Soft Tissues Inlamed fat Lymph nodes Gut Wall Caliber Peristalsis Clinical Interaction Palpable mass Maximal tenderness Sonographic Murphy sign Sonographic McBurney sign

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FIG. 8.29 Value of Gas for Sonographic Diagnosis in Two Patients. (A) Pneumoperitoneum. Sonogram shows a bright, echogenic focus representing free air between the abdominal wall and liver. Also shown is enhancement of the peritoneal stripe. (B) Conirmatory plain ilm. (C) Transvaginal image shows a large, gas-containing abscess (arrows) posterior to the uterus (U), secondary to acute diverticulitis in a renal transplant recipient. (D) Conirmatory CT scan shows the air containing deep abscess (arrows).

indistinguishable from inlammatory iniltration on ultrasound (see Fig. 8.8C and D). Mesenteric adenopathy is another manifestation of both inlammatory and neoplastic processes of the gut that should be speciically sought when performing abdominal sonography. As elsewhere, lymph nodes tend to change in size and shape when replaced by abnormal tissue. A normal, oval or lattened lymph node with a normal linear hilar echo becomes increasingly round and hypoechoic with either inlammatory or neoplastic replacement. In contrast to the sonographic appearance of loops of gut, mesenteric lymph nodes typically appear as focal, discrete hypoechoic masses of varying size (see Fig. 8.16). heir identiication on sonography suggests enlargement because they are not usually seen on routine examinations. In the presence of mesenteric adenopathy, abnormal masses related to or causing a GI tract abnormality should also be sought; these most oten are neoplastic or inlammatory in origin.

Right Lower Quadrant Pain Acute Appendicitis Acute appendicitis is the most common explanation for the “acute abdomen presentation” to an emergency department. Patients typically have right lower quadrant (RLQ) pain, tenderness, and leukocytosis. A mass may also be palpable. he patient with a classic presentation may have an appendectomy without preoperative imaging. his approach oten becomes complicated when a normal appendix is removed in a patient with symptoms caused by other factors. On the other hand, surgery may be delayed in some patients with acute appendicitis if the presentation is atypical. his approach may lead to perforation before the surgery, making it a complicated and diicult procedure, oten followed by abscess formation. In older clinical literature before routine cross-sectional imaging was available, laparotomy resulted in removal of normal, noninlamed appendices in 16% to 47% of cases (mean, 26%).42,43 Also, perforation occurred in up to 35%

CHAPTER 8 of patients.44 It is a balance between this negative laparotomy rate and the perforation rate at surgery that motivates crosssectional imaging before initiating treatment for the patient with acute RLQ pain. For a patient with suspected appendicitis, the sonographic objectives are to identify the patient with acute appendicitis, to identify the patient without acute appendicitis, and, in this latter population, to identify an alternate explanation for the RLQ pain. Symptoms of appendicitis, RLQ pain, and elevated white blood cell count overlap with a variety of other GI conditions, including typhlitis, mesenteric adenitis, Crohn disease, right-sided diverticulitis, segmental infarction of the omentum, and, in women, acute gynecologic conditions such as ruptured or torsion of an adnexal cyst or pelvic inlammatory disease.45 Urologic disease, especially stone-related and right-sided segmental omental infarction, may also mimic acute appendicitis. Addressing the value of sonography in establishing an alternative diagnosis in patients with suspected acute appendicitis, Gaensler et al.46 found that 70% of patients with another diagnosis had abnormalities visualized on the sonogram. From a retrospective review of 462 patients with suspected appendicitis who underwent appendectomy, Bendeck et al.47 found that women in particular beneit most from preoperative imaging, with a statistically signiicant, lower negative appendectomy rate than women with no preoperative imaging. Both CT and ultrasound provide sensitive and accurate diagnosis of appendicitis. he choice of imaging modality is determined somewhat by local expertise.48 Some institutions also screen patients on the basis of their weight, sending thin patients for ultrasound and reserving CT for larger patients. hese considerations aside, we recommend sonographic evaluation of all women (and children)—with the addition of transvaginal scan for all patients whose pain is still not explained ater completion of a traditional suprapubic pelvic sonogram. he pathophysiology of acute appendicitis likely involves obstruction of the appendiceal lumen, with 35% of cases demonstrating a fecalith.49 Mucosal secretions continue, increasing the intraluminal pressure and compromising venous return. he mucosa becomes hypoxic and ulcerates. Bacterial infection ensues,

Acute Appendicitis: Sonographic Diagnosis IDENTIFY APPENDIX Blind ended Noncompressible Aperistaltic tube Gut signature Arising from base of cecum (typically appendix is caudal to the base of the cecum but it may also be retrocecal and retroileal) Diameter greater than 6 mm (some use 7 mm for greater speciicity) SUPPORTIVE FEATURES Inlamed perienteric fat Pericecal collections Appendicolith

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eventually with gangrene and perforation. A walled-of abscess is more common than free peritoneal contamination. Acute appendicitis begins with transient, visceral, or referred crampy pain in the periumbilical area associated with nausea and vomiting. Coincident with inlammation of the serosa of the appendix, the pain shits to the RLQ and may be associated with physical signs of peritoneal irritation. Both clinical and experimental data support the belief that some patients have repeated attacks of appendicitis.50,51 In 1986 Puylaert6 described the value of graded compression sonography in the evaluation of 60 consecutive patients suspected of having acute appendicitis. Puylaert’s initial reports of success in diagnosing acute appendicitis depended solely on visualization of the abnormal appendix, a blind-ended, noncompressible, aperistaltic tube arising from the tip of the cecum with a gut signature (Fig. 8.30). However, other investigators reported seeing normal appendices on a sonogram.52,53 he normal appendix is compressible, with a wall thickness of 3 mm or less54 (Fig. 8.31, Video 8.13). Jefrey et al.55 concluded that size can diferentiate the normal from the acutely inlamed appendix. hreshold levels for the diameter of the appendix, above which acute appendicitis is highly likely, have been set at either 6 mm or 7 mm, with a resultant change in sensitivity and speciicity. Sonographic visualization of an appendix with an appendicolith, regardless of appendiceal diameter, should also be regarded as a positive test. Rettenbacher et al.56 added assessment of appendiceal morphology in conirming suspicion of appendicitis. A round or partly round appendix had a high correlation with acute appendicitis, whereas an ovoid appendix did not. Color Doppler is also contributory, showing hyperemia in the appendiceal wall in the acutely inlamed appendix. Lee et al.57 described visualization of the appendix in 485 of 570 patients (85%) using graded compression sonography alone. Use of a posterior manual compression technique allowed for identiication of the appendix in an additional 57 of the remaining 85 patients, increasing the percentage of identiied appendices to 95%. he appendix positioned in the true pelvis may show subtle evidence of inlammation on a suprapubic scan because the pathology may be deep in the pelvic cavity. In our experience, this occurs most oten in women, possibly related to a more capacious pelvis, and the clinical presentation is frequently that of pelvic inlammatory disease. his particular disease is optimally studied with transvaginal placement of the ultrasound probe because the appendix is oten intimately related to either the uterus or the ovaries. he origin of such an appendix from the base of the cecum may be impossible to determine on transvaginal sonography, and compression with the ultrasound probe is oten not feasible. Nonetheless, the identiication of the blind-ended tip of the appendix with an increased diameter, luminal distention, and inlammation of the surrounding fat is obvious (Fig. 8.32). If rupture of a pelvic appendix has occurred before the sonogram, the identiication of a pelvic abscess without identiication of the appendix itself may produce an equivocal result as to the source of the pelvic inlammatory problem. Although the sensitivity of sonography for the diagnosis of appendicitis decreases with perforation, features associated with

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FIG. 8.30 Acute Appendicitis in Three Patients. (A), (C), and (E) Long-axis views show the blind-ended tip of the appendix. (C) Tip is directed to the left of the image as the appendix ascends cephalad from its origin from the cecum. (B), (D), and (F) Corresponding cross-sectional views. The appendix looks round in short axis on all cases, and the lumen is distended with luid. The appendix is surrounded with inlamed fat. The gut signature is preserved in the top two cases (A-D). The bottom case (E and F) shows loss of deinition of the wall layers, suggesting gangrenous change.

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FIG. 8.31 Normal Appendix. (A) Long-axis image and (B) cross-sectional image show the normal appendix (A) arising from the base of the cecum (C). The appendix shows a gut signature, a blind end, and measures 6 mm or less in diameter. See also Video 8.13.

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FIG. 8.32 Value of Transvaginal Sonography for Diagnosis of Acute Appendicitis. (A) Long-axis view of the appendix on transvaginal sonography was the only view to show the blind-ended tip of the luid-distended appendix. (B) Appendix is a large, luid-illed, thick-walled structure and shows a shadowing appendicolith.

Sonography of Appendiceal Perforation Loculated pericecal luid Phlegmon Abscess Prominent pericecal fat Circumferential loss of submucosal layer of the appendix

its occurrence include loculated pericecal luid, phlegmon or abscess, prominent pericecal or periappendiceal fat, and circumferential loss of the submucosal layer of the appendix58 (Fig. 8.33, Video 8.14). False-positive diagnosis for acute appendicitis may occur if a normal appendix or a thickened terminal ileum is mistaken for an inlamed appendix.

Crohn Appendicitis Patients with Crohn disease may have acute appendicitis caused by IBD involvement of the appendix, in contrast to acute suppurative appendicitis. he wall of the appendix typically is extremely thickened and hyperemic with wall layer preservation, and the luminal surfaces are oten in apposition59 (Fig. 8.34). his appearance contrasts with that in suppurative appendicitis,

where luminal distention is the expectation and wall thickening is moderate at best. Crohn appendicitis is a self-limited process,60,61 and treatment may be conservative if the appropriate diagnosis can be established with noninvasive techniques. In a small number of the patients for whom we have suggested this diagnosis, follow-up sonograms have shown resolution of the sonographic indings with no disease progression. Patients with Crohn disease who present with Crohn appendicitis account for about 10% of total presentations. his patient population typically has a more benign course. If the appendix is removed surgically in the mistaken belief that the patient has acute suppurative appendicitis, recurrence or progression of Crohn disease is rare.

Right-Sided Diverticulitis Acute inlammation of a right-sided diverticulum is distinct from the more common diverticulitis that is encountered in the let hemicolon. hese diverticula occur more oten in women than in men and have a predilection for Asian populations. Most patients are young adults. Right-sided diverticula are usually solitary and are congenital in origin. hey are true diverticula and therefore have all layers of the gut wall. heir inlammation is associated with RLQ pain, tenderness, and leukocytosis, with a mistaken diagnosis of appendicitis in virtually all cases.

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FIG. 8.33 Perforation of Appendix in Three Patients. (A) Long-axis image and (B) cross-sectional image show the blind-ended appendix. There is loss of deinition of the wall layers, and the appendix is surrounded by an echogenic mass effect representing inlamed fat in the mesoappendix. (A) Arrow points to a bubble of extraluminal gas at the tip of the appendix; tip perforation was conirmed at surgery. (C) Sonogram and (D) CT scan show a periappendiceal abscess. The decompressed appendix is seen centrally on the sonogram. (E) Long-axis and (F) transverse images in the right lower quadrant show an abscess with an escaped appendicolith with acoustic shadowing. The appendix is no longer visible. See also Video 8.14. (C with permission from Birnbaum B, Wilson S. Appendicitis at the millennium. Radiology. 2000;215[2]:337-348.48)

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FIG. 8.34 Crohn Appendicitis. (A) Transverse sonogram in the right lower quadrant shows a thick-walled loop of gut surrounded by inlamed fat. (B) Cross-sectional and (C) long-axis high-frequency linear images of this loop of gut show that it is blind ended. There is massive mural thickening and hyperemia. The luminal surfaces are in apposition. All changes resolved completely with conservative management. (With permission from Wilson SR. The bowel wall looks thickened: what does that mean? In: Cooperberg PL, editor. RSNA categorical course syllabus. Chicago: RSNA; 2002. pp. 219-228.1)

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On sonography, acute diverticulitis is associated with inlammation of the pericolonic fat. he diverticula may be located in the cecum or the adjacent ascending colon. When inlamed, they may have one of two appearances.62 Most oten, the diverticulum may show as a pouch or saclike structure arising from the colonic wall63 (Fig. 8.35). Wall layers are continued into the wall of the congenital diverticulum. Hyperemia of the diverticulum and the inlamed fat is typical. If a fecalith is present within the diverticulum, it may show as a bright, echogenic focus located within or beyond a segment of thickened colonic wall. Occasionally, the culprit diverticulum is not evident and the only observations are those of inlamed fat and focal thickening of the colonic

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wall. In the appropriate clinical milieu, this is highly suspicious for acute diverticulitis. Treatment of acute diverticulitis is conservative and not surgical, emphasizing the importance of preoperative imaging in patients with RLQ pain attributed to this condition.

Acute Typhlitis Immunocompromised patients are most oten afected with acute typhlitis. Although infrequent today in North America, AIDS patients previously accounted for the overwhelming majority of cases of acute typhlitis seen since 1990. Cytomegalovirus (CMV) and Cryptosporidium are the pathogens isolated most oten in

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FIG. 8.35 Right-Sided Diverticulitis in Two Patients. Transverse sonograms through the ascending colon (AC) show a hypoechoic pouchlike projection, representing the inlamed diverticulum, which arises from (A) the lateral wall of the gut and (B) the medial border of the gut. Both are surrounded by inlamed fat (arrows).

patients with typhlitis and colitis, although other organisms have been implicated. Sonographic study most oten shows striking concentric, uniform thickening of the colon wall, usually localized to the cecum and the adjacent ascending colon64 (Fig. 8.36). he colon wall may be several times the normal thickness, relecting inlammatory iniltration throughout the gut wall.65,66 Acute abdominal catastrophe in patients with AIDS is usually a complication of CMV colitis with deep ulceration and may result in hemorrhage, perforation, and peritonitis.67 Tuberculous colitis may similarly afect the right colon and is frequently associated with lymphadenopathy (particularly involving the mesenteric and omental nodes), splenomegaly, intrasplenic masses, ascites, and peritoneal masses, all of which may be assessed using sonography.

Mesenteric Adenitis With Terminal Ileitis Mesenteric adenitis, in association with acute terminal ileitis, is the most frequent GI cause of misdiagnosis of acute appendicitis. Patients typically have RLQ pain and tenderness. On the sonographic examination, enlarged mesenteric lymph nodes and mural thickening of the terminal ileum are noted. Yersinia enterocolitica and Campylobacter jejuni are the most common causative agents.68,69 Right-Sided Segmental Omental Infarction Right-sided segmental infarction of the omentum is a rare condition invariably mistaken clinically for acute appendicitis.70 Of unknown origin, it is postulated to occur with an anomalous and fragile blood supply to the right lower omentum, making it susceptible to painful infarction. Patients experience RLQ pain

and tenderness and are diagnosed clinically with acute appendicitis. On sonography, a plaque or cakelike area of increased echogenicity, suggesting inlamed or iniltrated fat, is seen supericially in the right lank with adherence to the peritoneum70 (Fig. 8.37). No underlying gut abnormality is shown. Because segmental infarction is a self-limited process, its correct diagnosis will prevent unnecessary surgery. CT scan is conirmatory, showing streaky fat in a masslike coniguration in the right side of the omentum.

Left Lower Quadrant Pain he sonographic evaluation of the patient with let lower quadrant (LLQ) pain is less problematic than that of the patient with pain on the right side as acute diverticulitis is the explanation for the overwhelming majority of cases for which a valid explanation for the pain is found. he diagnostic features of acute diverticulitis are also less variable than those for acute appendicitis, making a suspicion of diverticulitis a good indication for the use of sonographic examination.

Acute Diverticulitis Diverticula of the colon are usually acquired deformities and are found most frequently in Western urban populations.71 he incidence of diverticula increases with age,72 afecting approximately half the population by the ninth decade. Muscular dysfunction and hypertrophy are constant associated features. Diverticula are usually multiple, and their most common location is the sigmoid and let colon. Both acute diverticulitis and spastic diverticulosis may be associated with a classic triad of presentation: LLQ pain, fever, and leukocytosis. Diverticula may also be

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FIG. 8.36 Acute Typhlitis in AIDS Patient With Cytomegalovirus Colitis. (A) Long-axis view of the ascending colon shows marked mural thickening of the cecum and the wall of the ascending colon. Wall layer preservation is noted. (B) Crosssectional view of the thickened colon (at level of left arrow in A), with luminal surfaces in apposition. (C) Cross-sectional view of the cecum (at level of right arrow in A), which is thick walled and shows a luid-illed lumen. (With permission from Wilson SR. The bowel wall looks thickened: what does that mean? In: Cooperberg PL, editor. RSNA categorical course syllabus. Chicago: RSNA; 2002. pp. 219-228.1)

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FIG. 8.37 Acute Omental Infarction. (A) Sonogram shows a large, tender mass in the right lower quadrant (RLQ; arrows) in older man with acute RLQ pain. The mass is uniformly echogenic and attenuating, with an ultrasound appearance suggesting inlamed fat. (B) Conirmatory CT scan shows the heterogeneous supericial fatty mass.

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found singly and in the right colon, where no association with muscular hypertrophy or dysfunction has been established. Inspissated fecal material is believed to incite the initial inlammation in the apex of the diverticulum leading to acute diverticulitis.73 Spread to the peridiverticular tissues and microperforation or macroperforation may follow. Localized abscess formation occurs more oten than peritonitis. Fistula formation, with communication to the bladder, vagina, skin, or other bowel loops, is present in a minority of cases. Surgical specimens demonstrate shortening and thickening of the involved segment of colon, associated with muscular hypertrophy. he peridiverticular inlammatory response may be minimal or extensive. Sonography appears to be of value in early assessment of patients thought to have acute diverticulitis.74,75 Classic features include segmental thickened gut and inlamed diverticula and inlamed perienteric fat. A negative scan combined with a low clinical suspicion is usually a good indication to stop investigation. However, a negative scan in a patient with a highly suggestive clinical picture justiies a CT scan. Similarly, demonstration of extensive pericolonic inlammatory changes on the sonogram may be appropriately followed by CT scan to deine better the nature and extent of the pericolonic disease before surgery or other intervention. Because diverticula and smooth muscle hypertrophy of the colon are so prevalent, it seems likely that they would be frequently seen on routine sonography, but this is not the usual experience. However, with the development of acute diverticulitis, both the inlamed diverticulum and the thickened colon become evident. Presumably, the impacted fecalith, with or without microabscess formation, accentuates the diverticulum, whereas smooth muscle spasm, inlammation, and edema accentuate the gut wall thickening. Identiication of diverticula on the sonogram strongly indicates diverticulitis.76 Diverticula are arranged in parallel rows along the margins of the teniae coli, so careful technique is required to make their identiication. Ater demonstration of a thickened loop of gut, the long axis of the loop should be determined (Fig. 8.38). Slight tilting of the transducer to the margins of the loop will increase visualization of the diverticula, because they may be on the lateral and medial edges of the loop rather than directly anterior or posterior (Fig. 8.39). Cross-sectional views are then obtained along the entire length of the thickened gut. Abnormalities must be conirmed on both views. Errors related to overlapping gut loops, in particular, can be virtually eliminated with this careful technique. Identiication of diverticula on sonography is correlated highly with inlammation, because it is unusual to show the diverticula in the absence of inlammation (Fig. 8.40). Failure to identify gas-containing abscesses or interloop abscesses is the major source of error when using sonography to evaluate patients with suspected diverticulitis. he meticulous technique of following involved thickened segments of colon in long-axis and transverse section will help detect even small amounts of extraluminal gas. Sonographic features of diverticulitis include segmental concentric thickening of the gut wall that is frequently strikingly hypoechoic, relecting the predominant thickening in the muscle

layer; inlamed diverticula, seen as bright, echogenic foci with acoustic shadowing or ring-down artifact within or beyond the thickened gut wall; acute inlammatory changes in the pericolonic fat, seen as poorly deined hyperechoic zones without obvious gas or luid content (Fig. 8.41, Video 8.15); and abscess formation, seen as loculated luid collections in an intramural, pericolonic, or remote location. With the development of extraluminal inlammatory masses, the diverticulum may no longer be identiied on sonography, presumably being incorporated into the inlammatory process. herefore demonstration of a thickened segment of colon with an adjacent inlammatory mass may be consistent with diverticulitis, but also with neoplastic or other inlammatory disease. Intramural sinus tracts appear as highamplitude, linear echoes, oten with ring-down artifact, within the gut wall. Typically, the tracts are deep, between the muscularis propria and the serosa. Fistulas appear as linear tracts that extend from the involved segment of gut to the bladder, vagina, or adjacent loops. heir echogenicity depends on their content, usually gas or luid. hickening of the mesentery and inlamed mesenteric fat may also be seen (Fig. 8.41). he sonographic and clinical features of diverticulitis are more speciic than those of acute appendicitis, and errors of diagnosis occur less oten. However, torsion of appendices epiploicae (omentales) may produce a sonographic appearance so closely resembling acute diverticulitis that diferentiation may be dificult.76 he inlamed or infarcted fat of the appendix shows as shadowing of increased echogenicity related to the margin of the colon, mimicking an inlamed diverticulum. However, regional perienteric inlammatory change is usually minimal, with fewer systemic symptoms. he noninlamed colonic appendices epiploicae are not visible, except with ascites, where they are seen as uniformly spaced, echogenic foci along the margins of the colon.

Sonography of Diverticulitis GUT Segmental concentric thickening of wall Hypoechoic relecting muscular hypertrophy INFLAMED DIVERTICULA Echogenic foci within or beyond gut wall Intramural sinus tracts High-amplitude linear echoes within gut wall Acoustic shadowing or ring-down artifact PERIENTERIC SOFT TISSUE Inlammation of pericolonic fat Hyperechoic mass effect Thickening of the mesentery Abscess formation Loculated luid collection Often with gas component Fistulas Linear tracts from gut to bladder, vagina, or adjacent loops Hypoechoic or hyperechoic

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FIG. 8.38 Muscular Hypertrophy From Diverticular Colon Disease. (A) Long-axis sonogram of the sigmoid colon shows prominence of the outer muscular layer, the muscularis propria, which appears hypoechoic. The outer longitudinal muscle ibers are slightly more echogenic than the inner circular muscle ibers. (B) Cross-sectional view. (C) Characteristic CT scan shows the effects of the smooth muscle hypertrophy.

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FIG. 8.39 Diverticulum of Colon. (A) Long-axis sonogram and (B) correlative CT scan show a small pouch (arrows) arising from the wall of the descending colon. There is mild inlammatory change in the perienteric fat.

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FIG. 8.40 Acute Diverticulitis of Sigmoid Colon in Three Patients. Cross-sectional views of part of the left colon. (A) Mild prominence of the muscular layer. The diverticulum (arrow) shows as a bright, echogenic shadowing focus, possibly related to a fecalith within. The wall of the diverticulum is not evident. There is minimal inlamed fat. (B) Diverticulum (arrow) has a thick, hypoechoic wall. There is a small, bright focus centrally but no shadowing. (C) Larger focus of echogenicity and shadowing related to an abscess that formed at the base of the inlamed diverticulum. Diverticula frequently show optimally on the cross-sectional images.

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FIG. 8.41 Pericolonic Changes With Diverticulitis in Two Patients. (A) Long-axis view of descending colon shows a long segment of thickened gut with prominent muscularis propria. Edema of the perienteric fat is striking and shows as a homogeneous echogenic mass effect deep to the gut. (B) Similarly inlamed fat; phlegmonous change (P) shows as a hypoechoic zone centrally within the fat. G, Gut. See also Video 8.15.

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OTHER ABNORMALITIES Occlusion of the GI tract lumen producing obstruction may be either mechanical, where an actual physical impediment to the progression of the luminal content exists, or functional, where paralysis of the intestinal musculature impedes progression (paralytic ileus).

Mechanical Bowel Obstruction Mechanical bowel obstruction (MBO) is characterized by (1) dilation of the GI tract proximal to the site of luminal occlusion, (2) accumulation of large quantities of luid and gas, and (3) hyperperistalsis as the gut attempts to pass the luminal content beyond the obstruction. If the process is prolonged, exhaustion and overdistention of the bowel loops may occur, with a secondary decrease in peristaltic activity. here are three broad categories of mechanical obstruction: obturation obstruction, related to blockage of the lumen by material in the lumen; intrinsic abnormalities of the gut wall, associated with luminal narrowing; and extrinsic bowel lesions, including adhesions. Strangulation obstruction develops when the circulation of the obstructed intestinal loop becomes impaired. Sonography in patients with suspected MBO is frequently unhelpful as adhesions, the most common cause of intestinal obstruction, are not visible on the sonogram. Also, the presence of abundant gas in the intestinal tract, characteristic of most patients with obstruction, frequently produces sonograms of nondiagnostic quality. However, in the minority of patients with MBO who do not have signiicant gaseous distention, sonography may be helpful. In a prospective study of 48 patients, Meiser and Meissner77 found that ultrasound was positive in 25% of patients with a “normal” plain ilm. Ultrasound alone allowed complete diagnosis of the cause of obstruction in 6 patients in a retrospective study of sonography on 26 patients with known colonic obstruction; it also correctly predicted the location of colonic obstruction in 22 cases (85%) and the cause of the obstruction in 21 cases (81%).11 Of 13 patients ultimately conirmed to have adenocarcinoma, 5 had a mass on sonography, 5 had segmental thickening, and 11 others showed a target sign of intussusception. Sonographic study of potential MBO should include assessment of the following: • GI tract caliber from the stomach to the rectum, noting any point at which the caliber alters (Fig. 8.42). • Content of any dilated loops, with special attention to their luid and gaseous nature (Fig. 8.43; see also Videos 8.9, 8.10, and 8.16). • Peristaltic activity within the dilated loops, which is typically greatly exaggerated and abnormal, frequently producing a to-and-fro motion of the luminal content. With strangulation, peristalsis may decrease or cease. • Site of obstruction for luminal (large gallstones, bezoars,78 foreign bodies, intussusception, occasional polypoid tumors), intrinsic (segmental gut wall thickening and stricture formation from Crohn disease, annular carcinomas), and extrinsic (abscesses, endometriomas) abnormality as a cause of the obstruction (Video 8.16).

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• Location of gut loops, noting any abnormal position. Obstruction associated with external hernias is ideal for sonographic detection in that dilated loops of gut may be traced to a portion of the gut with normal caliber but abnormal location (Fig. 8.44). Spigelian and inguinal hernias are the types most frequently seen on sonograms. Unique sonographic features are seen in the following: Closed-loop obstruction occurs if the bowel lumen is occluded at two points along its length, a serious condition that facilitates strangulation and necrosis. As the obstructed loop is closed of from the more proximal portion of the GI tract, little or no gas is present within the obstructed segments, which may become dilated and luid illed. Consequently, the abdominal radiograph may be unremarkable (Fig. 8.45A), and sonography may be most helpful by showing the dilated involved segments (Fig. 8.45B) and oten the normal-caliber bowel distal to the point of obstruction. he features of closed-loop obstruction are well described on ultrasound and include dilated small bowel, a C- or U-shaped bowel loop (Fig. 8.45C), a whirl sign, and two adjacent collapsed loops.79,80 his last important observation is diicult to observe on ultrasound, in contrast to CT scan. However, we have correctly suspected closed-loop obstruction in many patients on the basis of virtually normal plain ilms, small bowel dilation, and a U- or C-shaped bowel loop, especially if there is gut wall thickening or pneumatosis intestinalis suggesting gut infarction. Aferent loop obstruction is an uncommon complication of subtotal gastrectomy, with Billroth II gastrojejunostomy, that may occur by twisting at the anastomosis, internal hernias, or anastomotic stricture. Again, a gasless, dilated loop may be readily recognized on sonography in a location consistent with the enteroenteric anastomosis coursing from the right upper quadrant across the midline. Its detection, location, and shape should allow for correct sonographic diagnosis of aferent loop obstruction.81 Intussusception, invagination of a bowel segment (the intussusceptum) into the next distal segment (the intussuscipiens), is seen on sonography of the abdomen most oten as a transient and infrequent occurrence. However, it is a relatively infrequent cause of MBO in the adult, usually associated with a tumor as a lead point. In our experience, this is oten a lipoma that appears as a highly echogenic, intraluminal mass related to its fat content. A sonographic appearance of multiple concentric rings, related to the invaginating layers of the telescoped bowel and seen in cross section, is virtually pathognomonic82 (Fig. 8.46A). Occasionally, only a target appearance may be seen.83,84 he longitudinal appearance suggesting a “hay fork”84 is not as reliably detected. In both projections, the mesenteric fat invaginating with the intussusceptum will show as an eccentric area of increased echogenicity. A lipoma, as a lead point, similarly shows as a focus of increased echogenicity (Fig. 8.46B and C). Midgut malrotation predisposes to MBO and infarction. It is infrequently encountered in adults. A sonographic abnormality related to the superior mesenteric vessels suggests malrotation.85 On transverse sonograms, the superior mesenteric vein is seen on the let ventral aspect of the superior mesenteric artery, a reversal of the normal relationship.

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FIG. 8.42 Mechanical Small Bowel Obstruction. (A) Sagittal image of right lank shows multiple, adjacent, long loops of dilated, luid-illed small bowel with the classic morphology for a distal mechanical small bowel obstruction. (B) Transverse image in the left lower quadrant conirms the multiplicity of dilated loops involved in the process. A small amount of ascites is seen between the dilated loops.

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FIG. 8.43 Dilated Hypoperistaltic Segments. (A) Sagittal sonogram in the right lank of a patient with a Crohn stricture shows gross dilation of the ascending colon. A long, luid-sediment level is seen as a relection of the hypoperistalsis of this segment of obstructed gut. (B) Sagittal sonogram in a patient with paralytic ileus shows extensive small bowel dilation. Loops are luid illed and quiet with luid-luid level (arrowheads). See also Video 8.16. K, Kidney. (A with permission from Sarrazin J, Wilson SR. Manifestations of Crohn disease at US. Radiographics. 1996;16[3]:499-520.21)

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FIG. 8.44 Mechanical Small Bowel Obstruction: Ventral Hernia. (A) Sonogram shows dilated luid-illed loops of small bowel with edematous valvulae conniventes. (B) Transverse paraumbilical sonogram shows normal-caliber gut lying in abnormal supericial location between two dilated loops of small bowel (SB).

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Paralytic Ileus Paralytic ileus is a type of bowel obstruction related to adynamic function of the bowel wall. Paralysis of the intestinal musculature, in response to general or local insult, may impede the progression of luminal contents. Although the lumen remains patent, no progression occurs. Sonography is usually of little value because these patients characteristically have poor-quality sonograms resulting from large quantities of gas in the intestinal tract. However, on rare occasions, the sonogram may demonstrate dilated, luid-illed, very quiet, or aperistaltic loops of intestine. A luid-luid level in a dilated loop is characteristic of paralytic ileus, relecting lack of movement of the intestinal contents (see Fig. 8.43).

Gut Edema Patients with acute vasculitis of various causes may present with acute abdominal pain and ascites, with massive edema of the small bowel wall seen as the major abnormality on imaging.

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FIG. 8.45 Closed-Loop Obstruction. (A) Plain ilm is unremarkable. (B) Sonogram shows grossly dilated, gasless, luid-illed, small bowel loops. (C) Single loop shows a suggestive C or U shape.

Hypoalbuminemia, congestive heart failure, and spontaneous venous thrombosis may also show difuse edema of the gut wall. Prominent, thickened, hypoechoic valvulae conniventes (Fig. 8.47) and gastric rugae are relatively easy to recognize on the sonographic study, which should also include Doppler evaluation of the mesenteric and portal veins.

Gastrointestinal Tract Infections Although luid-illed, actively peristaltic gut may be seen with infectious viral or bacterial gastroenteritis, most afected patients do not demonstrate a sonographic abnormality. However, some pathogens, notably Yersinia enterocolitica, Mycobacterium tuberculosis, and Campylobacter jejuni, produce highly suggestive sonographic abnormalities in the ileocecal area, as described earlier. Certain high-risk populations, such as those with AIDS and neutropenia,64 appear to be susceptible to acute typhlitis and colitis, which also have a highly suggestive sonographic appearance.

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Abdominal and Pelvic Sonography FIG. 8.46 Intussusception in Two Patients (A) Sonogram shows multiple concentric rings representative of the invaginating intussuscipiens and the intussusceptum. Submucosal metastatic nodule as lead point. (B) Sonogram of the right lower quadrant shows a highly echogenic lead point related to a lipoma (arrow). The invaginating fat in the mesentery is also echogenic. (C) Conirmatory CT scan for image B. (B and C with permission from Wilson SR. The bowel wall looks thickened: what does that mean? In: Cooperberg PL, editor. RSNA categorical course syllabus. Chicago: RSNA; 2002. pp. 219-228.1)

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AIDS Patients Today, efective antiviral medications for HIV infection have drastically changed the outlook for those living with AIDS in the Western world. Nonetheless, patients with AIDS are at increased risk for development of both GI tract neoplasia, especially lymphoma (see Fig. 8.10C and D), and unusual opportunistic infections, most oten Candida esophagitis and CMV colitis65,66 (see Fig. 8.36). Pseudomembranous Colitis Pseudomembranous colitis is a necrotizing inlammatory bowel condition that may occur as a response to a heterogeneous group of insults. At present, antibiotic therapy with efects from the toxin of Clostridium diicile, a normal inhabitant of the GI tract, is most oten implicated. Watery diarrhea is the most common symptom and usually occurs during antibiotic therapy but may

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be quite remotely associated, occurring up to 6 weeks later. Endoscopic demonstration of pseudomembranous exudative plaques on the mucosal surface of the gut and culture of the enterotoxin of C. diicile are diagnostic. Supericial ulceration of the mucosa is associated with inlammatory iniltration of the lamina propria and the submucosa, which may be thickened to many times the normal size.86 Sonography is frequently performed before pseudomembranous colitis is diagnosed, oten based on a history of fever, abdominal pain, and watery diarrhea. Sonographic features have only rarely been described87,88 but are suggestive of pseudomembranous colitis. Usually the entire colon is involved in a process that may produce striking thickening of the colon wall. Exaggerated haustral markings and a nonhomogeneous thickened submucosa, with virtual apposition of the mucosal surfaces of the thickened walls, are characteristic63 (Fig. 8.48).

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FIG. 8.47 Small Bowel Edema Secondary to Vasculitis. (A) and (B) Sonograms show marked edema of the valvulae conniventes of the entire small bowel. (C) is a conirmatory CT scan with identical observations. (With permission from Wilson S. Evaluation of the small intestine by ultrasonography. In: Gourtsoyiannis N, editor. Radiologic imaging of the small intestine. Heidelberg: Springer-Verlag; 2002. pp. 73-86.18)

Pseudomembranous colitis should be suspected in any patient with difuse colonic wall thickening but without a previous history of IBD. Because the history of concurrent or prior antibiotic therapy is not always given, direct questioning of the patient is frequently helpful.

Congenital Cysts Duplication cysts, characterized by the presence of the normal layers of the gut wall, can occur in any portion of the GI tract. hese cysts may be visualized on sonogram, either routine or endoscopic, and should be considered as diagnostic possibilities whenever unexplained abdominal cysts are seen. Tailgut cysts are variants of abdominal cysts that are seen in the presacral region and are related to the rectum (Fig. 8.49). Ischemic Bowel Disease Ischemic bowel disease most oten afects the colon and is most prevalent in older persons with arteriosclerosis. In younger patients, it may complicate cardiac arrhythmia, vasculitis, coagulopathy, embolism, shock, or sepsis.12 Sonographic features

of ischemic bowel disease have been poorly described, although gut wall thickening may be encountered. Pneumatosis intestinalis may complicate gut ischemia with a characteristic sonographic appearance.

Pneumatosis Intestinalis Pneumatosis intestinalis is a relatively rare condition in which intramural pockets of gas are found throughout the GI tract. It has been associated with a wide variety of underlying conditions, including chronic obstructive pulmonary disease, collagen vascular disease, IBD, traumatic endoscopy, and post–jejunoileal bypass. In many situations, afected patients are asymptomatic and the observation is incidental. However, its demonstration is of great clinical signiicance when necrotizing enterocolitis or ischemic bowel disease is present. Both conditions are associated with mucosal necrosis in which gas from the lumen passes to the gut wall. Sonographic description of pneumatosis intestinalis is limited to isolated case reports. High-amplitude echoes may be demonstrated in the gut wall, with typical air artifact or shadowing89,90

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FIG. 8.48 Pseudomembranous Colitis. (A) Long-axis view and (B) cross-sectional view of the ascending colon show striking mural thickening of the gut wall. (With permission from O’Malley M, Wilson S. US of gastrointestinal tract abnormalities with CT correlation. Radiographics. 2003;23[1]:59-72.63)

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FIG. 8.49 Congenital Cysts. (A) Sagittal and (B) transverse sonograms in the epigastrium show an incidental gastric duplication cyst adjacent to the lesser curve of the stomach (S). (C) Suprapubic and (D) transvaginal pelvic scans show a complex, presacral pelvic mass, an incidental tailgut cyst.

CHAPTER 8 (Fig. 8.50). Gut wall thickening may be noted if the pneumatosis is associated with underlying IBD. If gut ischemia is suspected, careful evaluation of the liver is recommended to look for evidence of portal venous air.

Mucocele of Appendix Mucocele of the appendix is relatively uncommon, occurring in 0.25% of 43,000 appendectomy specimens in one series. Many patients with this condition are asymptomatic. A mass may be

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palpated in approximately 50% of cases. Benign and malignant varieties occur in a ratio of approximately 10 : 1.91 In the benign form the appendiceal lumen is obstructed by either inlammatory scarring or fecaliths. he glandular mucosa in the isolated segment continues to secrete sterile mucus. he neoplastic variety of mucocele is associated with primary mucous cystadenoma or cystadenocarcinoma of the appendix. Although the gross morphology of the appendix may be similar in the benign and malignant varieties, the malignant form is oten associated with pseudomyxoma peritonei if rupture occurs.92 On sonography, mucoceles typically produce large, hypoechoic, well-deined RLQ cystic masses with variable internal echogenicity, wall thickness, and wall calciication (Fig. 8.51). he internal contents oten show a laminated or whorled appearance. hese masses are frequently retrocecal and may be mobile.

Gastrointestinal Tract Hematoma Blunt abdominal trauma, complicated by duodenal hematoma and rectal trauma, either sexual or iatrogenic ater rectal biopsy, are the major causes of local hematomas seen on sonography. Hematoma is usually localized to the submucosa. Larger or more difuse hematomas may complicate anticoagulation therapy or bleeding disorders associated with leukemia. If hematomas are large, difuse gut wall thickening may be seen on sonograms.

FIG. 8.50 Pneumatosis Intestinalis. Sonogram shows three loops of gut with bright, high-amplitude echoes (arrows) originating within the gut wall.

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Peptic Ulcer Peptic ulcer, a defect in the epithelium to the depth of the submucosa, may be seen in either gastric or duodenal locations. Although rarely visualized, peptic ulcer has a fairly characteristic sonographic appearance. A gas-illed ulcer crater is seen as a bright, echogenic focus with ring-down artifact, either in a focal area of wall thickening or beyond the wall, depending on the depth of penetration (Fig. 8.52). Edema in the acute phase and ibrosis in the chronic phase may produce localized wall thickening and deformity.

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FIG. 8.51 Mucocele of the Appendix. (A) Sonogram and (B) CT scan show a large, mucus-illed appendix as an incidental observation. The whorled appearance on the sonogram is characteristic. There is a leck of calciication in the wall on the CT scan.

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FIG. 8.52 Peptic Ulcer. (A) Cross-sectional sonogram of the stomach shows a hypoechoic eccentric mass with a bright, central echogenic focus representing air in the ulcer crater. (B) Conirmatory scan with barium swallow.

Bezoars Bezoars are masses of foreign material or food, typically found in the stomach ater surgery for peptic ulcer disease (phytobezoars) or ater ingestion of indigestible organic substances such as hair (trichobezoars). hese masses may produce shadowing intraluminal densities on the sonogram and have been documented as a rare cause of small bowel obstruction.78 hey may also form in the small bowel in association with chronic stasis. Intraluminal Foreign Bodies Large foreign bodies, including bottles, candles, sexual vibrators, contraband, tools, and food, may be identiied in the GI tract, particularly in the rectum and sigmoid colon, where they produce fairly sharp, distinct specular echoes with sharp, acoustic shadows. heir recognition is enhanced by suspicion of their presence. Celiac Disease Undiagnosed adult patients with celiac disease are encountered infrequently in general ultrasound departments. Nonetheless, I have occasionally seen patients in whom sonography is the irst test to suggest the correct diagnosis. Sonographic observations include abnormal luid-illed small intestine with moderate dilation of the involved loops. Abnormal morphology is observed, which Dietrich et al.93 describe as a reduction in Kerckring plicae circulares (valvulae conniventes) with loss of density and uniformity. Peristalsis is increased above normal. An increase in the caliber of the superior mesenteric artery and portal vein may also be seen.94 Cystic Fibrosis Aggressive treatment of the pulmonary problems of cystic ibrosis (CF) increases the likelihood of encountering adult patients in a general ultrasound department that performs abdominal

sonography. hickening of the gut wall, particularly of the right hemicolon and to a lesser extent the let colon and small bowel, may be seen in association with iniltration of both the pericolonic and the mesenteric fat.95 hese may oten be incidental observations without signiicant associated symptomatology. In advanced CF, a ibrosing colonopathy with stricture may be seen.96,97 he culture of C. diicile is also documented in some patients with CF and colon wall thickening, without the accompanying symptoms of abdominal pain and diarrhea.98 However, positive stool culture is not the rule in CF patients with detectable colon wall thickening.

ENDOSONOGRAPHY Endoscopic sonography, performed with high-frequency transducers in the lumen of the gut, allows for detection of mucosal abnormality, delineation of the layers of the gut wall, and deinition of the surrounding sot tissues to a depth of 8 to 10 cm from the transducer crystal. hus tumors hidden below normal mucosa, tumor penetration into the layers of the gut wall, and tumor involvement of surrounding vital structures or lymph nodes may be well evaluated. Staging of previously identiied mucosal tumors is one of the major applications of endosonographic technique.

Upper Gastrointestinal Tract Rotating, high-frequency transducers, using 7.5-MHz crystals itted into a iberoptic endoscope, are most suitable for endosonography of the esophagus, stomach, and duodenum. Light sedation of the patient is usually required. he patient is placed in the let lateral decubitus position and the endoscope inserted to the desired location. Intraluminal gas is aspirated, and a balloon covering the transducer crystal is inlated with deaerated water. Localization is determined from the distance of insertion from

CHAPTER 8 the teeth and identiication of anatomic landmarks, such as the spleen, liver, pancreas, and gallbladder. Rotation and delection of the transducer tip allow scanning of visualized lesions in diferent planes.99 Identiication, localization, and characterization of benign masses are possible with endosonography. Varices are seen as compressible hypoechoic or cystic masses deep to the submucosa or in the outer layers of the esophagus, gastroesophageal junction, or gastric fundus.100 Benign tumors such as ibromas or leiomyomas are well-deined, solid masses without mucosal involvement that can be localized to the layer of the wall from which they arise, usually the submucosa and the muscularis propria, respectively. Peptic ulcer typically produces marked thickening of all layers of the gastric wall, with a demonstrated ulcer crater. Ménétrier disease produces thickening of the mucosal folds. Staging of esophageal carcinoma involves assessment of depth of tumor invasion and evaluation of involvement of the local lymph nodes and adjacent vital structures.101 Constricting lesions that do not allow passage of the endoscope may produce technically unsatisfactory or incomplete examinations. Gastric lymphoma is typically very hypoechoic; its invasion is along the gastric wall or horizontal, and involvement of extramural structures and lymph nodes is less than with gastric carcinoma. hus, localized mucosal ulceration with extensive iniltration of the deeper layers suggests lymphoma, which may also grow with a polypoid pattern or as a difuse iniltration without ulceration.102 Gastric carcinoma, in contrast, arises from the gastric mucosa, is usually more echogenic, tends to invade vertically or through the gastric wall, and frequently involves the perigastric lymph nodes at diagnosis.

Rectum: Tumor Staging of Rectal Carcinoma Transrectal (endorectal) sonography is an established modality for the staging of rectal carcinoma.103-105 Its resolution of the layers of the rectum surpasses the performance of both CT and MRI. Although a variety of pathologic conditions may be assessed with endorectal sonography, the staging of previously detected rectal carcinoma is its major role. Patients are scanned in the let lateral decubitus position following a cleansing enema. Both axial and sagittal images are obtained. A variety of rigid intrarectal probes are commercially available, using a range of transducer technologies with phased array, mechanical sector, and rotating crystals. Further, we have also been routinely evaluating women with rectal carcinoma using a transvaginal probe placed in the vagina ater a Fleet enema. his technique is excellent, especially for larger tumors, because the rectovaginal septum, the tumor, and the lymph nodes in the mesorectum are more optimally seen.106 Tumors are staged according to the Astler-Coller modiication107 of the Dukes Classiication, or more simply with the primary tumor component of the Union Internationale Contre le Cancer (UICC) TNM classiication,108 where T represents the primary tumor, N the nodal involvement, and M the distant metastases (Fig. 8.53).

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T4

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FIG. 8.53 Schematic of Tumor (T) Component of TNM Staging of Rectal Cancer on Sonography. Tumors (red) exhibit progressively deeper invasion beginning at 10 o’clock, where T supericial noninvasive lesion involves only supericial layers of intestinal wall. At 7 o’clock, T1 lesion invades submucosa (yellow). At 5 o’clock, T2 lesion invades muscularis propria (blue). At 2 o’clock, T3 lesion exhibits full-thickness invasion through layers of rectal wall, with invasion of surrounding perirectal fat. In directly anterior aspect (12 o’clock), T4 lesion exhibits invasion of prostate gland.

Rectal carcinoma arises from the mucosal surface of the gut. Tumors appear as relatively hypoechoic masses that may distort the rectal lumen. Invasion of the deeper layers, the submucosa, the muscularis propria, and the perirectal fat produces discontinuity of these layers on the sonogram (Fig. 8.54). Supericial ulceration or crevices that allow small bubbles of gas to be trapped deep to the crystal surface may demonstrate ring-down artifact and shadowing, with loss of layer deinition deep to the ulceration. Lymph nodes appear as round or oval, hypoechoic masses in the perirectal fat (Fig. 8.54C). Color Doppler is an excellent addition to transrectal probes, showing the extent of tumors on the basis of their hypervascularity (Fig. 8.55) Infrequently, actual deposits may be shown within enlarged nodes. herefore deinitive staging requires pathologic assessment of both the tumor and the regional nodes. Limitations of rectal sonography include the following: inability to identify microscopic tumor invasion, to image stenotic tumors, and to image tumors greater than 15 cm from the anal verge. It is also limited for distinguishing nodes involved with tumor from those with reactive change and to identify normalsized nodes with microscopic tumor invasion.

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FIG. 8.54 Rectal Tumors Seen at Transrectal Sonography. (A) Rectal carcinoma: T1. Hypoechoic mass between 6 o’clock and 8 o’clock is noted. The submucosa (the echogenic line) and the muscularis propria (the external hypoechoic line) are intact. (B) Rectal carcinoma: T2. Tumor is seen anteriorly. The muscularis propria (arrows) is the hypoechoic line that is thickened and nodular, consistent with tumor involvement. (C) Rectal carcinoma: T3. A large tumor involves the entire right lateral wall of the rectum. Invasion of the perirectal fat (arrows) is noted in several locations. A large node is seen at the 6 o’clock position; smaller nodes are seen at 5 o’clock and 8 o’clock. (D) Metastatic prostate carcinoma to rectal wall. Hypoechoic mass is seen between 10 o’clock and 1 o’clock. It involves the deep layers of the rectal wall and not the rectal mucosa. There is a small lymph node (arrow). (With permission from Berton F, Gola G, Wilson S. Perspective on the role of transrectal and transvaginal sonography of tumors of the rectum and anal canal. AJR Am J Roentgenol. 2008;190[6]:1495-1504.106)

Recurrent rectal cancer ater local resection is usually extraluminal, involving the resection margin secondarily. Serial transrectal sonography may be used in conjunction with serum carcinoembryonic antigen levels to detect these recurrences. A pericolic hypoechoic mass or local thickening of the rectal wall, in either deep or supericial layers, is taken as evidence of recurrence. Previous radiation treatment may produce a difuse thickening of the entire rectal wall, usually of moderate or high echogenicity, with an appearance that is usually easily diferentiated from the focal hypoechoic appearance of recurrent cancer. Sonographic-guided biopsy of a detected abnormality facilitates histologic diferentiation of recurrence from postoperative, inlammatory, or postradiation change. Prostatic carcinoma may invade the rectum directly, or more remote tumors may involve the rectum, usually as a result of

seeding to the posterior peritoneal pouch. Because these tumors initially involve the deeper layers of the rectal wall, with mucosal involvement occurring as the disease progresses, their sonographic appearance is distinct from that of primary rectal carcinoma (see Fig. 8.54D). Benign mesenchymal tumors, especially of smooth muscle origin, are uncommon in the rectum. When seen, their sonographic features are the same as elsewhere (Fig. 8.56). Mucous retention cysts, resulting from obstruction of mucous glands, produce cystic masses of varying size that are located deep in the rectal wall.

Anal Canal Cancer of the anal canal is a very rare tumor that is well shown on anal sonography (Fig. 8.57).

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FIG. 8.55 Contribution of Color Doppler at Transrectal Sonography to Staging and Diagnosis of Rectal Cancer. (A) and (B) T2 rectal cancer in 58-year-old man. (A) Axial image shows hypoechoic tumor. Destruction of submucosa is evident with involvement of muscularis propria on right side of image. (B) Color Doppler shows typical hypervascularity. Color demarcates tumor from normal rectal wall on left side of image. (C) and (D) Small rectal adenocarcinoma originating in adenomatous polyp in 55-year-old man. (C) Axial image shows an isoechoic polypoid mass with a broad base surrounded by luid within the rectal lumen. Mass involves the submucosal layer only. (D) Color Doppler image shows profuse vascularity and vascular stalk of the polypoid mass. (E) and (F) tubulovillous adenoma in 58-year-old woman. (E) Axial transvaginal image shows a mixed-echogenic mass that seems to ill the lumen of the rectum. (F) Color Doppler frequently shows this type of stellate, branching vascularity in tubulovillous tumors. (With permission from Berton F, Gola G, Wilson S. Perspective on the role of transrectal and transvaginal sonography of tumors of the rectum and anal canal. AJR Am J Roentgenol. 2008;190[6]:1495-1504.106)

FIG. 8.56 Gastrointestinal Stromal Tumor (GIST) of Rectum. Transrectal sonographic image shows solid, well-deined, round mass arising from muscularis propria layer in 59-year-old woman with asymptomatic palpable mass found at routine physical examination. Tumor is growing with submucosal pattern, and mucosal surface bulges into luid-illed lumen.

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FIG. 8.57 Cancer of Anal Canal. (A) Long-axis image and (B) cross-sectional image show a hypoechoic tumor disrupting the normal planes of the anal canal. (C) Sonogram shows the vascularity of the tumor. (With permission from Berton F, Gola G, Wilson S. Perspective on the role of transrectal and transvaginal sonography of tumors of the rectum and anal canal. AJR Am J Roentgenol. 2008;190[6]:1495-1504.106)

CHAPTER 8 Fecal Incontinence Anal endosonography, performed with the addition of a hard cone attachment to a radial 7.5-MHz probe, allows accurate assessment of the anal canal, including the internal and external sphincters.109 Performed primarily for assessment of fecal incontinence, this test shows the integrity of the sphincters with documentation of the degree and size of muscle defects. We do not use this technique any longer, preferring instead assessment of the sphincter and perianal sot tissues with a combination of transvaginal and transperineal scan.37,110-113 Young women, following traumatic obstetric delivery, are most oten alicted with fecal incontinence. he internal anal sphincter, in continuity with the muscularis propria of the rectum above, is seen as a thick circular hypoechoic or hypoechoic ring just deep to the convoluted mucosal echoes (Fig. 8.58). he external

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anal sphincter, in contrast, is less well deined and more echogenic, appearing gray on the ultrasound examination, and in continuity with ibers from the puborectalis sling. Traumatic disruption of the muscle layers will show as defects in the continuity of the normal muscle texture, most oten anterior (Fig. 8.59). Posttraumatic scarring may be associated with a change of shape of the anal canal from round to oval.

Perianal Inlammatory Disease Perianal inlammatory disease is seen in two distinct patient populations: (1) those with Crohn disease who develop perianal inlammation as part of their disease and (2) those who develop a perianal abscess or perianal istula as a spontaneous event. he irst group is described earlier in the section on Crohn disease. In other patients, perianal infection arises in small,

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FIG. 8.58 Normal Rectum and Anal Canal. (A) Transvaginal approach. Cross-sectional image of rectum taken with vaginal probe showing the normal, convoluted rectal mucosa; prominent submucosa (white); and the muscularis propria as a thin, hypoechoic rim (arrows). The rectum is usually oval, as shown here. (B) Transperineal approach. Anal canal shows the thick, well-deined internal anal sphincter (arrows) as a continuous hypoechoic ring continuous with the muscularis propria of the rectal wall above. The external anal sphincter is less well deined and echogenic. (C) Transperineal approach. Rotation of the probe by 90 degrees from image B shows the anal canal in long axis (arrows, internal anal sphincter).

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FIG. 8.59 Traumatic Disruption of Anal Sphincter in Two Patients. (A) Cross-sectional and (B) long-axis views of the anal canal from a transvaginal approach show disruption of the sphincter anteriorly from 9 to 3 o’clock. The arrow on the sagittal image shows the cephalad extent of the internal anal sphincter. (C) Cross-sectional and (D) long-axis views of the anal canal show full-thickness disruption of the anterior anal canal between 11 and 1 o’clock. The arrow in each image shows air bubbles within an anovaginal istula.

intersphincteric anal glands predominantly located at the dentate line. his occurs most frequently in young adult men. Documentation of luid collections and the relationship of inlammatory tracts to the sphincter mechanism are important for surgical treatment. We prefer transvaginal sonography (Video 8.17) in conjunction with transperineal sonography in women and transperineal sonography in men for evaluation of this problem. Scans are performed with curved and high-frequency linear probes placed irmly on the skin of the perineum between the introitus and the anal canal in women and between the scrotum and the anal canal in men.111 Firm pressure on the transducer is required to aford good visualization of the anal canal. We begin the procedure with the transducer in the transverse plane relative to the body. he transducer should be directed cephalad and anterior to the plane of the anal canal, then angled slowly through the plane of the anal canal, which will show it in cross section from the anorectal junction to the external anal

Sonography of Perianal Inlammatory Disease Internal opening in the anal canal or rectum Tracts and their relationship to anal sphincter External openings Fluid collections

opening. Rotation of the transducer by 90 degrees will allow for imaging in the longitudinal plane. Tracts and collections in the perineum, buttocks, scrotum, and labia can also be assessed and followed in a retrograde direction to their connection with the anal canal. Perianal inlammatory tracts and masses are classiied according to Parks et al.114 heir classiication provides an anatomic description of istulous tracts, which acts as a guide to operative

CHAPTER 8 treatment. he four main subtypes are intersphincteric (between internal and external sphincter), transsphincteric (crossing both internal and external anal sphincter into ischiorectal or ischioanal fossa), suprasphincteric, and extrasphincteric. In each patient, we also document the internal opening and the external openings, as possible. Tracts show on the ultrasound scan as hypoechoic linear areas or luid-containing tubular areas, depending on their size and activity (Fig. 8.60). As with istulas elsewhere, air bubbles within the tract show as bright, echogenic foci that

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may move during the scan, helping with their identiication. In our initial experience with 54 patients with perianal inlammatory masses, sonographic indings were conirmed in 22 of 26 patients (85%) who underwent surgical treatment for their disease.

Acknowledgment he author would like to acknowledge Gordana Popovich for her artwork.

A

B

C

D

E

F

G

H

I

FIG. 8.60 Perianal Inlammatory Disease in Nine Patients. Top row, Simple inlammatory openings and tracts (arrows). Cross-sectional images of the anal canal show internal opening at 1 o’clock with (A) transsphincteric tract running to a small collection; (B) intersphincteric tract; (C) larger extrasphincteric tract. Middle row, More complex tracts (arrows). (D) Anterior extrasphincteric tract shows luid within. (E) Bilateral, complex, intersphincteric tracts and collections show bright, echogenic foci representing extraluminal air. (F) Boomerang, or horseshoe, tract surrounds the anal canal posteriorly and laterally. There are internal openings at 2, 4, and 9 o’clock. Bottom row, Perianal abscesses (A). (G) Abscess on left posterolateral aspect of the anal canal is particle illed. (H) Large, posterior abscess is complex, with a dependent debris level. (I) Large, posterior abscess shows a large internal opening posteriorly at 6 o’clock.

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PART II

Abdominal and Pelvic Sonography

REFERENCES 1. Wilson SR. he bowel wall looks thickened: what does that mean? In: Cooperberg PL, editor. RSNA categorical course syllabus. Chicago: RSNA; 2002. pp. 219-228. 2. Heyder N, Kaarmann H, Giedl J. Experimental investigations into the possibility of diferentiating early from invasive carcinoma of the stomach by means of ultrasound. Endoscopy. 1987;19(6):228-232. 3. Kimmey MB, Martin RW, Haggitt RC, et al. Histologic correlates of gastrointestinal ultrasound images. Gastroenterology. 1989;96(2 Pt 1): 433-441. 4. Lutz HT, Petzoldt R. Ultrasonic patterns of space occupying lesions of the stomach and the intestine. Ultrasound Med Biol. 1976;2(2):129-132. 5. Bluth E, Merritt C, Sullivan M. Ultrasonic evaluation of the stomach, small bowel, and colon. Radiology. 1979;133(3 Pt 1):677-680. 6. Puylaert JB. Acute appendicitis: US evaluation using graded compression. Radiology. 1986;158(2):355-360. 7. Teefey SA, Roarke MC, Brink JA, et al. Bowel wall thickening: diferentiation of inlammation from ischemia with color Doppler and duplex US. Radiology. 1996;198(2):547-551. 8. Romanini L, Passamonti M, Navarria M, et al. Quantitative analysis of contrast-enhanced ultrasonography of the bowel wall can predict disease activity in inlammatory bowel disease. Eur J Radiol. 2014;83(8):1317-1323. 9. Dillman JR, Stidham RW, Higgins PDR, et al. Ultrasound shear wave elastography helps discriminate low-grade from high-grade bowel wall ibrosis in ex vivo human intestinal specimens. J Ultrasound Med. 2014;33(12):2115-2123. 10. Lim JH. Colorectal cancer: sonographic indings. AJR Am J Roentgenol. 1996;167(1):45-47. 11. Lim JH, Ko YT, Lee DH, et al. Determining the site and causes of colonic obstruction with sonography. AJR Am J Roentgenol. 1994;163(5):1113-1117. 12. Shorter RG. Gastrointestinal pathology: an atlas and text. Mayo Clin Proc. 1989;64(12):1567-1568. 13. Katori J, Aharon M, Kleinhaus U. Sonographic features of gastrointestinal leiomyosarcoma. J Clin Ultrasound. 1981;9(1):11-15. 14. Derchi LE, Banderali A, Bossi C, et al. he sonographic appearances of gastric lymphoma. J Ultrasound Med. 1984;3(6):251-256. 15. Salem S, Hiltz C. Ultrasonographic appearance of gastric lymphosarcoma. J Clin Ultrasound. 1978;6(6):429-430. 16. Telerman A, Gerard B, Van den Heule B, Bleiberg H. Gastrointestinal metastases from extra-abdominal tumors. Endoscopy. 1985;17(3):99-101. 17. Yeh H. Ultrasonography of peritoneal tumors. Radiology. 1979;133(2):419-424. 18. Wilson S. Evaluation of the small intestine by ultrasonography. In: Gourtsoyiannis N, editor. Radiologic imaging of the small intestine. Heidelberg: Springer-Verlag; 2002. pp. 73-86. 19. Horsthuis K, Bipat S, Bennink R, Stoker J. Inlammatory bowel disease diagnosed with US, MR, scintigraphy, and CT: meta-analysis of prospective studies. Radiology. 2008;247(1):64-79. 20. Panés J, Bouzas R, Chaparro M, et al. Systematic review: the use of ultrasonography, computed tomography and magnetic resonance imaging for the diagnosis, assessment of activity and abdominal complications of Crohn’s disease. Aliment Pharmacol her. 2011;34(2):125-145. 21. Sarrazin J, Wilson SR. Manifestations of Crohn disease at US. Radiographics. 1996;16(3):499-520. 22. Gasche C, Moser G, Turetschek K, et al. Transabdominal bowel sonography for the detection of intestinal complications in Crohn’s disease. Gut. 1999;44(1):112-117. 23. Medellin-Kowalewski A, Wilkens R, Wilson A, et al. Quantitative contrastenhanced ultrasound parameters in Crohn disease: their role in disease activity determination with ultrasound. AJR Am J Roentgenol. 2016;206(1):64-73. 24. DiCandio G, Mosca F, Campatelli A, et al. Sonographic detection of postsurgical recurrence of Crohn disease. AJR Am J Roentgenol. 1986;146(3):523-526. 25. Fraquelli M, Colli A, Casazza G, et al. Role of US in detection of Crohn disease: meta-analysis 1. Radiology. 2005;236(1):95-101. 26. Dubbins PA. Ultrasound demonstration of bowel wall thickness in inlammatory bowel disease. Clin Radiol. 1984;35(3):227-231. 27. Worlicek H, Lutz H, Heyder N, Matek W. Ultrasound indings in Crohn’s disease and ulcerative colitis: a prospective study. J Clin Ultrasound. 1987;15(3):153-163.

28. Spalinger J, Patriquin H, Miron M, et al. Doppler US in patients with Crohn disease: vessel density in the diseased bowel relects disease activity. Radiology. 2000;217(3):787-791. 29. Ripollés T, Martínez M, Paredes J, et al. Crohn disease: correlation of indings at contrast-enhanced US with severity at endoscopy. Radiology. 2009;253(1):241-248. 30. Ripollés T, Rausell N, Paredes J, et al. Efectiveness of contrast-enhanced ultrasound for characterisation of intestinal inlammation in Crohn’s disease: a comparison with surgical histopathology analysis. J Crohns Colitis. 2013;7(2):120-128. 31. Parente F, Maconi G, Bollani S, et al. Bowel ultrasound in assessment of Crohn’s disease and detection of related small bowel strictures: a prospective comparative study versus x ray and intraoperative indings. Gut. 2002;50(4):490-495. 32. Ferraioli G, Tinelli C, Lissandrin R, et al. Point shear wave elastography method for assessing liver stifness. World J Gastroenterol. 2014;20(16):4787-4796. 33. Dillman J, Stidham R, Higgins P, et al. US elastography–derived shear wave velocity helps distinguish acutely inlamed from ibrotic bowel in a Crohn Disease animal model. Radiology. 2013;267(3):757-766. 34. Lu C, Gui X, Chen W, et al. Ultrasound shear wave elastography identiies muscle wall hypertrophy and is a novel surrogate for inlammation in Crohn’s disease. United European Gastroenterol J. 2015;3:P0333. 35. Ripollés T, Martínez-Pérez M, Blanc E, et al. Contrast-enhanced ultrasound (CEUS) in Crohn’s disease: technique, image interpretation and clinical applications. Insights Imaging. 2011;2(6):639-652. 36. Stewart LK, McGee J, Wilson SR. Transperineal and transvaginal sonography of perianal inlammatory disease. AJR Am J Roentgenol. 2001;177(3):627-632. 37. Damani N, Wilson S. Nongynecologic applications of transvaginal US. Radiographics. 1999;19(Spec No):S179-S200. 38. Puylaert J. Ultrasound of acute GI tract conditions. Eur Radiol. 2001;11(10):1867-1877. 39. Seibert JJ, Williamson SL, Golladay ES, et al. he distended gasless abdomen: a fertile ield for ultrasound. J Ultrasound Med. 1986;5(6):301-308. 40. Lee DH, Lim JH, Ko YT, Yoon Y. Sonographic detection of pneumoperitoneum in patients with acute abdomen. AJR Am J Roentgenol. 1990;154(1):107-109. 41. Muradali D, Wilson S, Burns PN, et al. A speciic sign of pneumoperitoneum on sonography: enhancement of the peritoneal stripe. AJR Am J Roentgenol. 1999;173(5):1257-1262. 42. Pieper R, Forsell P, Kager L. Perforating appendicitis. A nine-year survey of treatment and results. Acta Chir Scand Suppl. 1986;530:51-57. 43. Kazarian K, Roeder W, Mersheimer W. Decreasing mortality and increasing morbidity from acute appendicitis. Am J Surg. 1970;119(6):681-685. 44. Van Way 3rd CW, Murphy JR, Dunn EL, Elerding SC. A feasibility study of computer aided diagnosis in appendicitis. Surg Gynecol Obstet. 1982;155(5):685-688. 45. Berry J, Malt R. Appendicitis near Its centenary. Ann Surg. 1984;200(5): 567-575. 46. Gaensler EH, Jefrey RB, Laing FC, Townsend RR. Sonography in patients with suspected acute appendicitis: value in establishing alternative diagnoses. AJR Am J Roentgenol. 1989;152(1):49-51. 47. Bendeck S, Nino-Murcia M, Berry G, Jefrey R. Imaging for suspected appendicitis: negative appendectomy and perforation rates. Radiology. 2002;225(1):131-136. 48. Birnbaum B, Wilson S. Appendicitis at the millennium. Radiology. 2000;215(2):337-348. 49. Shaw R. Appendix calculi and acute appendicitis. Br J Surg. 1965;52(6):451-459. 50. Savrin R, Clausen K, Martin E, Cooperman M. Chronic and recurrent appendicitis. Am J Surg. 1979;137(3):355-357. 51. Dachman AH, Nichols JB, Patrick DH, Lichtenstein JE. Natural history of the obstructed rabbit appendix: observations with radiography, sonography, and CT. AJR Am J Roentgenol. 1987;148(2):281-284. 52. Jefrey RB, Laing FC, Townsend RR. Acute appendicitis: sonographic criteria based on 250 cases. Radiology. 1988;167(2):327-329. 53. Abu-Yousef MM, Bleicher JJ, Maher JW, et al. High-resolution sonography of acute appendicitis. AJR Am J Roentgenol. 1987;149(1):53-58. 54. Rioux M. Sonographic detection of the normal and abnormal appendix. AJR Am J Roentgenol. 1992;158(4):773-778. 55. Jefrey RB, Laing FC, Lewis FR. Acute appendicitis: high-resolution real-time US indings. Radiology. 1987;163(1):11-14.

CHAPTER 8 56. Rettenbacher T, Hollerweger A, Macheiner P, et al. Ovoid shape of the vermiform appendix: a criterion to exclude acute appendicitis—evaluation with US. Radiology. 2003;226(1):95-100. 57. Lee J, Jeong Y, Hwang J, et al. Graded compression sonography with adjuvant use of a posterior manual compression technique in the sonographic diagnosis of acute appendicitis. AJR Am J Roentgenol. 2002;178(4):863-868. 58. Borushok KF, Jefrey Jr RB, Laing FC, Townsend RR. Sonographic diagnosis of perforation in patients with acute appendicitis. AJR Am J Roentgenol. 1990;154(2):275-278. 59. Agha FP, Ghahremani GG, Panella JS, Kaufman MW. Appendicitis as the initial manifestation of Crohn’s disease: radiologic features and prognosis. AJR Am J Roentgenol. 1987;149(3):515-518. 60. Roth T, Zimmer G, Tschantz P. Maladie de Crohn appendiculaire. Ann Chir. 2000;125(7):665-667. 61. Higgins MJ, Walsh M, Kennedy SM, et al. Granulomatous appendicitis revisited: report of a case. Dig Surg. 2001;18(3):245-248. 62. Chou Y, Chiou H, Tiu C, et al. Sonography of acute right side colonic diverticulitis. Am J Surg. 2001;181(2):122-127. 63. O’Malley M, Wilson S. US of gastrointestinal tract abnormalities with CT correlation. Radiographics. 2003;23(1):59-72. 64. Teefey SA, Montana MA, Goldfogel GA, Shuman WP. Sonographic diagnosis of neutropenic typhlitis. AJR Am J Roentgenol. 1987;149(4):731-733. 65. Frager DH, Frager JD, Brandt LJ, et al. Gastrointestinal complications of AIDS: radiologic features. Radiology. 1986;158(3):597-603. 66. Balthazar EJ, Megibow AJ, Fazzini E, et al. Cytomegalovirus colitis in AIDS: radiographic indings in 11 patients. Radiology. 1985;155(3):585-589. 67. Teixidor HS, Honig CL, Norsoph E, et al. Cytomegalovirus infection of the alimentary canal: radiologic indings with pathologic correlation. Radiology. 1987;163(2):317-323. 68. Puylaert JB. Mesenteric adenitis and acute terminal ileitis: US evaluation using graded compression. Radiology. 1986;161(3):691-695. 69. Puylaert JB, Lalisang RI, van der Werf SD, Doornbos L. Campylobacter ileocolitis mimicking acute appendicitis: diferentiation with gradedcompression US. Radiology. 1988;166(3):737-740. 70. Puylaert JB. Right-sided segmental infarction of the omentum: clinical, US, and CT indings. Radiology. 1992;185(1):169-172. 71. Painter NS, Burkitt DP. Diverticular disease of the colon, a 20th century problem. Clin Gastroenterol. 1975;4(1):3-21. 72. Parks TG. Natural history of diverticular disease of the colon. A review of 521 cases. Br Med J. 1969;4(5684):639-642. 73. Fleischner F, Ming S. Revised concepts on diverticular disease of the colon. Radiology. 1965;84(4):599-609. 74. Wilson SR, Toi A. he value of sonography in the diagnosis of acute diverticulitis of the colon. AJR Am J Roentgenol. 1990;154(6): 1199-1202. 75. Parulekar SG. Sonography of colonic diverticulitis. J Ultrasound Med. 1985;4(12):659-666. 76. Derchi LE, Reggiani L, Rebaudi F, Bruschetta M. Appendices epiploicae of the large bowel. Sonographic appearance and diferentiation from peritoneal seeding. J Ultrasound Med. 1988;7(1):11-14. 77. Meiser G, Meissner K. [Sonographic diferential diagnosis of intestinal obstruction—results of a prospective study of 48 patients]. Ultraschall Med. 1985;6(1):39-45. 78. Tennenhouse JE, Wilson SR. Sonographic detection of a small-bowel bezoar. J Ultrasound Med. 1990;9(10):603-605. 79. Siewert B, Raptopoulos V. CT of the acute abdomen: indings and impact on diagnosis and treatment. AJR Am J Roentgenol. 1994;163(6):1317-1324. 80. Balthazar EJ. George W. Holmes Lecture. CT of small-bowel obstruction. AJR Am J Roentgenol. 1994;162(2):255-261. 81. Lee DH, Lim JH, Ko YT. Aferent loop syndrome: sonographic indings in seven cases. AJR Am J Roentgenol. 1991;157(1):41-43. 82. Parienty RA, Lepreux JF, Gruson B. Sonographic and CT features of ileocolic intussusception. AJR Am J Roentgenol. 1981;136(3):608-610. 83. Weissberg D, Scheible W, Leopold G. Ultrasonographic appearance of adult intussusception. Radiology. 1977;124(3):791-792. 84. Alessi V, Salerno G. he “Hay-fork” sign in the ultrasonographic diagnosis of intussusception. Gastrointest Radiol. 1985;10(1):177-179. 85. Gaines PA, Saunders AJS, Drake D. Midgut malrotation diagnosed by ultrasound. Clin Radiol. 1987;38(1):51-53.

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86. Totten MA, Gregg JA, Fremont-Smith P, Legg M. Clinical and pathological spectrum of antibiotic-associated colitis. Am J Gastroenterol. 1978;69(3 Pt 1):311-319. 87. Downey DB, Wilson SR. Pseudomembranous colitis: sonographic features. Radiology. 1991;180(1):61-64. 88. Bolondi L, Ferrentino M, Trevisani F, et al. Sonographic appearance of pseudomembranous colitis. J Ultrasound Med. 1985;4(9):489-492. 89. Vernacchia FS, Jefrey RB, Laing FC, Wing VW. Sonographic recognition of pneumatosis intestinalis. AJR Am J Roentgenol. 1985;145(1):51-52. 90. Sigel B, Machi J, Ramos JR, et al. Ultrasonic features of pneumatosis intestinalis. J Clin Ultrasound. 1985;13(9):675-678. 91. Cotrin RS, Kumar V, Collins T, editors. Robbins pathologic basis of disease. 6th ed. Philadelphia: Saunders; 1999. pp. 1583-1584. 92. Young R, Gilks C, Scully R. Mucinous tumors of the appendix associated with mucinous tumors of the ovary and pseudomyxoma peritonei. Am J Surg Pathol. 1991;15(5):415-429. 93. Dietrich CF, Brunner V, Seifert H, et al. [Intestinal B-mode sonography in patients with endemic sprue. Intestinal sonography in endemic sprue]. Ultraschall Med. 1999;20(6):242-247. 94. Rettenbacher T, Hollerweger A, Macheiner P, et al. Adult celiac disease: US signs. Radiology. 1999;211(2):389-394. 95. Pickhardt PJ, Yagan N, Siegel MJ, et al. Cystic ibrosis: CT indings of colonic disease. Radiology. 1998;206(3):725-730. 96. Haber HP, Benda N, Fitzke G, et al. Colonic wall thickness measured by ultrasound: striking diferences in patients with cystic ibrosis versus healthy controls. Gut. 1997;40(3):406-411. 97. Connett G, Lucas J, Atchley J, et al. Colonic wall thickening is related to age and not dose of high strength pancreatin microspheres in children with cystic ibrosis. Eur J Gastroenterol Hepatol. 1999;11(2):181-184. 98. Welkon CJ, Long SS, hompson Jr CM, Gilligan PH. Clostridium diicile in patients with cystic ibrosis. Am J Dis Child. 1985;139(8):805-808. 99. Shorvon PJ, Lees WR, Frost RA, Cotton PB. Upper gastrointestinal endoscopic ultrasonography in gastroenterology. Br J Radiol. 1987;60(713):429-438. 100. Strohm WD, Classen M. Benign lesions of the upper GI tract by means of endoscopic ultrasonography. Scand J Gastroenterol Suppl. 1986;21(123): 41-46. 101. Takemoto T, Ito T, Aibe T, Okita K. Endoscopic ultrasonography in the diagnosis of esophageal carcinoma, with particular regard to staging it for operability. Endoscopy. 1986;18(Suppl. 3):22-25. 102. Bolondi L, Casanova P, Caletti GC, et al. Primary gastric lymphoma versus gastric carcinoma: endoscopic US evaluation. Radiology. 1987;165(3):821-826. 103. Hildebrandt U, Feifel G. Preoperative staging of rectal cancer by intrarectal ultrasound. Dis Colon Rectum. 1985;28(1):42-46. 104. Wang KY, Kimmey MB, Nyberg DA, et al. Colorectal neoplasms: accuracy of US in demonstrating the depth of invasion. Radiology. 1987;165(3): 827-829. 105. Yamashita Y, Machi J, Shirouzu K, et al. Evaluation of endorectal ultrasound for the assessment of wall invasion of rectal cancer. Dis Colon Rectum. 1988;31(8):617-623. 106. Berton F, Gola G, Wilson S. Perspective on the role of transrectal and transvaginal sonography of tumors of the rectum and anal canal. AJR Am J Roentgenol. 2008;190(6):1495-1504. 107. Astler V, Coller F. he prognostic signiicance of direct extension of carcinoma of the colon and rectum. Ann Surg. 1954;139(6):846-852. 108. Spiessl B, Beahrs OH, Hermanek P, et al., editors. TNM atlas: illustrated guide to the TNM/pTNM-classiication of malignant tumours. 3rd ed. Berlin: Springer Verlag; 2003. 109. Law P, Bartram C. Anal endosonography: technique and normal anatomy. Gastrointest Radiol. 1989;14(1):349-353. 110. Rikin MD, Ehrlich SM, Marks G. Staging of rectal carcinoma: prospective comparison of endorectal US and CT. Radiology. 1989;170(2):319-322. 111. Berton F, Gola G, Wilson S. Sonography of benign conditions of the anal canal: an update. AJR Am J Roentgenol. 2007;189(4):765-773. 112. Stewart LK, Wilson SR. Transvaginal sonography of the anal sphincter: reliable, or not? AJR Am J Roentgenol. 1999;173(1):179-185. 113. Sudakof G, Quiroz F, Foley W. Sonography of anorectal, rectal, and perirectal abnormalities. AJR Am J Roentgenol. 2002;179(1):131-136. 114. Parks AG, Gordon PH, Hardcastle JD. A classiication of istula-in-ano. Br J Surg. 1976;63(1):1-12.

CHAPTER

9

The Kidney and Urinary Tract Mitchell Tublin, Deborah Levine, Wendy Thurston, and Stephanie R. Wilson

SUMMARY OF KEY POINTS • Renal ultrasound is the screening modality of choice for the initial evaluation of renal insuficiency. Relevant imaging markers include parenchymal echogenicity, renal length, and collecting system dilatation. • The primary role for ultrasound in the evaluation of renal masses is to differentiate between cystic and solid lesions, although an appropriate differential diagnosis may be given based on clinical history and cyst complexity. • Echogenic renal masses are problematic, and although several discriminatory features have been proposed, renal computed tomography or magnetic resonance imaging is typically employed for larger lesions to

differentiate between renal cell carcinoma and angiomyolipoma. • The role of ultrasound in the evaluation of hematuria continues to evolve. Ultrasound is an effective screening modality for typical “urologic” causes of hematuria (namely, renal calculi) in younger patients. • Focal and diffuse bladder wall thickening at ultrasound is nonspeciic and may be caused by a variety of infectious, inlammatory reactions or neoplastic processes. Urine analysis, clinical history, and potentially cystoscopy are typically performed after thickening is identiied at sonography.

CHAPTER OUTLINE EMBRYOLOGY Development of the Kidneys and Ureter Development of the Bladder Development of the Urethra ANATOMY Kidney Ureter Bladder SONOGRAPHIC TECHNIQUE Kidney Ureter Bladder and Urethra HYDRONEPHROSIS PITFALLS IN ASSESSMENT OF OBSTRUCTION CONGENITAL ANOMALIES Anomalies Related to Renal Growth Hypoplasia Fetal Lobation Compensatory Hypertrophy Anomalies Related to Ascent of Kidney Ectopia Crossed Renal Ectopia Horseshoe Kidney Anomalies Related to Ureteral Bud Renal Agenesis Supernumerary Kidney Duplex Collecting System and Ureterocele Ureteropelvic Junction Obstruction

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Congenital Megacalices Congenital Megaureter Anomalies Related to Vascular Development Aberrant Vessels Retrocaval Ureter Anomalies Related to Bladder Development Bladder Agenesis Bladder Duplication Bladder Exstrophy Urachal Anomalies Anomalies Related to Urethral Development: Diverticula GENITOURINARY INFECTIONS Pyelonephritis Acute Pyelonephritis Renal and Perinephric Abscess Pyonephrosis Emphysematous Pyelonephritis Emphysematous Pyelitis Chronic Pyelonephritis Xanthogranulomatous Pyelonephritis Papillary Necrosis Tuberculosis Fungal Infections Candida Albicans Parasitic Infections Schistosomiasis Echinococcal (Hydatid) Disease

Acquired Immunodeiciency Syndrome Cystitis Infectious Cystitis Malacoplakia Emphysematous Cystitis Chronic Cystitis FISTULAS, STONES (CALCULI), AND CALCIFICATION Bladder Fistulas Renal Calculi Ureteral Calculi Bladder Calculi Nephrocalcinosis GENITOURINARY TUMORS Renal Cell Carcinoma Imaging and Treatment Approaches Sonographic Appearance Biopsy and Prognosis Pitfalls in Interpretation Transitional Cell Carcinoma Renal Tumors Ureteral Tumors Bladder Tumors Squamous Cell Carcinoma Adenocarcinoma Oncocytoma Angiomyolipoma Lymphoma Kidney Ureter

CHAPTER 9 Bladder Leukemia Metastases Kidney Ureter Bladder Urachal Adenocarcinoma Rare Neoplasms Kidney Bladder RENAL CYSTIC DISEASE Cortical Cysts Parapelvic Cysts Medullary Cysts Medullary Sponge Kidney Medullary Cystic Disease Polycystic Kidney Disease Multicystic Dysplastic Kidney Lithium Nephropathy

The Kidney and Urinary Tract

Multilocular Cystic Nephroma Localized Cystic Disease Neoplasm-Associated Renal Cystic Disease Acquired Cystic Kidney Disease Von Hippel–Lindau Disease Tuberous Sclerosis TRAUMA Renal Injuries Ureteral Injuries Bladder Injuries VASCULAR ABNORMALITIES Renal Vascular Doppler Sonography Renal Artery Occlusion and Infarction Arteriovenous Fistula and Malformation Renal Artery Stenosis Renal Artery Aneurysm Renal Vein Thrombosis Ovarian Vein Thrombosis

T

he prime function of the kidney is excretion of metabolic waste products. he kidneys do this by converting more than 1700 liters of blood per day into 1 liter of highly concentrated urine.1 he kidney is an endocrine organ that secretes many hormones, including erythropoietin, renin, and prostaglandins. he kidneys also function to maintain homeostasis by regulating water-salt and acid-base balance. he renal collecting system, ureters, and urethra function as conduits, and the bladder serves as a reservoir for urinary excretion.

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MEDICAL GENITOURINARY DISEASES Acute Tubular Necrosis Acute Cortical Necrosis Glomerulonephritis Acute Interstitial Nephritis Diabetes Mellitus Amyloidosis Endometriosis Interstitial Cystitis NEUROGENIC BLADDER BLADDER DIVERTICULA POSTSURGICAL EVALUATION Nephrectomy Urinary Diversion CONCLUSION Acknowledgment

and a dorsal rectum. he bladder develops from the urogenital sinus. Initially, the bladder is continuous with the allantois, which eventually becomes a ibrous cord called the urachus, the adult median umbilical ligament. As the bladder enlarges, the distal portion of the mesonephric ducts is incorporated as connective tissue into the bladder trigone. At the same time, the ureters come to open separately into the bladder.2 In infants and children the bladder is an abdominal organ; it is not until ater puberty that it becomes a true pelvic structure2 (Fig. 9.2).

Development of the Urethra

EMBRYOLOGY Development of the Kidneys and Ureter hree sets of kidneys develop in human embryos: the pronephros, mesonephros, and metanephros (deinitive or permanent kidney).2 he pronephroi appear early in the fourth embryologic week and are rudimentary and nonfunctioning. he mesonephroi form late in the fourth week and function as interim kidneys until the developing metanephroi begin to function (ninth week). he metanephroi (permanent kidneys) develop from two sources: the ureteric bud and metanephrogenic blastema.2 he ureteric bud forms the ureter, renal pelvis, calices, and collecting ducts, interacting with and penetrating the metanephrogenic blastema. his interaction is necessary to initiate ureteric bud branching and diferentiation of nephrons within the blastema (Fig. 9.1). Initially, the permanent kidneys are found in the pelvis. With fetal growth, the kidneys come to lie in the upper retroperitoneum. With ascent, the kidneys rotate medially 90 degrees so that the renal pelvis is directed anteromedially. he kidneys are in their adult location and position by the ninth gestational week. As the kidneys ascend, they derive their blood supply from nearby vessels; adult blood supply is from the abdominal aorta.

Development of the Bladder In the seventh gestational week the urorectal septum fuses with the cloacal membrane, dividing it into a ventral urogenital sinus

he epithelium of most of the male urethra and the entire female urethra is derived from the endoderm of the urogenital sinus. he urethral connective tissue and smooth muscle form from adjacent splanchnic mesenchyme.2

ANATOMY Kidney In the adult, each kidney measures approximately 11 cm long, 2.5 cm thick, and 5 cm wide and weighs 120 to 170 grams.3 Emamian et al.4 demonstrated that the parenchymal volume of the right kidney is smaller than that of the let kidney, possibly because of a relatively larger potential space for let renal growth (growth of right kidney inhibited by liver) or relatively increased let renal blood low (let renal artery typically shorter than right renal artery). Renal length correlates best with body height, and renal size decreases with advancing age because of parenchymal reduction. he let kidney usually lies 1 to 2 cm higher than the right kidney.3 he kidneys are mobile and will move depending on body position. In the supine position, the superior pole of the let kidney is at the level of the 12th thoracic vertebra, and the inferior pole is at the level of the third lumbar vertebra. he normal adult kidney is bean shaped with a smooth, convex contour anteriorly, posteriorly, and laterally. Medially,

Mesonephric duct

Remnant of pronephros

Metanephric mass of mesoderm

B

Ureteric bud Mesonephros Developing liver

Pelvis

C

Nephrogenic cord

Major calix Ureter

Minor calix

Cloaca Pelvis

Mesonephric duct

D Metanephric diverticulum or ureteric bud

A

Mesenchymal cell cluster

Metanephric mass of intermedate mesoderm

Straight collecting tubule

Primordium of metanephros

Metanephric mass of mesoderm

E

Groove between lobes Lobe

Arched collecting tubule

FIG. 9.1 Embryology of the Kidney and Ureter. (A) Lateral view of a 5-week embryo shows the three embryologic kidneys. (B)-(E) Successive stages of development of the ureteric bud (ifth to eighth week) into the ureter, pelvis, calices, and collecting tubules. (With permission from The urogenital system. In: Moore KL, Persaud TVN, editors. The developing human: clinically oriented embryology. 5th ed. Philadelphia: Saunders; 1993. pp. 265-303.2) Allantois

Primitive urigenital sinus Mesonephros

Mesonephros

Ureteric bud Urorectal septum

Mesonephric duct

Hindgut

B

Cloacal membrane Vesical part Pelvic part

C Genital tubercle

Urogenital membrane

Phallic part

Mesonephros

Urogenital sinus

A

Metanephros

Gonad

D Mesonephros

Mesonephros

Metanephros

Metanephros

E FIG. 9.2 Embryology of the Bladder and Urethra. Diagrams show division of the cloaca into the urogenital sinus and rectum; absorption of the mesonephric ducts; development of the urinary bladder, urethra, and urachus; and change in location of the ureters. (A) and (B) Five-week embryo. (C)-(H) Seven- to 12-week embryo. (A, C, E, and G, female; B, D, F, and H, male.) (With permission from The urogenital system. In: Moore KL, Persaud TVN, editors. The developing human: clinically oriented embryology. 5th ed. Philadelphia: Saunders; 1993. pp. 265-303.2)

Urachus

Rectum

Ureter

Urinary bladder

Mesonephric duct

Ureter

Pelvic portion of urogenital sinus

Uterine tube

F Urinary bladder

Kidney

Kidney

Testis

Ovary

Ureter

Uterus Clitoris

G

Ductus deferens

Vagina Penis Spongy urethra

H

CHAPTER 9 the surface is concave; the medial surface is known as the renal hilum. he renal hilum is continuous with a central cavity called the renal sinus. Within the renal sinus are the major branches of the renal artery, major tributaries of the renal vein, and the collecting system.3 he remainder of the renal sinus is packed with fat. he collecting system (renal pelvis) lies posterior to the renal vessels in the renal hilum (Fig. 9.3). Renal parenchyma is composed of cortex and medullary pyramids. he renal medullary pyramids are hypoechoic relative to the renal cortex and can be identiied in most normal adults (Fig. 9.4). Normal renal cortex is typically less echogenic than adjacent liver and spleen. Platt et al.5 found that 72% of 153 patients with renal cortical echogenicity equal to that of the liver had normal renal function. Greater renal echogenicity than liver echogenicity showed a speciicity and a positive predictive value for abnormal renal function of 96% and 67%, respectively. However, the sensitivity of this ultrasound criterion was poor (20%). During normal development, two parenchymal masses called ranunculi partially fuse. Parenchymal junctional defects occur at the site of fusion and must not be confused with pathologic processes (e.g., renal scar, angiomyolipoma). he junctional parenchymal defect is most oten located anteriorly and superiorly, typically at the junction of the upper and middle thirds of the kidney, and can be traced medially and inferiorly into the renal sinus. Usually, it is oriented more horizontally than vertically and therefore it is best appreciated on sagittal scans6 (Fig. 9.5). Junctional cortical defects are more oten shown within the right kidney, although let junctional cortical defects may be detected with favorable acoustic windows. A hypertrophied column of Bertin (HCB) is a normal variant; it represents unresorbed polar parenchyma from one or both of the two subkidneys that fuse to form the normal kidney.7 Sonographic features that may aid in the demarcation of HCB include indentation of the renal sinus laterally and a border formed by the junctional parenchymal defect. Hypertrophied columns are usually located at the junction of the upper and middle thirds of the kidney and contain renal cortex that is continuous with the adjacent renal cortex of the same subkidney.

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FIG. 9.3 Anatomy of the Kidney, Ureter, and Bladder.

B

FIG. 9.4 Normal Kidney. (A) Sagittal and (B) transverse sonograms of normal anatomy with corticomedullary differentiation show relatively hypoechoic medullary pyramids, with cortex slightly less echogenic than the liver and spleen.

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Bladder

FIG. 9.5 Anterior Junction Line. Sagittal sonogram demonstrates an echogenic line that extends from the renal sinus to perinephric fat. The defect is typically located at the junction of the upper and middle thirds of the kidney, as in this example.

Sonographic Criteria for Hypertrophied Column of Bertin Indentation of renal sinus laterally Bordered by junctional parenchymal defect Location at junction of upper and middle thirds Continuous with adjacent renal cortex Similar color low to surrounding parenchyma Contains renal pyramids Less than 3 cm in size

Columns contain renal pyramids and usually measure less than 3 cm7,8 (Fig. 9.6). he echogenicity of HCB and adjacent renal cortex depend on the scan plane. Alterations in tissue orientation produce diferent acoustic relectivity.7 he echoes of the HCB are brighter than those of adjacent renal cortex when seen en face7 (Fig. 9.6). It may be diicult to diferentiate a small, hypovascular tumor from an HCB; however, demonstration of arcuate arteries by color Doppler ultrasound indicates an HCB rather than a tumor. Occasionally, contrast-enhanced computed tomography (CT) may be necessary to diferentiate between an HCB and a non–border-deforming renal lesion. he kidney has a thin, ibrous capsule. he capsule is surrounded by perirenal fat. Perirenal fat is encased anteriorly by Gerota fascia and posteriorly by Zuckerkandl fascia.9 he right perirenal space opens superiorly at the bare area of the liver, and both perirenal spaces communicate with the pelvic peritoneal space.10 Right and let perirenal spaces communicate with each other across the midline at the level of the third to ith lumbar vertebrae.10

he bladder is positioned in the pelvis, inferior and anterior to the peritoneal cavity and posterior to the pubic bones.3 Superiorly, the peritoneum is relected over the anterior aspect of the bladder. Within the bladder, the ureteric and urethral oriices demarcate an area known as the trigone; the urethral oriice also marks the bladder neck. he bladder neck and trigone remain constant in shape and position; however, the remainder of the bladder will change shape and position depending on the volume of urine within it. Deep to the peritoneum covering the bladder is a loose, connective tissue layer of subserosa that forms the adventitial layer of the bladder wall. Adjacent to the adventitia are three muscle layers: the outer (longitudinal), middle (circular), and internal longitudinal layers. Adjacent to the muscle, the innermost layer of the bladder is composed of mucosa. he bladder wall should be smooth and of uniform thickness. he wall thickness depends on the degree of bladder distention.

SONOGRAPHIC TECHNIQUE he ability to visualize organs of the genitourinary tract by ultrasound depends on the patient’s body habitus, operator experience, and scanner platform. High-frequency probes should be used for patients with a favorable body habitus. Harmonic imaging is oten useful for diicult-to-scan patients (e.g., obese patients). Compound imaging and speckle reduction may increase lesion conspicuity and decrease artifacts.

Kidney he kidneys should be assessed in the transverse and coronal plane. Optimal patient positioning varies; supine and lateral decubitus positions oten suice, although oblique and occasionally prone positioning may be necessary (e.g., obese patients). Usually, a combination of subcostal and intercostal approaches is required to evaluate the kidneys fully; the upper pole of the let kidney may be particularly diicult to image without a combination of approaches. When the collecting system is dilated, additional images should be taken to assess for the level of obstruction, any obstructing lesion, and appearance of the kidneys ater voiding (see “Hydronephrosis”).

Ureter he proximal ureter is best visualized using a coronal oblique view with the kidney as an acoustic window. he ureter is followed to the bladder, maintaining the same approach. A nondilated ureter may be impossible to visualize because of overlying bowel gas. Transverse scanning of the retroperitoneum oten demonstrates a dilated ureter, which can then be followed caudally with both transverse and sagittal imaging. In women, a dilated distal ureter is well seen with transvaginal scanning.

Ureter

Bladder and Urethra

he ureter is a long (30-34 cm), mucosal-lined conduit that delivers urine from the renal pelvis to the bladder. Each ureter varies in diameter from 2 to 8 mm.3 As it enters the pelvis, the ureter passes anterior to the common/external iliac artery. he ureter has an oblique course through the bladder wall (see Fig. 9.3).

he bladder is best evaluated when it is moderately illed; an overilled bladder causes patient discomfort. he bladder should be scanned in the transverse and sagittal planes. To better visualize the bladder wall in women, transvaginal scanning may be helpful. If the nature of a large, luid-illed mass in the pelvis is uncertain,

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B

C

E

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D

F

FIG. 9.6 Hypertrophied Column of Bertin. (A) Sagittal and (B) transverse sonograms show classic appearance of the column of Bertin. (C) Medullary pyramids can be seen within the hypertrophied column of Bertin. (D) Echogenicity of the column may vary based on orientation. (E) Transverse sonogram and (F) corresponding power Doppler image conirm a hypertrophied column.

voiding or insertion of a Foley catheter will clarify the location and appearance of the bladder relative to the luid-illed mass. Incomplete bladder emptying can be due to prostate enlargement, neurogenic bladder, or pelvic loor weakness. Bladder stones and infection are important complications. Initial assessment includes assessment of the kidneys and ureter for dilatation, as well as calculation of both a prevoid and postvoid residual. We typically calculate bladder volume by taking the three

orthogonal measurements and multiplying by .6 (this is diferent from most organs, which multiply by .52). his slightly larger value is because the shape of the bladder is more of a cuboidal shape than a prolate ellipse. he urethra in a woman can be scanned with transvaginal, transperineal, or translabial sonography11 (Fig. 9.7). he posterior or the prostatic urethra in men is best visualized with transrectal probes (Fig. 9.8).

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HYDRONEPHROSIS he term hydronephrosis refers to dilatation of the collecting system. Obstruction is oten present, but this is not always the case. here are many causes of a dilated renal collecting system, and ultrasound is the initial imaging modality of choice for the majority of these assessments (except as discussed in the previous section where noncontrast-enhanced CT may be used in the initial assessment of acute renal colic). Initial sonographic evaluation should include an assessment of the degree of dilatation, appearance of surrounding renal parenchyma, assessment for level of obstruction and any obstructing lesion. Numerous grading systems for the assessment of the degree of hydronephrosis have been proposed following Ellenbogen and colleagues’ original article on the topic.12 None has been readily adopted, however, and most radiologists continue to use descriptive terminology such as mild, moderate, and severe.13

FIG. 9.7 Translabial Ultrasound of Female Urethra. Sagittal sonogram shows the tubular hypoechoic urethra extending from the bladder to the skin surface.

A

A practical pearl for the ultrasound evaluation of hydronephrosis is to assess the degree of dilatation before and ater bladder voiding. Hydronephrosis that persists ater voiding suggests an anatomic obstruction. If collecting system dilatation diminishes postvoiding, then one might consider nonobstructive pelvicaliectasis (i.e., vesicoureteral relux). Most obstructing lesions are located within the pelvis (ibroids, prostatic hypertrophy, ovarian tumor, bladder tumor) and thus are obvious on sonographic evaluation. When the pelvis is normal, the length of the ureter should be assessed for dilatation and/or obstructing lesion. In pregnancy, it is helpful to have the patient lie in the decubitus position with the symptomatic side up to allow for the weight of the uterus to move of of the ureter. Over time the obstructed kidney will initially become enlarged. Later, renal damage may occur with parenchymal atrophy and blunting of calices. In pregnancy, the urinary tract frequently is dilated. Smooth muscle relaxation occurs as a result of elevated hormone levels. Mass efect on the ureter may be caused by the enlarged uterus. Because of the location of the ureters, the right ureter is frequently more dilated than the let ureter. Physiologic dilatation of the urinary tract in pregnancy is suggested when the distal ureters taper at the sacral promontory. Pregnant patients are also at increased risk for urinary tract infections (UTIs), which can complicate the assessment. In addition, stone disease can occur and this needs to be distinguished from the physiologic dilatation associated with pregnancy. In acute hydronephrosis of pregnancy, patients may present with severe lank or lower abdominal pain radiating to the groin due to ureteric obstruction. he obstruction usually occurs at the level of the pelvic brim. Symptoms may improve with change in posture with the patient in the lateral decubitus position, symptomatic side up. In extreme cases, ureteral stunting may be required. When severe overdistention syndrome occurs, rupture of the urinary tract may occur, which can be identiied as luid collection around the periphery of the kidney by ultrasound.

B

FIG. 9.8 Transrectal Ultrasound of Male Urethra. (A) Sagittal and (B) transverse sonograms show the urethra with calciications in the urethral glands (arrows) surrounded by the echo-poor muscle of the internal urethral sphincter. B, Bladder; arrowhead, ejaculatory duct; S, seminal vesicles. (Courtesy of Ants Toi, MD, Toronto Hospital.)

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317

Causes of Hydronephrosis Genitourinary Obstruction

Comments

Genitourinary Obstruction

Comments

Renal/ureteral stone

Look for stone in common sites of obstruction: ureterovesical junction and ureteropelvic junction Hematuria

Aneurysm

Should be obvious on Doppler assessment of vessels Mass typically seen in pelvis Ureter dilated to pelvic brim

Transitional cell carcinoma Sloughed papilla Blood clot Posterior urethral valves Ureterocele

Ureteropelvic junction obstruction Ureteral stricture (prior infection, surgery, radiation) Neurogenic bladder Extrinsic Obstruction Retrocaval ureter Prostatic hypertrophy Tumor (ibroid, ovarian carcinoma, lymphoma) Lymphadenopathy Retroperitoneal ibrosis

Hematuria Bilateral, pediatric diagnosis May be orthotopic or heterotopic If heterotopic, look for renal duplication abnormality Extrarenal pelvis may be dilated out of proportion to calices History aids in diagnosis

Endometriosis Pregnancy Nonobstructive Vesicoureteral relux Congenital megacalices

Check for postvoid residual

Prior obstruction

May need CT for diagnosis Enlarged prostate impinges on bladder Abnormal mass seen in pelvis Abnormal mass seen in pelvis Mass encasing the aorta CT may be needed for diagnosis

Infection

PITFALLS IN ASSESSMENT OF OBSTRUCTION Although obstruction typically causes dilatation, early in the process the renal collecting system may not dilate. In cases of renal failure, a poorly functioning kidney may not make suicient urine to demonstrate dilatation. In addition, in cases of severe obstruction, pelvocaliceal rupture may lead to decompression of the collecting system with a perinephric hematoma/urinoma. Hydronephrosis (a condition in which dilated calices communicate with central collecting system) should be distinguished from multiple parapelvic cysts (which do not communicate).

CONGENITAL ANOMALIES Anomalies Related to Renal Growth Hypoplasia Renal hypoplasia is a renal parenchymal anomaly in which there are too few nephrons. Renal function depends on the mass of the kidney. True hypoplasia is a rare anomaly. Many patients

High low states (diabetes insipidus, psychogenic polydipsia) Distended bladder

Cortical scarring, typically in upper poles May be unilateral or bilateral If associated with congenital megaureter, both dilated ureter and calices will be present May need contrastenhanced CT for diagnosis Prior severe dilatation may not return to normal Signs and symptoms of infection Typically mild dilatation

Returns to normal after bladder emptying

with unilateral hypoplasia are asymptomatic; the condition is typically an incidental inding. Patients with bilateral hypoplasia oten have renal insuiciency. Hypoplasia is believed to result from the ureteral bud making contact with the most caudal portion of the metanephrogenic blastema. his can occur with delayed development of the ureteric bud or from delayed contact of the bud with the cranially migrating blastema. Hypoplasia is established when fewer but otherwise histologically normal renal lobules are identiied.14 At ultrasound, the kidney is small but otherwise appears normal.

Fetal Lobation Fetal lobation is usually present until 4 or 5 years of age; however, persistent lobation is seen in 51% of adult kidneys.15 here is infolding of the cortex without loss of cortical parenchyma. At ultrasound, sharp clets are shown overlying the columns of Bertin.16 Compensatory Hypertrophy Compensatory hypertrophy may be difuse or focal. It occurs when existing healthy nephrons enlarge to allow healthy renal parenchyma to perform more work. he difuse form is seen

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with contralateral nephrectomy, renal agenesis, renal hypoplasia, renal atrophy, and renal dysplasia. Difuse compensatory hypertrophy is suggested at ultrasound when an enlarged but otherwise normal-appearing kidney is identiied. he focal form is seen when residual islands of normal tissue enlarge in an otherwise diseased kidney; focal compensatory hypertrophy may be particularly prominent in the setting of relux nephropathy. Large areas of nodular but normal renal tissue identiied between scars may mimic a solid renal mass.5

Anomalies Related to Ascent of Kidney Ectopia Failure of the kidney to ascend during embryologic development results in a pelvic kidney; prevalence is 1 in 724 pediatric autopsies.16 hese kidneys are oten small and abnormally rotated. Fity percent of pelvic kidneys have decreased function.16 he ureters are oten short; poor drainage and collecting system dilatation predispose pelvic kidneys to infection and stone formation. he blood supply is oten complex; multiple arteries may be derived from regional arteries (typically, internal iliac or common iliac). If the kidney ascends too high, it may pass through the foramen of Bochdalek and become a true thoracic kidney; this is usually of no clinical signiicance. A search for a pelvic kidney should be performed if the kidney is not identiied within renal fossae (Fig. 9.9). If the kidney has ascended too high, ultrasound is helpful to determine if the diaphragm is intact. Crossed Renal Ectopia In crossed renal ectopia, both kidneys are found on the same side. In 85% to 90% of cases, the ectopic kidney will be fused to the other kidney (crossed-fused ectopia). he upper pole of the ectopic kidney is usually fused to the lower pole of the other kidney, although fusion may occur anywhere. he incidence is 1 in 1000 to 1 in 1500 at autopsy.15 Fusion of metanephrogenic blastema does not allow proper rotation or ascent; thus both kidneys are more caudally located, although the ureterovesical

junctions (UVJs) are located normally. At sonography, both kidneys are on the same side and are typically fused (Fig. 9.10). In patients with renal colic, knowing that the UVJs are in the normal location is particularly important, since bilateral ureters need to be assessed.

Horseshoe Kidney he incidence of horseshoe kidneys in the general population is 0.01% to 0.25%. Horseshoe kidneys occur when metanephrogenic blastema fuse prior to ascent; fusion is usually at the lower poles (95%). Typically, the isthmus is composed of functioning renal tissue, although rarely it is made up of ibrous tissue. he horseshoe kidney sits anterior to the abdominal great vessels and derives its blood supply from the aorta and other regional vessels, such as inferior mesenteric, common iliac, internal iliac, and external iliac arteries. Abnormal rotation of renal pelves oten results in ureteropelvic junction (UPJ) obstruction; the horseshoe kidney is thus predisposed to infection and stone formation. Additional associated anomalies include vesicoureteral relux, collecting system duplication, renal dysplasia, retrocaval ureter, supernumerary kidney, anorectal malformation, esophageal atresia, rectovaginal istula, omphalocele, and cardiovascular and skeletal abnormalities. At sonography, horseshoe kidneys are usually lower than normal and the lower poles project medially. Transverse imaging of the retroperitoneum will demonstrate the renal isthmus crossing the midline anterior to abdominal great vessels (Fig. 9.11). Hydronephrosis (pyelocaliectasis) and collecting system calculi may be evident.

Anomalies Related to Ureteral Bud Renal Agenesis Renal agenesis may be unilateral or bilateral. Bilateral renal agenesis is a rare anomaly that is incompatible with life. he prevalence rate of bilateral agenesis at autopsies is 0.04%. he condition has a 3 : 1 male predominance.15 Unilateral renal

*

FIG. 9.9 Pelvic Kidney. Transverse sonogram demonstrates a left pelvic kidney posterior to the uterus (*).

FIG. 9.10 Cross-Fused Ectopia. Sagittal sonogram demonstrates two kidneys fused to each other.

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Horseshoe kidney

RK

LK

A

B

FIG. 9.11 Horseshoe Kidney. (A) Transverse sonogram shows the isthmus crossing anterior to the retroperitoneal great vessels, with the renal parenchyma of each limb of the horseshoe draping over the spine. (B) Conirmatory contrast-enhanced CT examination. LK, Left kidney; RK, right kidney.

agenesis is usually an incidental inding; the contralateral kidney of these patients may be quite large secondary to compensatory hypertrophy. Renal agenesis occurs when there is (1) absence of the metanephrogenic blastema, (2) absence of ureteral bud development, or (3) absence of interaction and penetration of the ureteral bud with the metanephrogenic blastema. Renal agenesis is associated with genital tract anomalies, which are oten cystic pelvic masses in both men and women. Other associated anomalies include skeletal abnormalities, anorectal malformations, and cryptorchidism. At ultrasound, although the kidney is absent, a normal adrenal gland is usually found. he adrenal gland will be absent in 8% to 17% of patients with renal agenesis.16 It may be diicult to diferentiate between renal agenesis and a small, hypoplastic or dysplastic kidney. With all these conditions, the contralateral kidney will be enlarged as a result of compensatory hypertrophy. Usually, the colon falls into the empty renal bed. Care should be taken not to confuse a loop of gut with a normal kidney.

Supernumerary Kidney Supernumerary kidney is an exceedingly rare anomaly. he supernumerary kidney is usually smaller than normal and can be found above, below, in front of, or behind the normal kidney. he supernumerary kidney oten has only a few calices and a single infundibulum. he formation of a supernumerary kidney is likely caused by the same mechanism that gives rise to a duplex collecting system.15 Two ureteric buds reach the metanephrogenic blastema, which then divides, or alternatively, there are initially two blastema. On sonography, an extra kidney will be found. Duplex Collecting System and Ureterocele Duplex collecting system is the most common congenital anomaly of the urinary tract, with an incidence of 0.5% to 10% of live births.15 he degree of duplication is variable. Duplication is complete when there are two separate collecting systems and two separate ureters, each with their own ureteral oriice. Duplication is incomplete when the ureters join and enter the bladder through a single ureteral oriice. Ureteropelvic duplication arises

when two ureteral buds form and join with the metanephrogenic blastema or when there is division of a single ureteral bud early in embryogenesis. Normally during embryologic development, the ureteral oriice migrates superiorly and laterally to become part of the bladder trigone. With complete duplication, the ureter from the lower pole of the kidney migrates to assume its normal location, whereas the ureter draining the superior pole of the kidney migrates abnormally to a more medial and inferior ureteral oriice. Patients have an increased incidence of UPJ obstruction and uterus didelphys.16 In complete duplication, the ureter draining the lower pole has a more perpendicular course through the bladder wall, making it more prone to relux. he ectopic ureter from the upper pole is prone to obstruction, relux, or both (Fig. 9.12). Obstruction can result in cystic dilatation of the intramural portion of the ureter, giving rise to a ureterocele. Ureteroceles may be unilateral or bilateral and may occur in normal, duplicated, or ectopic ureters. Ureteroceles may result in ureteral obstruction and give rise to recurrent or persistent UTIs. If large, they may block the contralateral ureteral oriice and the urethral oriice at the bladder neck. Treatment of these symptomatic ureteroceles is surgical. However, most ureteroceles are transient, incidental, and clinically insigniicant. At ultrasound, a duplex collecting system is seen as two central echogenic renal sinuses with intervening, bridging renal parenchyma. Unfortunately, this sign is insensitive and is only seen in 17% of duplex kidneys.17 Hydronephrosis of the upper-pole moiety and visualization of two distinct collecting systems and ureters are diagnostic. he bladder should always be carefully evaluated for the presence of a ureterocele. A ureterocele will appear as a round, cystlike structure within the bladder (Fig. 9.13). Occasionally, it may be large enough to occupy the entire bladder and will cause obstruction of the bladder neck. In female patients, transvaginal sonography can be helpful to identify small ureteroceles18 (Fig. 9.14). hese ureteroceles may be transient. Madeb et al.19 demonstrated that transvaginal sonography with color Doppler and spectral analysis can provide additional information about low dynamics, eliminating the need for invasive procedures.

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A

B

FIG. 9.12 Duplex Collecting System. (A) Sagittal sonogram shows an upper-pole cystic mass. Note collecting system dilatation and cortical thinning. (B) Delayed intravenous urogram shows duplicated left collecting system and dilated upper-pole moiety.

A

C

B

FIG. 9.13 Duplex Collecting System. (A) Sagittal sonogram shows dilatation of the lower-pole moiety, likely related to relux. (B) Sagittal sonogram shows central parenchyma separating the upper-pole and lower-pole moieties. There is moderate dilatation of both moieties. (C) Sagittal sonogram of the bladder and distal ureter of the patient in B. Note dilatation of the ureter from the upper-pole moiety and a large ureterocele.

CHAPTER 9 Ureteropelvic Junction Obstruction UPJ obstruction is a common anomaly with a 2 : 1 male predominance. he let kidney is afected twice as frequently as the right kidney. UPJ obstruction is bilateral in 10% to 30% of cases.20 Most adult patients present with chronic, vague, back or lank pain. Symptomatic patients and those with complications, including superimposed infection, stones, or impaired renal function, should be treated. Patients have an increased incidence of contralateral multicystic dysplastic kidney and renal agenesis. Most idiopathic UPJ obstructions are thought to be functional rather than anatomic.20 Histologic evaluation of afected specimens has demonstrated excessive collagen between muscle bundles, deicient or absent muscle, and excessive longitudinal muscle.20 Occasionally, intrinsic valves, true luminal stenosis, and aberrant arteries are the cause of obstruction. At ultrasound, hydronephrosis is present

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to the level of the UPJ (Fig. 9.15). Marked ballooning of the renal pelvis is oten shown, and if long-standing, there will be associated renal parenchymal atrophy. he caliber of the ureter, on the other hand, is normal. Careful evaluation of the contralateral kidney should be performed to exclude associated anomalies.

Congenital Megacalices Congenital megacalices refer to typically unilateral, nonobstructive enlargement of the calices. It is nonprogressive; overlying parenchyma and renal function are maintained. Infection and stone formation are increased because of caliceal enlargement. he exact pathogenesis is speculative; the most common association is with primary megaureter.21 At ultrasound, numerous enlarged clubbed calices are shown. Papillary impressions are absent, and cortical thickness is maintained. Congenital Megaureter Megaureter (congenital megaureter, megaloureter) results in functional ureteric obstruction. he most distal segment of ureter is aperistaltic: focal ureteral lack of peristalsis results in a wide spectrum of indings, from insigniicant distal ureterectasis to progressive hydronephrosis/hydroureter. As with UPJ obstructions, men are afected more oten, and the let ureter is typically involved.20 Bilateral involvement has been demonstrated in 8% to 50% of patients. he classic inding at ultrasound is fusiform dilatation of the distal third of the ureter (Fig. 9.16). Depending on the severity, associated pyelocaliectasis may or may not be present. Calculi may form just proximal to the adynamic segment.

Anomalies Related to Vascular Development FIG. 9.14 Small Bilateral Ureteroceles. Transverse transvaginal sonogram demonstrates two small cystic structures related to the bladder wall. With the probe in the vagina, the bladder trigone and the ureteric oriices are shown in the near ield of the transducer.

A

Aberrant Vessels As it ascends during embryologic development, the kidney derives its blood supply from successively higher levels of the aorta.

B

FIG. 9.15 Ureteropelvic Junction Obstruction. (A) Sagittal and (B) transverse sonograms demonstrate marked ballooning of the renal pelvis with associated proximal caliectasis.

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A

B

FIG. 9.16 Congenital Megaureter. (A) Sagittal sonogram shows marked dilatation of the distal ureter up to the ureterovesical junction. (B) Sagittal sonogram shows moderate midregion ureterectasis.

Aberrant renal arteries will be present if the vascular supply from the lower levels of the aorta persists. Aberrant vessels can compress the ureter anywhere along its course. Color Doppler ultrasound may be useful to identify obstructing vessels crossing at the UPJ.

Retrocaval Ureter Retrocaval ureter is a rare but well-recognized congenital anomaly with a 3 : 1 male predominance. Most patients present with pain in the second to fourth decade of life. Normally, the infrarenal inferior vena cava (IVC) develops from the supracardinal vein; if it develops from the subcardinal vein, the ureter will pass posterior to the IVC. he ureter then passes medially and anteriorly between the aorta and IVC to cross the right iliac vessels. It then enters the pelvis and bladder in a normal manner. Sonography shows collecting system and proximal ureteral dilatation. In easy-to-scan patients the compressed retrocaval ureter may be identiied.

Anomalies Related to Bladder Development Bladder Agenesis Bladder agenesis is a rare anomaly. Most infants with bladder agenesis are stillborn; virtually all surviving infants are female.22 Many associated anomalies are oten present. At ultrasound, the bladder is absent. Bladder Duplication Bladder duplication is divided into three types, as follows16: Type 1: A complete or incomplete peritoneal fold separates the two bladders. Type 2: An internal septum divides the bladder. he septum may be complete or incomplete and may be oriented in a sagittal or coronal plane. here may be multiple septa.

Type 3: A transverse band of muscle divides the bladder into two unequal cavities.

Bladder Exstrophy Bladder exstrophy occurs in 1 in 30,000 live births, with a 2 : 1 male predominance.16 Failure in development of the mesoderm below the umbilicus leads to absence of the lower abdominal and anterior bladder wall. here is a high incidence of associated musculoskeletal, gastrointestinal, and genital tract anomalies. hese patients have an increased (200-fold) incidence of bladder carcinoma (adenocarcinoma in 90%).16 Urachal Anomalies Normally, the urachus closes in the last half of fetal life.16 he four types of congenital urachal anomalies, in order of frequency, are as follows16,23,24 (Fig. 9.17): 1. Patent urachus (50%) 2. Urachal cyst (30%) 3. Urachal sinus (15%) 4. Urachal diverticulum (5%) Urachal anomalies have a 2 : 1 predominance in males. A patent urachus is usually associated with urethral obstruction and serves as a protective mechanism to allow normal fetal development. A urachal cyst forms if the urachus closes at the umbilical and bladder ends but remains patent in between. he cyst is usually situated in the lower third of the urachus. here is an increased incidence of adenocarcinoma. At ultrasound, a midline cyst with or without internal echoes is seen superior to the bladder. A urachal sinus forms when the urachus closes at the bladder end but remains patent at the umbilicus. A urachal diverticulum forms if the urachus closes at the umbilical end but remains patent at the bladder. Urachal diverticula are usually incidentally found. here is an increased incidence of carcinoma and stone formation.

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Anomalies Related to Urethral Development: Diverticula he majority of urethral diverticula are acquired secondary to injury or infection, although congenital diverticula occur rarely. Most urethral diverticula in women form as a result of infection of the periurethral glands; some may be related to childbirth. Most diverticula are found in the midurethra and are bilateral. Oten, a luctuant anterior vaginal mass is felt. Stones may develop because of urinary stasis. Transvaginal or translabial scanning may demonstrate a simple or complex cystic structure communicating with the urethra through a thin neck (Fig. 9.18).

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FIG. 9.17 Congenital Urachal Anomalies. (A) Patent urachus extends from the bladder to the umbilicus. (B) Urachal sinus. (C) Urachal diverticulum. (D) Urachal cyst.

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Acute Pyelonephritis Acute pyelonephritis is a tubulointerstitial inlammation of the kidney. Two routes may lead to inlammation: ascending infection (85%; e.g., Escherichia coli) and hematogenous seeding (15%; e.g., Staphylococcus aureus). Women age 15 to 35 years are most oten afected25; 2% of pregnant women will develop acute pyelonephritis.26 Most adults present with lank pain and fever and can be diagnosed clinically with the aid of laboratory studies (bacteriuria, pyuria, and leukocytosis). With appropriate antibiotics, both clinical and laboratory indings show rapid improvement. Imaging is necessary only when symptoms and laboratory abnormalities persist: imaging is useful to identify potential causes of insuiciently treated infection, including renal and perirenal abscesses, calculi, and urinary obstruction. he Society of Uroradiology proposed using acute pyelonephritis to describe acutely infected kidneys, eliminating the need for terms such as bacterial nephritis, lobar nephronia, renal cellulitis, lobar nephritis, renal phlegmon, and renal carbuncle.27

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FIG. 9.18 Urethral Diverticulum in Young Woman With Palpable Vaginal Mass. (A) Sagittal and (B) transverse translabial sonograms show a complex cystic mass adjacent to the anterior urethra.

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At ultrasound, the majority of kidneys with acute pyelonephritis appear normal. However, ultrasound indings of pyelonephritis include (Fig. 9.19) renal enlargement, compression of the renal sinus, decreased echogenicity (secondary to edema) or increased echogenicity (potentially from hemorrhage), loss of corticomedullary diferentiation, poorly marginated mass(es), gas within the renal parenchyma,26,27 and focal or difuse absence of color Doppler perfusion corresponding to the swollen inlamed areas. If the pyelonephritis is focal, the poorly marginated masses may be echogenic, hypoechoic, or of mixed echogenicity. Echogenic masses may be the most common appearance of focal pyelonephritis.28 Sonography, including power Doppler, is less sensitive than CT, magnetic resonance imaging (MRI), or technetium-99m single-photon emission computed tomography (99mTc-DMSA SPECT) renal cortical scintigraphy for demonstrating changes of acute pyelonephritis. However, ultrasound is more accessible

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and less expensive and thus an excellent screening modality for monitoring and follow-up of complications,29 as well as in the assessment of pregnant patients with acute pyelonephritis because of its lack of ionizing radiation.26,27 A unique renal infection known as alkaline-encrusted pyelitis has been described in renal transplants and native kidneys of

Acute Pyelonephritis on Sonography Renal enlargement Compression of renal sinus Abnormal echotexture (either increased or decreased) Loss of corticomedullary differentiation Poorly marginated mass(es) Gas within renal parenchyma Focal or diffuse absence of color Doppler perfusion corresponding to the swollen inlamed areas

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FIG. 9.19 Acute Pyelonephritis in Three Patients. (A) Subtle focal increased echogenic areas are seen in the anterior cortex of the right kidney. (B) Power Doppler perfusion defect in lower pole of kidney of patient with documented E. coli pyelonephritis. Note normal corresponding gray-scale image. (C) Sagittal and (D) transverse sonograms in a third patient show a swollen and edematous kidney with focal altered echogenicity and loss of corticomedullary differentiation. The renal sinus fat is attenuated by swollen parenchyma.

CHAPTER 9 debilitated and immunocompromised patients.30 his entity is most frequently caused by Corynebacterium urealyticum, a ureasplitting microorganism. Urothelial stone encrustation develops in the kidney and bladder. If the kidney is afected, the patient may present with hematuria, stone passage, or an ammonium odor to the urine. Dysuria and suprapubic pain are the most common clinical signs if the bladder is involved. Treatment is with antibiotics and local acidiication of the urine. On sonography, alkaline-encrusted pyelitis is suggested if thickened, calciied urothelium is identiied.30 he calciication can be thin and smooth or thick and irregular. Care should be taken to distinguish urothelial calciication from layering of collecting system calculi.30

Renal and Perinephric Abscess Untreated or inadequately treated acute pyelonephritis may lead to parenchymal necrosis and abscess formation. Patients at increased risk for renal abscesses include those with diabetes, compromised immunity, chronic debilitating diseases, urinary tract obstruction, infected renal calculi, and intravenous drug abuse.26,31 Renal abscesses tend to be solitary and may spontaneously decompress into the collecting system or perinephric space. Perinephric abscesses, also a complication of pyonephrosis, may result from direct extension of peritoneal or retroperitoneal infection or interventions.24 Small abscesses are treated conservatively with antibiotics, whereas larger abscesses oten require percutaneous drainage and, if drainage is unsuccessful, surgery. At ultrasound, renal abscesses appear as round, thick-walled, hypoechoic complex masses with through transmission (Fig. 9.20). Internal mobile debris and septations may be seen. Occasionally, “dirty shadowing” may be noted posterior to gas within the abscess. he diferential diagnosis includes (1) hemorrhagic or infected cysts, (2) parasitic cysts, (3) multiloculated cysts, and (4) cystic neoplasms. Although not as accurate as CT in determining the presence and extent of perinephric abscess extension,26

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sonography is an excellent modality for following conservatively treated patients with abscesses to document resolution.

Pyonephrosis Pyonephrosis implies purulent material in an obstructed collecting system. Depending on the level of obstruction, any portion of the collecting system, including the ureter, can be afected. Early diagnosis and treatment are crucial to prevent development of bacteremia and life-threatening septic shock. he mortality rates of bacteremia and septic shock are 25% and 50%, respectively32; 15% of patients are asymptomatic at presentation.33 In the young adult, UPJ obstruction and calculi are the most frequent cause of pyonephrosis, whereas malignant ureteral obstruction is typically the predisposing factor in older patients.26 Pyonephrosis is suggested when ultrasound shows mobile collecting system debris (with or without a luid-debris level), collecting system gas, and stones (Fig. 9.21). Emphysematous Pyelonephritis Emphysematous pyelonephritis (EPN) is an uncommon, lifethreatening infection of the renal parenchyma characterized by gas formation.34 Most patients are women (2 : 1) and diabetic (90%), with a mean age of 55 years. In diabetic patients, EPN tends to occur in nonobstructed collecting systems; the reverse is true in nondiabetic patients. Bilateral disease occurs in 5% to 10% of EPN patients. Escherichia coli is the ofending organism in 62% to 70% of cases; Klebsiella (9%), Pseudomonas (2%) Proteus, Aerobacter, and Candida are additional causative organisms.26,31 At presentation, most patients are extremely ill with fever, lank pain, hyperglycemia, acidosis, dehydration, and electrolyte imbalance35; 18% present only with fever of unknown origin.36 Wan et al.37 retrospectively studied 38 patients with EPN and identiied two types of disease: EPN1, characterized by parenchymal destruction and streaky or mottled gas, and EPN2,

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FIG. 9.20 Renal Abscess. (A) Sagittal ultrasound shows a complex cystic upper-pole lesion containing layering low level echoes. (B) Corresponding contrast-enhanced CT exam shows a large right upper-pole cystic lesion with a thick rind. The patient was successfully treated with ultrasound guided drain placement and antibiotics.

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FIG. 9.21 Pyonephrosis. (A) Sagittal ultrasound of an older male with Proteus mirabilis sepsis shows a deformed, chronically hydronephrotic kidney, with layering collecting system echoes. (B) Corresponding noncontrast-enhanced CT shows a large right hydronephrotic sac and perinephric iniltration. Clinical history and imaging indings prompted successful, emergent drainage.

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FIG. 9.22 Emphysematous Pyelonephritis Type 1 (EPN1). (A) Sagittal sonogram of right renal fossa shows extensive shadowing gas occupying most of the right kidney. (B) Corresponding noncontrast-enhanced CT demonstrates diffuse parenchymal destruction of the right kidney with extensive mottled gas. Nephrectomy was eventually performed in this septic, diabetic patient. Caution must be exercised to avoid missing EPN1 altogether on ultrasound. Failure to see a kidney in a septic patient should prompt alternative cross-sectional imaging.

characterized as renal or perirenal luid collections, with bubbly or loculated gas or with gas in the collecting system. Mortality rates for EPN1 and EPN2 were 69% and 18%, respectively. he authors postulated that the diferent clinical outcomes of EPN1 and EPN2 result from the patient’s immune status and the vascular supply of the afected kidney. Emergency nephrectomy is the treatment of choice for EPN1, whereas percutaneous drainage is recommended for EPN2. CT is the preferred method to image patients with EPN, to determine the location and extent of renal and perirenal gas. Sonographic evaluation of EPN1 or EPN2 may be diicult because dirty shadowing from parenchymal gas

will obscure deeper structures; shadowing might also prompt an erroneous interpretation of renal calculi or bowel gas38 (Fig. 9.22).

Emphysematous Pyelitis Emphysematous pyelitis refers to gas localized within the urinary collecting system.34 his disease entity is seen most oten in women with diabetes or obstructing stone disease; a mortality rate of 20% has been reported. It is important to exclude iatrogenic causes of gas within the collecting system. At ultrasound, nondependent linear echogenic lines with dirty distal posterior

CHAPTER 9 acoustic shadowing, indicative of gas are seen within the collecting system (Fig. 9.23). As with EPN, CT is oten required to identify emphysematous pyelitis because dirty acoustic shadowing from gas at ultrasound may obscure the exact extent of renal and perirenal disease.

Chronic Pyelonephritis Chronic pyelonephritis is an interstitial nephritis oten associated with vesicoureteric relux. Relux nephropathy is believed to cause 10% to 30% of all cases of end-stage renal disease (ESRD)39 (Fig. 9.24). Chronic pyelonephritis usually begins in childhood and is more common in women. he renal changes may be unilateral or bilateral but usually are asymmetric.

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Relux into the collecting tubules occurs when the papillary duct oriices are incompetent. his relux occurs more oten in compound papillae, which are typically found at the poles of the kidneys. Cortical scarring therefore tends to occur over polar calices. here is associated papillary retraction with caliceal clubbing. At ultrasound, a dilated blunt calix is seen, associated with overlying cortical scar or cortical atrophy40 (Fig. 9.25). hese changes may be multicentric and bilateral. If the disease is unilateral, there may be compensatory hypertrophy of the contralateral kidney. If the disease is multicentric, compensatory hypertrophy of normal intervening parenchyma may create an island of normal tissue simulating a tumor.

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FIG. 9.23 Emphysematous Pyelitis. (A) Transverse sonogram of left kidney shows “clean” shadowing posterior to a renal calculus (C) and “dirty” shadowing posterior to nondependent collecting system gas (G). (B) Conirmatory unenhanced CT image shows both a calculus and gas within the left collecting system.

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FIG. 9.24 Relux Nephropathy: Renal Transplantation Evaluation. (A) Sagittal sonogram shows marked right hydronephrosis and absence of overlying cortex. (B) Cystogram conirms massive bilateral ureteral relux.

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FIG. 9.25 Chronic Pyelonephritis. (A) Sagittal sonogram of a patient with a history of vesicoureteral relux shows upper-pole atrophy and severe cortical loss overlying a deformed, dilated calyx. (B) Sagittal sonogram shows an atrophic kidney with scarring and dilatation of the collecting system caused by relux. (C) Sagittal sonogram shows an echogenic wedge-shaped scar in the midpole of the kidney. (D) Conirmatory CT scan.

Xanthogranulomatous Pyelonephritis Xanthogranulomatous pyelonephritis (XGP) is a chronic, suppurative renal infection in which destroyed renal parenchyma is replaced with lipid-laden macrophages. XGP is typically unilateral and may be difuse, segmental, or focal. XGP is typically associated with nephrolithiasis (70%) and obstructive nephropathy.41-43 he disease most commonly occurs in middleaged women and diabetic patients.43 Presenting signs are nonspeciic: pain, mass, weight loss, and UTI (Proteus or E. coli).41 he difusely involved kidney is usually nonfunctional. Ultrasound indings of difuse XGP include renal enlargement, maintenance of a reniform shape, and lack of corticomedullary diferentiation. Multiple hypoechoic areas correspond to dilated calices or inlammatory parenchymal masses.41 hrough transmission is variable and depends on the degree of liquefaction of the parenchymal masses. Occasionally, the large, complex cystic masses may mimic pyonephrosis. A staghorn calculus will result in extensive shadowing from the central renal sinus (Fig. 9.26). Perinephric extension may occur, but this is oten best appreciated with CT. Difuse XGP has no speciic sonographic features but is suggested when parenchymal thinning, hydronephrosis, stones,

debris in a dilated collecting system, and perinephric luid collections are present.44 Segmental XGP will be seen as one or more hypoechoic masses, oten associated with a single calyx.41,45 An obstructing calculus may be seen near the papilla. Focal XGP arises in the renal cortex and does not communicate with the renal pelvis. It cannot be distinguished sonographically from tumor or abscess.41

Papillary Necrosis Causative factors implicated in the ischemia that leads to papillary necrosis include analgesic abuse, diabetes, UTI, renal vein thrombosis, prolonged hypotension, urinary tract obstruction, dehydration, sickle cell anemia, and hemophilia.46 Initially, the papilla swells (Fig. 9.27); then a communication with the caliceal system occurs. he central aspect of the papilla cavitates and may slough. With papillary cavitation, ultrasound shows cystic collections within the medullary pyramids. If the papilla sloughs, the afected adjacent calyx will be clubbed. he sloughed papilla can be seen in the collecting system as an echogenic nonshadowing structure. If the sloughed papilla calciies, distal acoustic shadowing simulating medullary nephrocalcinosis will be seen.47

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FIG. 9.26 Xanthogranulomatous Pyelonephritis. (A) Sagittal sonogram shows an enlarged hypoechoic kidney and a large showing staghorn calculus. (B) Corresponding contrast-enhanced CT demonstrates a diffusely enlarged left kidney, multiple intrarenal abscesses, and a large, central obstructing calculus.

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Sonographic Findings of Papillary Necrosis Swollen pyramids Papillary cavitation Adjacent clubbed calix Sloughed papilla in collecting system that can calcify and simulate a stone Sloughed papilla may cause obstruction

Hydronephrosis may develop if the sloughed papilla obstructs the ureter.

Tuberculosis Urinary tract tuberculosis (TB) occurs with hematogenous seeding of the kidney by Mycobacterium tuberculosis from an extraurinary

source (typically lung). Urinary tract TB usually manifests 5 to 10 years ater the initial pulmonary infection. Chest radiographs may be normal (35%-50% of patients) or may show active TB (10%) or inactive healed TB (40%-55%). Most patients present with lower urinary tract signs and symptoms that include frequency, dysuria, nocturia, urgency, and gross or microscopic hematuria, whereas 10% to 20% of patients are asymptomatic.48 Urinalysis indings include sterile pyuria, microscopic hematuria, and acidic pH. TB is deinitively diagnosed with acid-fast bacilli urine cultures; however, this usually requires 6 to 8 weeks for growth. Although both kidneys are seeded initially, clinical manifestations of urinary tract TB are typically unilateral. he early or acute changes include development of multiple small bilateral tuberculomas. Das et al.49 found that the most frequently encountered sonographic abnormality was focal renal lesions

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(Fig. 9.28). Small focal lesions (5-15 mm) were echogenic or were hypoechoic with an echogenic rim. Larger, mixedechogenicity focal lesions (>15 mm) were poorly deined. Bilateral disease was noted in 30% of patients. Most tuberculomas will heal spontaneously or ater antituberculous therapy. At some later date (perhaps years later), one or more of the tubercles may enlarge. With enlargement, cavitation and communication with the collecting system will occur. he resultant pathologic changes resemble papillary necrosis; papillary involvement is noted when a sonolucent linear tract is shown extending from the involved calix into the papilla. Sot tissue caliceal masses representing sloughed papilla may be seen. Ater rupture into the collecting system, M. tuberculosis bacilluria develops and allows the spread of the renal infection to other parts of the urinary tract. Spasm or edema in the region of the UVJ may occur, giving rise to hydronephrosis and hydroureter. Ureteric linear ulcers may also occur, typically within the distal ureter. Bladder involvement is seen in 33% of patients with genitourinary tract TB.49 Early bladder manifestations include mucosal edema and ulceration. Early clinical symptoms (dysuria and frequency) are also nonspeciic. If edema occurs at the bladder trigone, ureteric obstruction may occur. At ultrasound, early bladder involvement will appear as focal or difuse wall thickening; the thickening can be quite extensive (Fig. 9.29). he later or more chronic changes of genitourinary tract TB include ibrotic strictures, extensive cavitation, calciication, mass lesions, perinephric abscesses, and istulas.48 he chronic changes, in particular those related to ibrotic strictures, result in functional renal damage. Strictures may occur anywhere in the intrarenal collecting system and ureter. he obstruction then results in proximal collecting system dilatation and pressure atrophy of

the renal parenchyma. With time, calciication in the areas of caseation or sloughed papilla may occur. If renal infection ruptures into the perinephric space, an abscess may develop. Perinephric abscesses may ultimately result in istulas to adjacent viscera. he hallmark of chronic, upper tract renal TB is a small, nonfunctional, calciied kidney, the “putty” kidney. In the bladder, chronic infection and ibrosis result in a thickened, small-capacity bladder.48 Speckled or curvilinear calciication of the bladder wall may rarely occur.50 Most cases of genitourinary tract TB can be diagnosed with a combination of intravenous/retrograde urography, ultrasound, CT, and CT urography.51 Premkumar et al.52 demonstrated in 14 patients with advanced urinary tract TB that detailed morphologic information and functional renal status are best assessed with CT and urography. Das et al.53 reported that ultrasoundguided, ine-needle aspiration (1) may be diagnostic in patients with negative urine cultures and (2) may conirm a diagnosis of upper genitourinary tract TB in those patients with suspicious lesions and positive cultures.

FIG. 9.28 Progressive Renal Tuberculosis. Sagittal sonogram shows small, irregular hypoechoic medullary lesions. Areas of cavitation ultimately connect to the collecting system. (With permission from Wasnik AP. Tuberculosis, urinary tract. In: Kamaya A, Wong-You-Cheong J, editors. Diagnostic ultrasound: abdomen and pelvis. Philadelphia: Elsevier; 2016. pp. 490-493.51)

FIG. 9.29 Urinary Bladder Tuberculosis. Transverse sonogram shows irregular mucosal thickening, particularly at the ureteric oriice—a characteristic feature of early bladder tuberculosis. (With permission from Wasnik AP. Tuberculosis, urinary tract. In: Kamaya A, Wong-YouCheong J, editors. Diagnostic ultrasound: abdomen and pelvis. Philadelphia: Elsevier; 2016. pp. 490-493.51)

Fungal Infections Patients with a history of diabetes mellitus, chronic indwelling catheters, malignancy, hematopoietic disorders, chronic antibiotic or steroid therapy, transplantation, and intravenous drug abuse are at risk for developing fungal infections of the urinary tract.54

Candida Albicans Candida albicans is the most common fungal agent that afects the urinary tract. Renal parenchymal involvement, typically manifested by small parenchymal abscesses, occurs in the context of difuse systemic involvement. he abscesses may calcify over

CHAPTER 9 time.55 Extension into the perinephric space is also possible. Invasion of the collecting system ultimately results in fungus balls. Collecting system mycetomas may be diferentiated from blood clots, radiolucent stones, transitional cell tumors, sloughed papillae, ibroepithelial polyps, cholesteatomas, and leukoplakia based on clinical history and urine cultures.56-58 On sonography, candidal microabscesses are typically small, hypoechoic cortical lesions; the appearance is similar to other bacterial abscesses. Fungus balls appear as echogenic, nonshadowing sot tissue masses within the collecting system59 (Fig. 9.30). Fungus balls are mobile and may cause obstruction and hydronephrosis.

Parasitic Infections A wide variety of parasitic infections are common in developing countries. Sonographers should be particularly familiar with schistosomiasis and echinococcal (hydatid) disease.

Schistosomiasis Schistosoma haematobium is the most common agent to afect the urinary tract. he worms enter the human host by penetrating the skin. hey are then carried via the portal venous system to the liver, where they mature into their adult form. S. haematobium likely enters the perivesical venous plexus from the hemorrhoidal plexus.60 he female worm then deposits eggs into the venules of the bladder wall and ureter. Granuloma formation and obliterative endarteritis occur. Serologic tests demonstrating ova allow diagnosis. Hematuria is the most frequent complaint.60 At sonography, the kidneys are normal until late in the disease. Pseudotubercles develop in the ureter and bladder, and the urothelium becomes thickened (Fig. 9.31).61 Over time the pseudotubercles calcify; the calciication may be ine, granular and linear, or thick and irregular. If repeated infections occur, the bladder will become small and ibrotic. Bladder stasis results in an increased incidence of ureteral and bladder calculi.60 Patients with chronic disease also have an increased incidence of squamous cell carcinoma.60

FIG. 9.30 Fungus Ball. Sagittal sonogram shows an echogenic soft tissue mass within a dilated upper-pole cortex.

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Echinococcal (Hydatid) Disease he two major types of hydatid disease that afect the urinary tract are caused by Echinococcus multilocularis and the more common Echinococcus granulosus. Renal hydatid disease is found in 2% to 5% of patients with hydatid disease,60 is usually solitary, and typically involves the renal poles.62 Hydatid cysts may occur along the ureter or within the bladder. Each hydatid cyst consists of three layers: the pericyst, ectocyst, and endocyst. Echinococcal disease is oten silent until the cyst grows large enough to rupture or compress adjacent structures. he ultrasound manifestation of early hydatid disease is an anechoic cyst. Mural nodularity suggests scolices. When daughter cysts are present, a multiloculated cystic mass will be seen (Fig. 9.32). he membranes from the endocyst may detach and precipitate to the bottom of the hydatid luid to become “hydatid sand.”63 Varying patterns of calciication occur, ranging from eggshell to dense reticular calciication. Ring-shaped calciications inside a larger, calciied lesion suggest calciied daughter cysts.60,63 A speciic ultrasound diagnosis is diicult without an appropriate clinical history. However, several features may suggest hydatid disease, including loating membranes, daughter cysts, and thick, double-contour cyst walls.64

Acquired Immunodeiciency Syndrome he disease course and imaging manifestations of human immunodeiciency virus (HIV) infection, acquired immunodeiciency syndrome (AIDS), and HIV-associated nephropathy have rapidly evolved largely because of advances in the care of HIV-positive patients. Highly active antiretroviral therapy (HAART) has resulted in a decreased incidence of opportunistic infections and improved survival.

FIG. 9.31 Bladder Schistosomiasis. Transverse sonogram shows mild bladder wall thickening and linear anterior wall echogenicity due to early calciication. (With permission from Wasnik AP. Schistosomiasis, bladder. In: Kamaya A, Wong-You-Cheong J, editors. Diagnostic ultrasound: abdomen and pelvis. Philadelphia: Elsevier; 2016. pp. 548-549.61)

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FIG. 9.32 Renal Hydatid Cyst. (A) Sagittal sonogram shows a complex multiloculated lower-pole cystic mass (arrows). (B) Contrast-enhanced CT shows multiple conluent daughter cysts. (Courtesy of Drs. Vikram Dogra and Suleman Merchant.)

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FIG. 9.33 Proven Pneumocystis Nephropathy in a Patient With AIDS. (A) Sagittal and (B) transverse sonograms show multiple scattered echogenic foci within the renal parenchyma. Some foci demonstrate the distal acoustic shadowing of calciication. Similar indings are seen in the liver. (With permission from Spouge AR, Wilson S, Gopinath N, et al. Extrapulmonary Pneumocystis carinii in a patient with AIDS: sonographic indings. AJR Am J Roentgenol. 1990;155:76-78.66)

Early literature noted the increased incidence of opportunistic genitourinary infections (cytomegalovirus [CMV], Candida albicans, Cryptococcus, Pneumocystis jiroveci [formerly P. carinii], Mycobacterium avium-intracellulare, Mucormycosis) and tumors (lymphoma, Kaposi sarcoma) in these immunocompromised patients.65 he appearance of these infections is oten nonspeciic (and now rare), but difuse visceral/renal calciications suggest disseminated P. jiroveci, CMV, or M. avium-intracellulare infections66-68 (Fig. 9.33). he genitourinary infections that now occur in these patients, including pyelonephritis, renal abscesses, and cystitis, are similar to those seen in non–HIV-infected individuals. Use of HAART has also changed the spectrum of chronic renal diseases seen in HIV-positive patients. he incidence of ESRD in HIV patients decreased initially ater the institution of

HAART; however, the increased prevalence of HIV in the US population has resulted in an increased number of patients with HIV-associated nephropathy (HIVAN).69 In HIV-positive patients, HIVAN is the most common cause of chronic kidney disease; black patients are at particular risk. he histologic hallmark of HIVAN is focal segmental glomerulosclerosis. Nephropathy in HIV-positive patients may also be caused by HIV immune complex disease and HIV thrombotic microangiopathy. Adverse renal efects of various drugs also complicate the diagnosis of chronic renal failure.70 However, other disease processes not directly associated with HIV infection (e.g., hypertension, diabetic nephropathy, interstitial nephritis) may result in ESRD in patients successfully treated with HAART.71 Deinitive diagnosis of HIVAN is usually made ater renal biopsy. Renal sonography is useful in these patients to exclude obstruction

CHAPTER 9 and determine renal size. Early reports also suggested that greatly increased renal echogenicity is a fairly speciic inding of HIVAN (and heroin nephropathy)65,72,73 (Fig. 9.34). Other features in HIV-positive patients with renal insuiciency include globularappearing kidneys, decreased corticomedullary diferentiation, decreased renal sinus fat, and parenchymal heterogeneity.74

Cystitis Infectious Cystitis Women are at increased risk for cystitis because of colonization of the short female urethra by rectal lora. Bladder outlet obstruction or prostatitis results in cystitis in men. he most common pathogen is E. coli.75 Mucosal edema and decreased bladder capacity are common. Findings may be more prominent at the trigone and bladder neck. Patients will present with bladder irritability and hematuria. he most common inding at sonography is difuse bladder wall thickening. If cystitis is focal, pseudopolyps may form, which are impossible to diferentiate from tumor76 (Fig. 9.35A). Malacoplakia Malacoplakia is a rare granulomatous infection with a predilection for the urinary bladder. he disease is seen more oten in women (4 : 1), with a peak incidence in the sixth decade.77 he pathogenesis of malacoplakia is not known; however, an association with diabetes mellitus, alcoholic liver disease, mycobacterial infections, sarcoidosis, and transplantation suggests an altered immune response.78 Patients may present with hematuria and symptoms of bladder irritability. At sonography, single or multiple mucosal-based masses ranging from 0.5 to 3.0 cm are seen, typically at the bladder base. Malacoplakia may be locally invasive77 (Fig. 9.35B).

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Emphysematous Cystitis Emphysematous cystitis occurs most oten in female patients and those with diabetes. Patients present with symptoms of cystitis and occasionally have pneumaturia.75 he most common ofending organism is E. coli. Both intraluminal and intramural gas are present. In these severely ill patients, the urothelium is ulcerated and necrotic and may slough completely. Emphysematous cystitis is suggested at sonography when echogenic foci within the bladder wall are associated with ring-down artifact or dirty shadowing79 (Fig. 9.36A and B). Gas may be seen in the bladder lumen as well. he bladder wall is usually thickened and echogenic.34 A lack of bladder wall thickening may be a helpful sonographic feature to distinguish the gas of emphysematous cystitis from gas introduced by catheterization (Fig. 9.36C). Chronic Cystitis Chronic inlammation of the bladder may be caused by various agents. Although the histology may also vary, the imaging manifestations, including a small, thickened bladder, are nonspeciic. Chronic cystitis may result in invagination of solid “nests” of urothelium into the lamina propria (Brunn epithelial nests), which may result in morphologic changes that mimic neoplasia.80 If the central portion of a Brunn nest degenerates, a cyst results (cystitis cystica). If chronic irritation persists, the Brunn nests may develop into glandular structures (cystitis glandularis). hese may be precursors of adenocarcinoma.75 Cystitis cystica and cystitis glandularis may be manifested at ultrasound as bladder wall cysts or solid papillary masses (see Fig. 9.35C). Because the appearance of these conditions on imaging can be mistaken for malignancy, cystoscopy with biopsy is necessary for diagnostic conirmation.

Causes of Bladder Wall Thickening FOCAL Neoplasm Transitional cell carcinoma Squamous cell carcinoma Adenocarcinoma Lymphoma Metastases Infectious/Inlammatory Tuberculosis (acute) Schistosomiasis (acute) Cystitis Malacoplakia Cystitis cystica Cystitis glandularis Fistula Medical Diseases Endometriosis Amyloidosis FIG. 9.34 HIV-Associated Nephropathy (HIVAN). Sagittal sonogram shows an enlarged, markedly echogenic kidney. Biopsy conirmed focal segmental glomerulosclerosis.

Trauma Hematoma

DIFFUSE Neoplasm Transitional cell carcinoma Squamous cell carcinoma Adenocarcinoma Infectious/Inlammatory Cystitis Tuberculosis (chronic) Schistosomiasis (chronic) Medical Diseases Interstitial cystitis Amyloidosis Neurogenic Bladder Detrusor hyperrelexia Bladder Outlet Obstruction With muscular hypertrophy

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FISTULAS, STONES (CALCULI), AND CALCIFICATION Bladder Fistulas Bladder istulas can be congenital or acquired. Causes of acquired istulas include trauma, inlammation, radiation, and neoplasm. Fistula from the bladder to the vagina, gut, skin, uterus, and the ureter may occur. Vesicovaginal istulas are most oten related to gynecologic or urologic surgery, bladder carcinoma, and carcinoma of the cervix. Vesicoenteric istulas typically occur as a complication of diverticulitis or Crohn disease. Vesicocutaneous istulas result from surgery or trauma. Vesicouterine istulas are a rare complication of cesarean section. Vesicoureteral istulas are also rare and usually occur ater hysterectomy.81 All these istulas are diicult to identify directly by sonography because the tracts are oten thin and short. Occasionally, linear bands of varying echogenicity may be seen.82,83 If the bladder

FIG. 9.35 Infectious Cystitis. (A) Transverse decubitus sonogram reveals bladder wall thickening (arrowheads) with pseudopolyp formation (arrows). (B) Bladder malacoplakia. Transverse sonogram shows a mucosal-based mass with focal invasion of the prostate gland. (C) Cystitis glandularis. Transverse sonogram shows a solid papillary mass.

communicates with gut, vagina, or skin, an abnormal collection of gas may be seen in the bladder lumen. At ultrasound, this appears as a nondependent linear echogenic focus with distal dirty shadowing. Palpation of the abdomen during scanning may cause gas to percolate through the istula, enhancing its detection83 (Fig. 9.36D). For depicting oten short vesicovaginal istulas, color Doppler sonographic low jets may be shown with diluted microbubble contrast agents in the bladder.84

Renal Calculi Renal stones are common, with a reported prevalence of 12% in the general population.85 Stone disease increases with advancing age, and white men are most oten afected. From 60% to 80% of calculi are composed of calcium.86 Multiple predisposing conditions, including dehydration, urinary stasis, hyperuricemia, hyperparathyroidism, and hypercalciuria, may result in renal calculi, but no cause is identiied in most patients. Caliceal

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FIG. 9.36 Gas Within the Bladder; Emphysematous Cystitis. (A) Transverse sonogram shows intraluminal gas along left anterior bladder wall. Note “dirty” posterior shadowing. (B) Corresponding CT in this patient with conirmed emphysematous cystitis shows mild bladder wall thickening and adjacent gas. (Courtesy of Shweta Bhatt, MD.) (C) Iatrogenic air introduced at cystoscopy appears as a nondependent bright echogenic focus with multiple relection artifacts. (D) Enterovesical istula (arrow) showing gas in the bladder as multiple bright echogenic foci on a transvaginal sonogram.

calculi that are nonobstructing are usually asymptomatic. Patients with small caliceal calculi may have gross or microscopic hematuria and may have colic symptoms despite the lack of imaging indings suggestive of obstruction.87 A calculus that migrates and causes infundibular or UPJ obstruction oten results in clinical signs and symptoms of lank pain. If a stone passes into the ureter, the calculus may lodge in three areas of ureteric narrowing: just past the UPJ; where the ureter crosses the iliac vessels; and at the UVJ. he very small diameter of the UVJ (1-5 mm) accounts for the large percentage of calculi that lodge within the distal ureter.86 Approximately 80% of stones smaller than 5 mm will pass spontaneously.

Renal calculi can be detected using many diferent imaging modalities, including plain ilms, tomography, intravenous urography, ultrasound, and unenhanced CT. Sensitivities of 12% to 96% for the ultrasound detection of calculi have been reported. his wide discrepancy is a result of difering deinitions (renal or ureteral), composition, and sizes of calculi.88 Stones greater than 5 mm were detected with 100% sensitivity by ultrasound. Ultrasound with or without plain radiography competes favorably with unenhanced CT in select patients with ureteral colic.89-91 he sensitivity of ultrasound detection of urinary calculi in patients with acute lank pain is 77% to 93%.92-94 he 2016 European Association of Urology guidelines for diagnosis and

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treatment of urolithiasis list ultrasound as the primary diagnostic imaging tool.95 However, noncontrast-enhanced low-dose CT has higher sensitivity (95%) and speciicity (97%) for urolithiasis than does ultrasound.96 hus many centers use low-dose CT, particularly in patients in whom ureteral stones are suspected or patients whose initial screening ultrasound examination is negative or equivocal but clinical suspicion remains elevated. Operator technique clearly impacts the ability of ultrasound to depict renal calculi. On sonography, renal calculi are seen as echogenic foci with sharp, distal acoustic shadowing (Fig. 9.37). Even in favorable locations, however, small urinary tract calculi may be diicult to detect if they have a weak posterior acoustic shadow. he trade-of between tissue penetration and resolution should be considered when selecting probe frequency, with appropriate focal zones applied to maximize signature shadowing. Harmonic imaging should also be routinely used, particularly in obese patients. he application of color Doppler may also improve the detection of small, minimally shadowing calculi.97 Lee et al.98

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demonstrated that most urinary tract stones (83%) show color and power Doppler sonographic twinkling artifacts, although the artifact at least partially depends on stone composition99 (Fig. 9.38). he relevance of this adjunct technique in the screening of patients with potential urinary colic has been questioned, however. In a recent retrospective study, Dillman et al. demonstrated a high (51%) false positive rate for the twinkle artifact when using noncontrast-enhanced CT as a reference standard.100 Several features that mimic renal calculi at ultrasound can result in false positive examination results, including intrarenal gas (see Fig. 9.23), renal artery calciication (Fig. 9.39), calciied sloughed papilla, calciied transitional cell tumor, alkalineencrusted pyelitis, and encrusted ureteral stents. Although the ultrasound evaluation of the secondary manifestation of an obstructing ureteral calculus—collecting system dilatation—is usually straightforward, pitfalls include (1) evaluation before hydronephrosis develops, leading to a false negative result, and (2) mistaking parapelvic cysts and nonobstructive pyelocaliectasis as hydronephrosis.101

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FIG. 9.37 Renal Calculi. Sagittal sonograms. (A) Small, midpole echogenic foci with shadowing representing nonobstructing calculi. (B) Multiple lower-pole and renal pelvic calculi with associated mild hydronephrosis. (C) Large staghorn calculus with severe upper-pole caliectasis (arrowheads).

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FIG. 9.38 Twinkle Artifacts Indicating Renal Calculi. (A) Transverse sonogram and simultaneous Doppler image show shadowing calculi, posterior shadowing, and color Doppler twinkle artifact. (B) A follow-up CT shows the larger calculus. The color Doppler twinkle artifact may sometimes aid in detection of small calculi, although often no corresponding calculi are shown on noncontrast-enhanced CT. The reason for this discrepancy is not clear, although it may be due to relatively large (5-mm) collimation typically used for the CT evaluation of calculi.

FIG. 9.39 Sonographic Feature Mimicking Renal Calculus. Transverse sonogram shows a linear distal renal artery calciication.

Entities That Mimic Renal Calculi Intrarenal gas Renal artery calciication Calciied sloughed papilla Calciied transitional cell tumor Alkaline-encrusted pyelitis Encrusted calciication of ureteric stent

Ureteral Calculi he search for ureteral calculi may be particularly diicult at sonography because of overlying bowel gas and the deep retroperitoneal location of the ureter (Fig. 9.40). However, transvaginal or transperineal scanning aid in detection of distal ureteral calculi that are not seen with a transabdominal suprapubic approach.83,102,103

When the ureter is dilated, the distal 3 cm will be seen as a tubular hypoechoic structure entering the bladder obliquely. A stone will be identiied as an echogenic focus with sharp, distal acoustic shadowing within the ureteric lumen (Fig. 9.41). here may be associated mucosal edema at the bladder trigone. Transabdominal evaluation of the ureteral oriices for jets is helpful to assess for obstruction (Video 9.1).104 At gray-scale ultrasound, a stream of low-level echoes can be seen entering the bladder from the ureteral oriice. he jet is likely shown at ultrasound because of both motion and a density diference between the jet and urine in the bladder.105 Good hydration before the study maximizes the density diference between ureteral and bladder urine and aids in jet visualization.106 In addition to gray-scale evaluation, Doppler ultrasound improves detection of ureteric jets. Color Doppler allows for simultaneous visualization of both ureteral oriices104 (Fig. 9.42). Depending on the state of hydration, jet frequency may vary from less than one per minute to continuous low; however, jets should be symmetric in a healthy individual. Patients with highgrade ureteral obstruction will have either a completely absent jet or a continuous, low-level jet on the symptomatic side. Patients with low-grade obstruction may or may not have asymmetric jets.104 Semiqualitative assessment of relative jet frequency from the afected side107 may improve diagnostic accuracy, but this technique has not been widely adopted. hus centers that evaluate ureteral jets with color Doppler use the technique as an adjunct for assessing ureteric obstruction and the possibility of spontaneous ureteral stone passage. Initial studies suggested that the addition of renal duplex Doppler to the gray-scale ultrasound examination would allow diagnosis of both acute and chronic urinary tract obstruction.108 Several studies indicated that the complex hemodynamics that occur with unrelieved obstruction can be semiquantitatively assessed by measuring intrarenal arterial resistive indices (RI =

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FIG. 9.40 Distal Ureteral Calculi. Sagittal sonograms of the distal ureters in two patients. (A) Calculus is 1 cm from the ureterovesical junction (UVJ), with extensive edema of the distal ureteric mucosa. (B) Tiny calculus at UVJ with no obvious edema. Note posterior acoustic shadowing.

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FIG. 9.41 Ureterovesical Calculus. Transvaginal sonograms in two patients show the value of this technique. (A) Small calculus obstructs a mildly dilated ureter at UVJ. (B) Larger calculus with extensive surrounding ureteric edema.

peak systolic velocity–end diastolic velocity/peak systolic velocity). It is believed that with obstruction, renal pelvic wall tension increases, initially resulting in a short period of prostaglandinmediated vasodilation.109 With prolonged obstruction, many hormones, including renin-angiotensin, kallikrein-kinin, and prostaglandin-thromboxane, reduce vasodilation and produce difuse vasoconstriction. Geavlete et al.110 found that if there was an intravesical ureteric jet on the renal colic side associated with arcuate or intralobar RI values of 0.7 or less and diference between renal RI values of 0.06 or less, spontaneous passage of the stone occurred in 71% of cases. Platt et al.108 used a threshold RI greater than 0.70 to indicate obstruction, noting a diference in RI of

0.08 to 0.1 when comparing the patients’ obstructed and nonobstructed kidneys. Initial reports advocating the Doppler assessment of renal obstructive physiology were tempered by a series of less promising studies.101,109 he RI is largely dependent on tissue/vascular compliance (diminished compliance results in elevated RI, and vice versa) and driving pulse pressures, and thus is not uniformly afected by obstruction.111-114

Bladder Calculi Bladder calculi most oten result from either stone migration from the kidney or bladder stasis. Urinary stasis is usually related to a bladder outlet obstruction, cystocele, neurogenic bladder,

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FIG. 9.42 Color Doppler Evaluation of Ureteral Colic. Transverse images of the bladder in two patients. (A) Normal symmetrical bilateral ureteral jets. (B) Persistent left ureteral jet distal to a partially obstructing left UVJ calculus. Note twinkle artifact posterior to ureteral calculus.

Nephrocalcinosis

FIG. 9.43 Bladder Calculus. Sagittal sonogram shows a small dependent echogenic focus with posterior sharp acoustic shadowing. Note bladder wall trabeculation.

or a foreign body in the bladder. Bladder calculi may be asymptomatic. If symptomatic, patients will complain of bladder pain or foul-smelling urine with or without hematuria. At sonography, a mobile, echogenic mass with distal acoustic shadowing will be seen (Fig. 9.43). If the stone is large, edema of the ureteral oriices and thickening of the bladder wall may be visualized. Occasionally, stones can adhere to the bladder wall because of adjacent inlammation; these calculi are known as “hanging” bladder stones.

Nephrocalcinosis refers to renal parenchymal calciication. he calciication may be dystrophic or metastatic. With dystrophic calciication, there is deposition of calcium in devitalized (ischemic or necrotic) tissue.115 his type of parenchymal calciication occurs in tumors, abscesses, and hematomas. Metastatic nephrocalcinosis occurs most oten with hypercalcemic states caused by hyperparathyroidism, renal tubular acidosis, and renal failure. Metastatic nephrocalcinosis can be further categorized by the location of calcium deposition as cortical or medullary. Causes of cortical nephrocalcinosis include acute cortical necrosis, chronic glomerulonephritis, chronic hypercalcemic states, ethylene glycol poisoning, sickle cell disease, and renal transplant rejection. Causes of medullary nephrocalcinosis include hyperparathyroidism (40%), renal tubular acidosis (20%), medullary sponge kidney, bone metastases, chronic pyelonephritis, Cushing syndrome, hyperthyroidism, malignancy, renal papillary necrosis, sarcoidosis, sickle cell disease, vitamin D excess, and Wilson disease.115 he Anderson-Carr-Randall theory of stone progression postulates that the concentration of calcium is high in the luid around the renal tubules. he calcium is removed by lymphatics, and if the amount exceeds lymphatic capacity, deposits of calcium in the fornical tips and margins of the medulla will result. he ultrasound manifestation of early medullary calciication are nonshadowing echogenic rims surrounding medullary pyramids.116 However, increased medullary echogenicity can also be caused by medullary sponge kidney117 (Fig. 9.44); it can be a normal transient inding in neonates.118 Further calcium deposition results in acoustic shadowing (Fig. 9.45). he calciications may perforate the calix and form a nidus for further stone growth.119 Although the physiology of cortical nephrocalcinosis difers from that of medullary nephrocalcinosis, its ultrasound

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manifestations are similar; early cortical calciication may be suggested by increased cortical echogenicity. With progressive calciication, a continuous, shadowing calciied rim develops.

GENITOURINARY TUMORS Renal Cell Carcinoma Renal cell carcinoma (RCC) accounts for approximately 3% of all adult malignancies and 86% of all primary malignant renal parenchymal tumors.120 here is a 2 : 1 male predominance, and peak age is 50 to 70 years. he cause is unknown, although weak associations with smoking,121 chemical exposure, asbestosis, obesity, and hypertension have been shown. he vast majority of RCCs are sporadic, but an estimated 4% occur in the context of inherited syndromes.122,123 hese “inherited” RCCs occur at an earlier age, are multifocal and bilateral, and afect

FIG. 9.44 Medullary Sponge Kidney. Sagittal sonogram shows markedly increased renal medullary echogenicity (“medullary rings”).

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men and women equally.122 Von Hippel–Lindau (VHL) disease is the best known inherited RCC syndrome; 24% to 45% of patients who have VHL disease will develop RCC. Most of these lesions are multicentric and bilateral and are clear cell carcinomas.124-126 Other inherited renal cancer syndromes include hereditary papillary renal cancer, Birt-Hogg-Dubé syndrome, hereditary leiomyoma RCC, familial renal oncocytoma, hereditary nonpolyposis colon cancer, and medullary RCC. An increased incidence of RCC in patients with tuberous sclerosis has also been reported.123 Another important but nonsyndromic risk factor for RCC is the acquired cystic kidney disease that occurs in patients receiving long-term hemodialysis or peritoneal dialysis. he RCCs in these patients are small and hypovascular and tend to be relatively less aggressive.127,128 Histologic subtypes of RCC include clear cell (70%-75%), papillary (15%), chromophobe (5%), oncocytic (2%-3%), and collecting duct or medullary (12 cm in diameter) and contain numerous large, thin-walled cysts, which may replace most of the ovary. he associated ascites and pleural efusions may lead to depletion of intravascular luids and electrolytes, resulting in hemoconcentration with hypotension, oliguria, and electrolyte imbalance.46 Severe OHS is usually treated conservatively to correct the depleted intravascular volume and electrolyte imbalance and usually resolves within 2 to 3 weeks. heca lutein cysts are the largest of the functional ovarian cysts and are associated with high hCG levels. hese cysts typically occur in patients with gestational trophoblastic disease. However, theca lutein cysts are typically not seen in irst-trimester

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diagnosis of gestational trophoblastic disease, because the hCG level will not have been suiciently high for a long enough time for them to develop.47 heca lutein cysts can also be seen in OHS as a complication of drug therapy for infertility. Sonographically, theca lutein cysts are usually bilateral, multilocular, and very large. hey may undergo hemorrhage, rupture, and torsion. Hyperreactio luteinalis is caused by an abnormal response to circulating hCG in the absence of ovulation induction therapy. Approximately 60% of hyperreactio luteinalis cases occur in singleton pregnancies with normal circulating levels of hCG. Hyperreactio luteinalis usually occurs in the third trimester or less oten in the puerperium. he majority of patients are asymptomatic, although maternal virilization may be seen in up to 25% of patients. he incidence of hyperreactio luteinalis increases in women with polycystic ovarian disease.48 In contrast to OHS, body luid shits are rare. Sonographically, there are bilaterally enlarged ovaries with multiple cysts similar to OHS, although the ovaries tend not to be as large and the condition occurs later in pregnancy. Hyperreactio luteinalis is a self-limited condition that resolves spontaneously. Luteoma of pregnancy is the only solid mass in this group of pregnancy-related processes. It is a rare benign process unique to pregnancy that is due to stromal cells that may become hormonally active, producing androgens and replacing the normal ovarian parenchyma. Most patients are asymptomatic, although maternal virilization may occur in up to 30%. hese patients have a 50% risk of virilization of the female fetus.49 Sonographically, luteomas usually present as nonspeciic, heterogeneous, predominantly hypoechoic masses that may be highly vascular. An ovarian mass in a pregnant patient with signs of virilization should suggest this diagnosis, because luteoma is the most common cause of maternal virilization during pregnancy. Surgery is not indicated since the condition resolves spontaneously, typically ater delivery.

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FIG. 16.8 Ovarian Hyperstimulation Syndrome. (A) TVS shows a greatly enlarged ovary with multiple cysts, some hemorrhagic. (B) Sagittal sonogram in right upper quadrant shows large volume of free intraperitoneal luid.

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Surface Epithelial Inclusion Cysts Surface epithelial inclusion cysts are nonfunctional cysts usually seen in postmenopausal women, although they may be seen at any age, and are usually located peripherally in the cortex. hey arise from cortical invaginations of the ovarian surface epithelium.50 When very small, the cysts themselves may not be seen, but rather they may appear as punctate echogenicities in the surface of the ovary. Although usually tiny, unilocular, and thin walled, these cysts can measure up to several centimeters in diameter. Occasionally, surface epithelial inclusion cysts may be hemorrhagic, particularly if torsion has occurred.

Paraovarian and Paratubal Cysts Paraovarian and paratubal cysts are wolian or müllerian duct remnants in the mesosalpinx, oten located superior to the uterine fundus. hey are generally epithelium-lined simple cysts, rarely multiloculated or containing small wall nodularities. Echoes may also be occasionally seen with the cyst sonographically because of hemorrhage. hey show no cyclic changes. here is an estimated incidence of 3%, accounting for about 10% to 20% of all adnexal masses. Typically, these cysts are small but may range in size up to 8 cm. hey may occur at any age but are most commonly visualized in the third and fourth decades. Most are asymptomatic although patients with large cysts may have pelvic pain or the cysts may act as a fulcrum for torsion.51-53 A speciic diagnosis of a paraovarian cyst is possible only by demonstrating a normal ipsilateral ovary adjacent to, but separate from, the cyst.54,55 Benign neoplasms such as cystadenomas and cystadenoibromas of paraovarian origin are uncommon. Malignancy has been reported in 2% to 3% of parovarian cystic masses on histopathologic examination,56,57 although it occurs even less oten in masses smaller than 5 cm.54,58

Peritoneal Inclusion Cysts Peritoneal inclusion cysts are seen in patients with peritoneal adhesions, occurring mostly in premenopausal women with a history of previous abdominal surgery, but they may also be seen in patients with a history of trauma, PID, or endometriosis. In patients with peritoneal adhesions, luid produced by the ovary (which is the main producer of peritoneal luid in women13) may accumulate within the adhesions and entrap the ovaries, resulting in an adnexal mass.59-62 Peritoneal inclusion cysts are lined with mesothelial cells. Clinically, most patients present with pain and/or a pelvic mass. On sonography, peritoneal inclusion cysts are multiloculated cystic adnexal masses, oten with a bizarre shape frequently described as a spider web pattern63 (Fig. 16.9). he diagnostic inding is the presence of an intact ovary positioned eccentrically amid septations and luid.60-62 he septations represent mesothelial and ibrous strands. he luid is usually anechoic but may contain echoes in some compartments as a result of hemorrhage or proteinaceous luid. Doppler evaluation may demonstrate vascularity within septations, at times mimicking a malignancy. Peritoneal inclusion cysts must be diferentiated from other extraovarian conditions such as parovarian cysts and a hydrosalpinx. Paraovarian cysts are separate from the ovary, whereas

FIG. 16.9 Peritoneal Inclusion Cyst. TVS image shows a multilocular cyst with linear septations attached to the right ovary that projects within the structure and contains a hemorrhagic cyst. This represents adhesions attached to the right ovary.

the ovary lies inside a peritoneal inclusion cyst. Parovarian cysts are usually round or ovoid and not associated with a history of pelvic surgery, trauma, or inlammation. A hydrosalpinx appears as a tubular or ovoid cystic structure oten with visible folds, and the ovary is demonstrated as a separate entity. Accurate diagnosis of peritoneal inclusion cysts is important because the risk of recurrence ater surgical resection is 30% to 50%.64 Conservative therapy, such as ovarian suppression with oral contraceptives or luid aspiration, is recommended.62

Polycystic Ovarian Syndrome Polycystic ovarian syndrome (PCOS) is now known to be a multifaceted endocrinologic disorder of ovarian dysfunction that includes abnormal estrogen and/or androgen production resulting in chronic anovulation and hyperandrogenism. Pathologically, the ovaries contain an increased number of follicles in various stages of maturation and atresia, and increased local concentration of androgens produces stromal abnormality. PCOS is a common cause of infertility and a higher-than-usual rate of early pregnancy loss.65,66 Clinical manifestations of PCOS range from mild signs of hyperandrogenism in thin, normally menstruating women to the classic Stein-Leventhal syndrome (oligomenorrhea or amenorrhea, hirsutism, and obesity). he typical sonographic indings of PCOS are bilaterally enlarged ovaries containing multiple small, 2- to 9-mm follicles and increased stromal echogenicity (Fig. 16.10). he ovaries have a rounded shape, with the follicles usually located peripherally (“string of pearls”), although they can also occur randomly throughout the ovarian parenchyma. Because of its superior resolution, TVS is more sensitive than TAS in detecting the small follicles. However, many women with PCOS will not have these typical sonographic indings. Ovarian volume may be normal in 30% of patients.67,68 Using TVS, increased stromal echogenicity has also been reported as a sensitive and speciic sign of polycystic ovaries.69,70 In a small number of patients, the sonographic indings may be unilateral.66,71

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FIG. 16.10 Polycystic Ovaries: Typical Appearance on TVS in Woman With Hirsutism and Oligomenorrhea. (A) and (B) Enlarged ovaries (cursors) with mildly increased stromal echogenicity and multiple peripheral follicles, “string of pearls” sign.

A 2003 consensus meeting of the American Society for Reproductive Medicine and European Society of Human Reproduction and Embryology deined PCOS as requiring two of three criteria: (1) oligo-ovulation and/or anovulation, (2) hyperandrogenism (clinical and/or biochemical), and (3) polycystic ovaries.72 An elevated serum luteinizing hormone (LH) level and insulin resistance have also been characteristic features. Historically, an elevated serum LH level and elevated LH/FSH ratio had been used as diagnostic tools. However, based on data that include the variability of LH depending on proximity to ovulation and its questionable importance in management, recommendations no longer support its necessity for clinical diagnosis.73 According to decisions made at the 2003 Rotterdam consensus workshop, the sonographic indings of polycystic ovaries should include either 12 or more follicles within the entire ovary measuring 2 to 9 mm in diameter72 or increased ovarian volume greater than 10 mL. Although increased stromal echogenicity has been considered speciic for polycystic ovaries, because of its subjective nature it was not included in the criteria. he consensus makers thought that measurement of ovarian volume worked as well as stromal evaluation in clinical practice. hese criteria are not considered valid if the patient is taking oral contraceptives or has a dominant follicle greater than 10 mm. More recently, it has been reported that with the use of newer, higher resolution ultrasound technology and an oline reliable grid system to count follicles, a signiicantly higher follicle count threshold within the entire ovary is necessary to support the diagnosis of PCOS. Lujan et al.74 advocated the use of a count of 26 and Christ et al.75 a count of 28 follicles measuring 2 to 9 mm within the entire ovary as a better predictor of PCOS. Because anovulation plays a key role in this disorder, the follicles will persist on serial studies. Long-term follow-up is recommended in patients with PCOS because the resulting high-unopposed estrogen levels can be associated with an increased risk of endometrial and breast carcinoma.

Endometriosis Endometriosis is considered the most common benign gynecologic disorder. It is estimated that endometriosis afects between 5% and 45% of women in the reproductive age group, causes signiicant morbidity, and represents a major public health concern.76,77 Clinical symptoms include pelvic pain, dysmenorrhea, dyspareunia, dyschezia, urinary symptoms, and infertility.78 he process is deined as the presence of functioning endometrial tissue outside the uterus. Endometriosis may present in diferent forms that include adnexal cysts (endometriomas), peritoneal plaques and adhesions, and deep iniltrating endometriosis consisting of implants or nodules that contain glands and stroma. Besides the ovary, the most commonly involved areas in the pelvis are the fallopian tube, broad ligament, and posterior cul-de-sac, but endometriosis can occur almost anywhere in the body, including the bladder and bowel. he correct diagnosis and evaluation of the extent of disease are key in determining the best treatment approach. Ultrasound is well accepted as the initial imaging modality of choice, whereas MRI is considered the problem-solving tool. he most common manifestation of endometriotic tissue is the endometrioma, which is readily diagnosed by its appearance sonographically with difuse homogenous low level internal echoes. Endometriomas, oten referred to as chocolate cysts, are frequently multiple, with a variety of appearances, from an anechoic cyst to a solid-appearing mass caused by the degradation of blood products over time.79 he characteristic sonographic appearance is that of a well-deined, unilocular or multilocular, predominantly cystic mass containing difuse, homogeneous, low-level internal echoes (Fig. 16.11, Video 16.3).80 Color Doppler typically shows little if any vascularity within cyst walls (as opposed to the corpus luteum, which typically has pronounced low). he low-level internal echoes may be seen difusely throughout the mass or in the dependent portion. Occasionally, a luid-luid level may be seen, particularly if the woman has been lying in a similar position for suicient time for the blood

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FIG. 16.11 Endometriosis: Spectrum of Appearances. TVS images. (A)-(D) Uniform low-level echoes within a cystic ovarian mass. (A) Typical peripheral echogenic foci. (B) Fluid-luid level. (C) Avascular marginal echogenic nodules. (D) Bilateral disease. (E) Deep penetrating implant on posterior surface of uterus (arrows). (F) Filling the pouch of Douglas (arrows). U, Uterus. See also Videos 16.3, 16.4, and 16.5.

products to settle into layers. In a retrospective study, Patel et al.81 found difuse, low-level internal echoes in 95% of endometriomas. hey concluded that this inding in the absence of neoplastic features is highly likely to be an endometrioma, especially if multilocularity or hyperechoic wall foci are present, whereas an endometrioma is highly unlikely when no component of the mass contains low-level echoes. A prospective study by Dogan et al.82 found a positive predictive value of 97% for typically appearing endometriomas with low-level internal echoes, regular margins, round shape, and thick walls. Diferentiation of endometriosis from benign and malignant neoplasms is occasionally required. Papillary wall projections have been frequently described. Patel et al. demonstrated small, linear, hyperechoic foci sometimes present in the wall of the cyst that were thought to represent cholesterol deposits accumulating in the cyst wall.81 Guerriero et al.83 described papillations projecting within the cyst with a height of greater than 3 mm and no internal Doppler low that were felt to represent adjacent ibrin or blood products (Video 16.4). In rare cases in pregnant women, decidualization of the wall of an endometrioma may occur, resulting in a solid vascular mural mass that cannot be diferentiated from malignancy84,85 (Fig. 16.12). Calciication is occasionally present in an endometrioma and can be confused with a dermoid.86 Endometriomas may serve as precursors of borderline endometrioid and clear cell tumors that may eventually become low-grade invasive carcinoma and therefore, if not surgically removed, these are followed yearly.50,87

Endometriomas may be present in postmenopausal women, although their appearance generally difers. Instead of the unilocular cyst containing low-level echoes, the postmenopausal endometrioma more oten has the appearance of a multilocular mass. When cyst luid is present, it is more frequently anechoic or comprised of a more heterogeneous echogenicity.88 he appearance of an endometrioma may be similar to a hemorrhagic ovarian cyst because both are cystic masses that contain blood products of variable age. However, a hemorrhagic cyst more frequently demonstrates a reticular internal pattern rather than the pattern of homogeneous low-level echoes and is more frequently associated with free luid in the cul-de-sac. A hemorrhagic cyst will resolve or show a signiicant decrease in size over the next few menstrual cycles, whereas endometriomas tend to show little change in size and internal echo pattern. Clinically, most women with a symptomatic hemorrhagic cyst present with acute pelvic pain, whereas women with an endometrioma have more chronic discomfort associated with their menses. Endometriosis is frequently accompanied by the presence of pelvic adhesions. he evaluation of adhesions of the uterus and ovaries as well as obliteration of the pouch of Douglas can be challenging with ultrasound although techniques have been reported that can be performed successfully by experienced operators.89,90 Movement of the normally mobile uterus and ovaries by abdominal palpation or pressure with the abdominal probe can show adherence of these structures to the adjacent

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FIG. 16.12 Decidualization of Endometrioma in Pregnancy. (A) and (B) Sagittal gray-scale and color Doppler TVS images of a cyst containing low-level echoes and a peripheral echogenic nodule. The nodule demonstrates color Doppler low, a inding seen in a borderline neoplasm or a decidualized endometrioma in a pregnant patient.

broad ligament, pouch of Douglas, bladder, rectum, or peritoneum. he use of the sliding sign on TVS has been described to diagnose the obliteration of the pouch of Douglas.91,92 his procedure entails the placement of gentle pressure against the cervix with the TVS probe to determine if the posterior cervix slides easily along the anterior rectal and vaginal wall. Additionally, if luid is present within the pelvis, ine linear structures representing adhesions may be seen joining the ovary with attached endometrioma, uterus and cul-de-sac peritoneum. Deep iniltrating endometriosis is the most severe form of the disease although the extent of disease based laparoscopic staging may not correlate with the severity of symptoms.78 Variable accuracy of TVS in the identiication of deep iniltrating endometriosis has been reported. Most implants are found in dependent areas of the pelvis that is divided into the anterior and posterior compartment according to the deep iniltrating endometriosis classiication by Chapron et al.93 he anterior compartment is composed of the urinary bladder, and the posterior compartment includes the cul-de-sac, the uterosacral ligament, bowel wall, rectum and recto-sigmoid junction, vagina, and rectovaginal septum. Sonographically, implants appear as hypoechoic nodules or as difuse or nodular retroperitoneal thickening. Within the bowel wall, the lesion oten takes on the appearance of a fusiform swelling (Fig. 16.11E and F, Video 16.5). Few, if any, vessels are apparent using color Doppler evaluation.94-97

Adnexal Torsion Adnexal torsion is a relatively infrequent gynecologic emergency requiring prompt surgical intervention with a reported incidence of 3% in some series. he process primarily afects women of reproductive age or younger and is uncommon in the postmenopausal age group.98,99 Initially, there is twisting of the ovary, the fallopian tube, or both structures, causing venous and lymphatic compromise with resulting ovarian edema and adnexal enlargement. However, until venous and arterial thrombosis has occurred, reperfusion may permit complete recovery. Complete and unalleviated torsion can progress rapidly from interference with

venous and lymphatic drainage to arterial occlusion and eventually necrosis. Torsion may be partial or complete, and acute or chronic. Not infrequently, torsion may be intermittent with periods of spontaneous remission of symptoms. he diagnosis of torsion is complicated by its vague clinical presentation. he most consistent presenting symptom is abdominal and pelvic pain, with other nonspeciic signs and symptoms such as fever and nausea and vomiting more variably present. Early diagnosis and intervention prior to infarction permit ovarian preservation and prevent peritonitis. Because the only consistent symptom cited in most studies is abdominal pain, usually intense and progressive, and localized to a lower quadrant, diferential considerations include other gynecologic causes such as PID, ovarian cysts, and ectopic pregnancy as well as nongynecologic causes. Although oten diicult to palpate, a demonstrable mass may be present. A right-sided predominance also exists that is attributed to the protective presence of the sigmoid colon on the let and the hypermobility of the right-sided cecum. As a result, the presentation of ovarian torsion may mimic that of appendicitis.100,101 Most cases of ovarian torsion (50%-80%) are associated with adnexal pathologic conditions such as ovarian tumors or cysts. his usually involves an ipsilateral ovarian mass 5 to 10 cm in diameter that acts as a fulcrum to potentiate torsion due to increased ovarian volume or weight within adnexal structures. Although associated with a neoplasm in as many as 50% of cases, previous studies have indicated that the lesions are usually benign since the inlammatory and invasive changes caused by malignant lesions may be protective against ovarian mobility.102 It is associated with 1 in 1800 pregnancies, most commonly in the irst trimester or immediately postpartum.103 Women undergoing ovulation induction are at high risk secondary to the development of large theca lutein cysts.100 he initial role of sonography in the evaluation of patients at risk for ovarian torsion is to not only diagnose torsion but also exclude other causes of acute abdominal pain such as appendicitis,

CHAPTER 16 PID, ruptured ovarian cyst, and ectopic pregnancy. he most consistent inding of ovarian torsion is an enlarged edematous ovary (Fig. 16.13) or ovarian complex of ovary and adnexal mass. he location of the ovary is frequently medial and superior to its usual location (Fig. 16.14A).104 If the fallopian tube is involved, a hydrosalpinx will usually be demonstrated. Peripherally placed follicles and homogeneous echoes seen centrally consistent with areas of edema within enlarged ovaries have also been reported,105,106 although these descriptors are nonspeciic (Video 16.6). Entities such as endometriomas, polycystic ovaries, hemorrhagic cysts, tubo-ovarian complexes, and hyperstimulated ovaries undergoing ovulation induction are oten similarly described. he irregular internal texture of the ovary seems to correlate with intraovarian hemorrhage. Free luid within the cul-de-sac is another nonspeciic inding frequently associated with cases of ovarian torsion. he luid may be a transudate from the ovarian capsule secondary to obstruction of veins and lymphatic vessels.107

C

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FIG. 16.13 Ovarian Torsion: Doppler Evaluation of Enlarged Ovaries. TVS color Doppler image of a young woman presenting with acute pelvic pain shows no evidence of color Doppler low within an enlarged ovary containing irregular parenchyma; low is demonstrated distally within the iliac artery. See also Video 16.6.

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FIG. 16.14 Ovarian Torsion With Cyst as Fulcrum. (A) TAS sagittal image of a young woman with acute pain shows a large, simple cyst (C) that lies anterior to the uterus (U) and cephalad to the bladder (B). This unusual position should raise the suspicion of torsion. (B)-(D) Another young female patient who is postpartum presenting with acute pelvic pain. (B) TAS shows a large simple ovarian cyst superior to the uterus. (C) and (D) TAS spectral Doppler images show normal arterial and venous waveforms within the wall of the cyst.

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Doppler indings vary depending on degree of torsion and its chronicity. Lack of arterial and venous Doppler low should enable conident diagnosis although false positive diagnoses may be obtained as a result of the depth of penetration being greater than the capabilities of the ultrasound beam, improper Doppler or gray-scale priority settings, and too high ilter pulse repetition frequency (PRF) settings.108 hus it is helpful to scan the asymptomatic ovary irst to ensure that Doppler settings are appropriate. Conversely, both arterial and venous ovarian spectral Doppler signal has been frequently reported in cases of surgically proven torsion. Absent venous Doppler low has a positive predictive value as high as 94% for ovarian torsion despite persistence of arterial signal.107 Explanations proposed include venous occlusion leading to symptoms before arterial occlusion occurs and that persistent adnexal arterial low is related to the dual-ovarian arterial blood supply (ovarian artery and ovarian branches of uterine artery).109 Occasionally, a twisted vascular pedicle (consisting of broad ligament, fallopian tube, and adnexal and ovarian branches of uterine artery and vein) may be demonstrated as a round hyperechoic structure with multiple concentric hypoechoic stripes (target appearance) or as an ellipsoid or tubular structure with internal heterogeneous echoes.110 Using color or power Doppler ultrasound, the presence of circular or coiled twisted vessels within the vascular pedicle (whirlpool sign) is helpful in diagnosing torsion.110 Absence of blood low within the vascular pedicle suggests a nonviable ovary.110,111 Comparison with the morphologic appearance and low patterns of the contralateral ovary can also be helpful since decreased or abnormal low may be present in the torsed ovary.107,112 Massive edema of the ovary is a rare condition resulting from partial or intermittent torsion of the ovary, causing venous and lymphatic obstruction but not arterial occlusion, leading to marked stromal edema. he few cases described in the literature show a large, edematous multicystic adnexal mass.113-115 he use of duplex and color Doppler imaging is most useful in making the diagnosis in the absence of Doppler low although the presence of Doppler signal cannot eliminate the diagnosis. In the appropriate clinical setting, an enlarged ovary or ovary and adnexal mass complex should suggest torsion even in the presence of ovarian Doppler low112,116 Torsion is extremely unlikely if the ovary is morphologically normal and of normal size regardless of Doppler indings.

NEOPLASMS Ovarian Cancer Ovarian cancer is the ith leading cause of cancer death among US women and causes more deaths than any other cancer of the female reproductive system. he American Cancer Society estimated 21,980 new cases of ovarian cancer in the United States in 2014, with about 14,270 deaths.117 Between 1987 and 2010, the incidence decreased at a rate of 0.9% a year.117,118 Ovarian cancer represents approximately 25% of all gynecologic malignancies, with peak incidence in the sixth decade of life. Ovarian cancer has the highest mortality rate of all gynecologic malignancies, mostly a result of late diagnosis. Because there are few

clinical symptoms, 60% to 70% of women have advanced disease (stages III or IV) at diagnosis. he overall 5-year survival rate is 20% to 30%, but with early detection in stage I, the rate rises to 80% to 90%. herefore eforts have been directed at developing methods of early diagnosis of ovarian cancer. Increasing age, nulliparity, a family history of ovarian cancer, and a patient history of breast, endometrial, or colon cancer are associated with increased risk of ovarian cancer. he lifetime risk of a woman developing ovarian cancer is 1 in 70 (1.4%). However, if a woman has a irst-degree relative (mother, daughter, sister) or second-degree relative (aunt or grandmother) who has had ovarian cancer, the risk is 5%. With two or more relatives who have had ovarian cancer, the lifetime risk increases to 7%.119 About 3% to 5% of women with a family history of ovarian cancer have a hereditary ovarian cancer syndrome. he three main hereditary syndromes associated with ovarian cancer are the breast-ovarian cancer syndrome, the most common, caused by mutations in the suppressor genes BRCA1 and BRCA2, with a high frequency of both cancers; the hereditary nonpolyposis colorectal cancer syndrome (Lynch II), in which ovarian cancer occurs in association with nonpolyposis colorectal cancer or endometrial cancer, or both; and site-speciic ovarian cancer syndrome, the least common, without an excess of breast or colorectal cancer.120 Hereditary ovarian cancer syndromes are thought to have an autosomal dominant inheritance, and the lifetime risk of ovarian cancer in these patients is 40% to 50%. hey have an earlier age of onset (10-15 years earlier) than do other ovarian cancers.120 herefore oophorectomy is commonly advocated ater child-bearing in these women. A number of clinical screening trials of asymptomatic women have been reported using TVS (either alone or in combination with Doppler sonography) and/or biologic markers such as cancer antigen (CA) 125.121-126 CA 125 is a high-molecular-weight glycoprotein recognized by the OC 125 monoclonal antibody. It has proved extremely useful in following the clinical course of patients undergoing chemotherapy and in detecting recurrent subclinical disease.127,128 Although serum CA 125 is elevated in approximately 80% of women with epithelial ovarian cancer, it detects less than 50% of stage I disease and is insensitive to mucinous and germ cell tumors.128 Other malignancies, as well as many benign conditions, are associated with elevated serum CA 125. he use of serum CA 125 and/or sonography as a screening test for ovarian cancer is not currently recommended for routine clinical use.129 Routine screening has resulted in unnecessary surgery with its attendant risks.129 he largest screening trial to date is the United Kingdom Collaborative Trial of Ovarian Cancer Screening (UKCTOCS), a randomized study evaluating annual screening using either TVS or serum CA 125 with TVS as a second-line test (multimodal screening). Preliminary results are encouraging, with superior sensitivity and positive predictive value reported with the multimodal screening strategy compared to TVS alone for detecting primary invasive epithelial ovarian and fallopian tube cancers.130 Histologically, epithelial neoplasms represent 65% to 75% of ovarian tumors and 90% of ovarian malignancies50 (Table 16.1). he remaining neoplasms consist of germ cell tumors (15%-20%), sex cord–stromal tumors (5%-10%), and metastatic

CHAPTER 16

TABLE 16.1 Ovarian Neoplasms Tumor

Incidence

Examples

Surface epithelial– stromal tumors

65%-75%

Germ cell tumors

15%-20%

Sex cord–stromal tumors

5%-10%

Metastatic tumors

5%-10%

Serous cystadenoma/ carcinoma Mucinous cystadenoma/ carcinoma Endometrioid carcinoma Clear cell carcinoma Transitional cell tumor Teratoma Dysgerminoma Yolk sac tumor Granulosa cell tumor Sertoli-Leydig cell tumor Thecoma and ibroma Uterus Stomach, colon, breast Lymphoma

tumors (5%-10%). Sonographically, ovarian cancer usually presents as an adnexal mass. Well-deined anechoic cysts are more likely to be benign, whereas lesions with irregular walls, thick irregular septations, mural nodules, and solid elements with low are more likely to be malignant.131,132 Many scoring systems and mathematical models based on the morphologic characteristics have been proposed for distinguishing between benign and malignant masses. However, subjective evaluation of the ultrasound morphologic features (pattern recognition) by an experienced interpreting physician has been shown to be the superior method.133,134 Using this method, a physician should be able to distinguish benign from malignant masses in approximately 90% of cases.135 Color and pulsed Doppler sonography have been advocated for distinguishing benign from malignant ovarian masses. Support is based on the premise that malignant masses, because of internal neovascularization, will have high diastolic low. Malignant tumor growth depends on angiogenesis, with the development of abnormal tumor vessels.136 hese abnormal vessels lack smooth muscle within their walls, which, along with arteriovenous shunting, leads to decreased vascular resistance and thus higher diastolic low velocity. herefore the pulsatility index (PI) and resistive index (RI) should be lower in malignant lesions. Although many reports have found a tendency for both PI and RI to be lower in malignant lesions, there is too much overlap to diferentiate reliably between benign and malignant lesions in individual patients.137-142 Other parameters such as vessel location have been suggested to improve the speciicity of Doppler ultrasound assessment of ovarian masses.143 Malignant lesions tend to have more central low, whereas benign lesions tend to have more peripheral low. However, Stein et al.138 found considerable overlap, with 21% of malignant lesions having only peripheral low and 31% of benign lesions having central low. Guerriero et al.144 found a higher accuracy in predicting malignancy when color Doppler ultrasound demonstrated arterial low within the solid portions of the mass.

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Studies comparing the morphologic features on sonography with the Doppler indings found that Doppler ultrasound showed no more diagnostic information than morphologic assessment alone.133,139,140,145 Valentin133 concluded that, in experienced hands, morphologic assessment is the best method for discriminating between benign and malignant masses. he main advantage of adding Doppler ultrasound would be to increase the conidence with which a correct diagnosis is made. Others have found that Doppler ultrasound, when added to sonographic morphologic assessment, improves speciicity and positive predictive value.142,146148 Brown et al.149 found that a nonhyperechoic solid component was the most statistically signiicant predictor of malignancy. Schelling et al.150 also found that a solid component in an adnexal mass with central vascularity achieved high accuracy, sensitivity, and speciicity in predicting malignancy. A meta-analysis of 46 published studies concluded that ultrasound techniques that combine morphologic assessment with color Doppler low imaging is signiicantly better in characterizing ovarian masses than morphologic assessment, color Doppler low imaging, or Doppler indices alone.151 Doppler ultrasound is probably not needed if the mass has a characteristic benign morphology, because morphologic assessment is highly accurate in this group of lesions.138,141 Doppler ultrasound is likely valuable in assessing the mass that is morphologically indeterminate or suggestive of malignancy. Doppler indings should be combined with morphologic assessment, clinical indings, patient age, and phase of menstrual cycle for optimal evaluation of an adnexal mass.152 Recently, contrast-enhanced TVS (CE-TVS) has been used to evaluate ovarian tumor neovascularity. With dynamic CE-TVS, malignant tumor neovascularity usually demonstrates more prolonged contrast washout compared with benign tumors. he diference in contrast enhancement patterns between benign and malignant ovarian masses results in potential improvement in diferentiating benign from malignant lesions with CE-TVS compared with conventional TVS.153

Surface Epithelial–Stromal Tumors In the past, epithelial-stromal tumors were generally considered to arise from the surface epithelium that covers the ovary and the underlying ovarian stroma. It has since been proposed that epithelial ovarian cancer is a collection of diseases arising from varying cells of origin. Evidence suggests that the majority of primary ovarian cancers (in particular, high-grade serous cancers) are derived from the fallopian tube rather than the ovary. A dualistic model that categorizes ovarian cancer into two groups (type I and type II) has been described. Type I tumors usually present at a low stage and include low-grade serous, low-grade endometrioid, clear cell, and mucinous carcinomas. Type II tumors include high-grade serous carcinomas, high-grade endometrioid carcinomas, carcinosarcomas, and undiferentiated carcinomas. Type I tumors tend to be clinically indolent, whereas type II tumors are typically highly aggressive.154,155 Epithelial-stromal tumors can be divided into ive broad categories based on epithelial diferentiation: serous, mucinous, endometrioid, clear cell, and transitional cell (Brenner).50 his group of tumors accounts for 65% to 75% of all ovarian neoplasms and 80% to 90% of all ovarian malignancies. he mode of spread

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of the malignant tumors is primarily intraperitoneal, although direct extension to contiguous structures can occur. Lymphatic spread is predominantly to the paraortic nodes. Hematogenous spread usually occurs late in the course of the disease.

Serous Cystadenoma and Cystadenocarcinoma Serous tumors are the most common surface epithelial–stromal tumors, representing 30% of all ovarian neoplasms. Approximately 50% to 70% of serous tumors are benign. Serous cystadenomas account for about 25% of all benign ovarian neoplasms, and serous cystadenocarcinomas account for about 50% of all malignant ovarian neoplasms.50 he peak incidence of serous cystadenomas is in the fourth and ith decades, whereas serous

cystadenocarcinomas most frequently occur in perimenopausal and postmenopausal women. Approximately 20% of benign serous tumors and 50% of malignant serous tumors are bilateral. heir sizes vary greatly, but in general they are smaller than mucinous tumors. Sonographically, serous cystadenomas are usually large, thin-walled cysts. hey are typically unilocular, but may contain thin septations (Fig. 16.15A and B). Papillary projections are occasionally seen. Serous cystadenocarcinomas may be quite large and usually present as multilocular cystic masses containing multiple papillary projections arising from the cyst walls and septa (Fig. 16.15G-I) he septa and walls may be thick. Echogenic solid material may be seen within the loculations. Papillary

A

B

C

D

E

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10

–15.3 cm/s 60 30 cm/s

G

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–30

FIG. 16.15 Epithelial Ovarian Neoplasms: Spectrum of Appearances. (A) and (B) Serous cystadenomas. (A) Septations within a cystic mass are fairly thin. (B) Septations are thicker. (C) Serous cystadenoma of low malignant potential. Low-level echogenic particles and mural nodules. (D) and (E) Mucinous cystadenomas. (F) Mucinous cystadenocarcinoma. Large size and septations are characteristic; septal nodularity is marked (arrows). (G)-(I) Patient with serous cystadenocarcinoma. Extensive nodularity shows vascularity, conirming the morphologic suspicion of a malignant mass. There is high diastolic low resulting in a low resistive index.

CHAPTER 16

FIG. 16.16 Mucinous Cystadenoma. Gross pathologic specimen shows multiple cystic loculations.

projections may form on the surface of the cyst and surrounding organs, resulting in ixation of the mass. Ascites is frequently seen.

Mucinous Cystadenoma and Cystadenocarcinoma Mucinous tumors are the second most common ovarian epithelial tumor, accounting for 20% to 25% of ovarian neoplasms. Mucinous cystadenomas constitute 20% to 25% of all benign ovarian neoplasms, and mucinous cystadenocarcinomas make up 5% to 10% of all primary malignant ovarian neoplasms.50 Mucinous cystadenomas occur most oten in the third to sixth decades but may be seen in very young women, whereas mucinous cystadenocarcinomas most frequently occur in the fourth to seventh decades. Mucinous tumors are less frequently bilateral than their serous counterparts, with only 5% of the benign and 15% to 20% of the malignant lesions occurring on both sides. A high percentage, 80% to 85%, of mucinous tumors are benign.156 Mucinous cystadenomas can be huge cystic masses, measuring up 30 cm and illing the entire pelvis and abdomen (Figs. 16.15D and E and 16.16). Multiple thin septa are present, and low-level echoes caused by the mucoid material may be seen in the loculations. Papillary projections are less frequently seen than in the serous counterpart. Mucinous cystadenocarcinomas are usually large, multiloculated cystic masses containing papillary projections and echogenic material; they generally have a sonographic appearance similar to that of serous cystadenocarcinomas (Fig. 16.15F). Penetration of the tumor capsule or rupture may lead to intraperitoneal spread of mucin-secreting cells that ill the peritoneal cavity with a gelatinous material. his condition, known as pseudomyxoma peritonei, may be similar sonographically to ascites or may contain multiple septations or loating debris in the luid that ills much of the pelvis and abdomen. his condition may occur in mucinous cystadenomas and in mucinous cystadenocarcinomas. A ruptured mucocele of the appendix and mucinous tumors of the appendix and colon can also lead to pseudomyxoma peritonei. Borderline (Low Malignant Potential) Tumors here is an intermediate group of epithelial tumors that are histologically categorized as “borderline” or of “low malignant

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potential.” hey occur in about 10% to 15% of serous and mucinous tumors. hese tumors have cytologic features of malignancy but do not invade the stroma and, although malignant, have a much better prognosis. hey present at an earlier age than cystadenocarcinomas and have 5-year and 20-year survival of 95% and 80%, respectively. hey may be treated by ovarysparing surgery to preserve fertility. Sonographic features suggestive of low malignant potential tumors are a small- to medium-sized cyst containing low-level echoes (similar to an endometrioma) with vascular mural nodules (Figs. 16.15C) or a cystic mass with a well-deined multilocular (honeycomb) nodule.157,158 Normal ovarian tissue may be seen adjacent to the lesion and may be helpful in excluding invasive ovarian cancer.157,159 his has been referred to as the ovarian crescent sign.159 Although the presence of this sign decreases the likelihood of invasive adnexal malignancy, it was found to be a poor discriminator between benign and malignant adnexal masses in a prospective study by Van Holsbeke et al.160

Endometrioid Tumor Almost all endometrioid tumors are malignant. hey are the second most common epithelial malignancy, representing 20% to 25% of ovarian malignancies; 25% to 30% are bilateral, and they occur most frequently in the ith and sixth decades. heir histologic characteristics are identical to those of endometrial adenocarcinoma, and approximately 30% of patients have associated endometrial adenocarcinoma, which is thought to represent an independent primary tumor. Approximately 15% to 20% of endometrioid cancer is associated with endometriosis, which may occur within the endometriosis, the ipsilateral or contralateral ovary.50 he endometrioid tumor has a better prognosis than other epithelial malignancies, probably related to diagnosis at an earlier stage. Sonographically, it usually presents as a cystic mass containing papillary projections, although some endometrioid tumors are predominantly a solid mass that may contain areas of hemorrhage or necrosis.156 Clear Cell Tumor his tumor is considered to be of müllerian duct origin and a variant of endometrioid carcinoma. Clear cell tumor is almost always malignant and constitutes 5% to 10% of primary ovarian carcinomas. It occurs most frequently in the ith to seventh decades and is bilateral in about 20% of patients. Associated pelvic endometriosis is present in 50% to 70% of clear cell carcinomas, and approximately one-third arise within the lining of endometriomas.50 Sonographically, it usually presents as a nonspeciic, complex, predominantly cystic mass (Fig. 16.17, Video 16.7).156 Transitional Cell Tumor Also known as Brenner tumor, transitional cell tumor is derived from the surface epithelium that undergoes metaplasia to form typical uroepithelial-like components.156 It is uncommon, accounting for 2% to 3% of all ovarian neoplasms, and is almost always benign; 6% to 7% are bilateral. Most patients are asymptomatic, and the tumor is discovered incidentally on sonographic examination or at surgery. About 30% are associated with cystic neoplasms,

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Abdominal and Pelvic Sonography neoplasms, with 95% being benign cystic teratomas (dermoids). he others, including dysgerminomas and endodermal sinus (yolk sac) tumors, occur mainly in children and young adults and are almost always malignant. Germ cell tumors are the most common ovarian malignancies in children and young adults. When a large, predominantly solid ovarian mass is present in a girl or young woman, the diagnosis of a malignant germ cell tumor should be strongly considered163 (Video 16.8).

FIG. 16.17 Clear Cell Carcinoma in Endometrioma. TVS shows a complex cyst with homogenous low-level internal echoes centrally and solid nodules peripherally. See also Video 16.7

C

Cystic Teratoma Cystic teratomas make up approximately 15% to 25% of ovarian neoplasms; 10% to 15% are bilateral. hey are composed of well-diferentiated derivatives of the three germ layers: ectoderm, mesoderm, and endoderm. Because ectodermal elements generally predominate, cystic teratomas are virtually always benign. Cystic teratomas are frequently seen in the reproductive years but can occur at any age and can be seen in postmenopausal women. hese tumors may present as a palpable mass. Cystic teratomas are usually asymptomatic and oten are discovered incidentally during sonography. In approximately 10% of cases, the tumor is diagnosed during pregnancy.50 Torsion is the most common complication, whereas rupture is uncommon, occurring in 1% of patients and causing a secondary chemical peritonitis. Malignant transformation is also uncommon, occurring in 2% of patients, usually older women,50 and is almost exclusively due to squamous cell carcinoma.28 Sonographically, cystic teratomas have a variable appearance ranging from completely anechoic to completely hyperechoic. However, certain features are considered speciic (Fig. 16.19). hese include a predominantly cystic mass with a highly echogenic mural nodule, the dermoid plug.164 he dermoid plug usually contains hair, teeth, or fat and frequently casts an acoustic shadow. In many cases the cystic component is pure sebum (which is liquid at body temperature) rather than simple luid.165 Cystic Teratomas: Sonographic Features

FIG. 16.18 Transitional Cell (Brenner) Tumor in Wall of Mucinous Cystadenoma. TAS shows a large, well-deined cystic mass (C) with a solid hypoechoic mural nodule (arrow). Pathologic examination showed a Brenner tumor within the wall of a large, mucinous cystadenoma.

usually serous or mucinous cystadenomas or cystic teratomas, frequently in the ipsilateral ovary161 (Fig. 16.18). Sonographically, Brenner tumors are hypoechoic solid masses. Calciication may occur in the outer wall. A cystic component is uncommon, but when present, usually results from a coexistent cystadenoma.156,162 Pathologically, transitional cell masses are solid tumors composed of dense ibrous stroma. hey appear similar to ovarian ibromas and thecomas and to uterine leiomyomas, both sonographically and pathologically.

Germ Cell Tumors Germ cell tumors are derived from the primitive germ cells of the embryonic gonad. hey account for 15% to 20% of ovarian

Dermoid plug “Tip of the iceberg” sign Dermoid mesh Mobile spherules (rare) Fat-luid level

A mixture of matted hair and sebum is highly echogenic because of multiple tissue interfaces, and it produces poorly deined acoustic shadowing that obscures the posterior wall of the lesion. his has been termed the “tip of the iceberg” sign166 (Fig. 16.19B). Highly echogenic foci with well-deined acoustic shadowing may arise from other elements, including teeth and bone. Multiple linear hyperechogenic interfaces, oten described as lines and dots, may be seen loating within the cyst and have been shown to be hair ibers.167 his is also considered a speciic sign and has been referred to as the dermoid mesh168 (Fig. 16.19G). A fat-luid or hair-luid level may also be seen (Fig. 16.19D and E). In most cases, as in other lesions such as endometriomas and hemorrhagic cysts, the dependent layer will be more echogenic. However, in approximately 30% of dermoids,

CHAPTER 16

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583

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B

C

D

E

F

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FIG. 16.19 Dermoid Cysts: Spectrum of Appearances. (A) Small, highly echogenic mass in an otherwise normal ovary. (B) Transverse TAS shows the uterus (U). In the right adnexal region, there is a highly echogenic and attenuating mass (arrows), the “tip of the iceberg” sign. (C) Highly echogenic intraovarian mass with no normal ovarian tissue. (D) Mass of varying echogenicity with hair-luid level (straight arrow) and highly echogenic, fat-containing dermoid plug (curved arrow) with shadowing. (E) Mass with fat-luid level (arrow), with dependent layer more echogenic. (F) Mass containing uniform echoes, small cystic area, and calciication (arrows) with shadowing. (G) Combination of dermoid mesh and dermoid plug appearances. (H) Dermoid mesh, multiple linear hyperechogenic interfaces (lines and dots) loating within cystic mass. (I) Multiple mobile spherical echogenic structures loating in a large, cystic pelvic mass.

the nondependent layer will be more echogenic.169 Another rare but characteristic feature is multiple mobile spherical echogenic structures loating in a large, cystic pelvic mass170 (Fig. 16.19I). hese spheres are typically composed of desquamative keratincontaining ibrin, hemosiderin, and hair. Patel et al.171 found that an adnexal mass showing two or more characteristic sonographic dermoid features had a positive predictive value of 100%. Pitfalls in the diagnosis of cystic teratomas have been described.172 Acute hemorrhage into an ovarian

cyst or an endometrioma may be so echogenic that it resembles a dermoid plug. However, posterior sound enhancement is usually seen with acute hemorrhage, whereas the dermoid plug tends to attenuate sound. Other pitfalls include pedunculated ibroids, especially lipoleiomyomas, and perforated appendicitis with an appendicolith. An echogenic dermoid may appear similar to bowel gas and may be overlooked. If a deinite pelvic mass is clinically palpable and the sonogram appears normal, the patient should be reexamined, to carefully assess for a dermoid.

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Doppler evaluation of a benign teratoma may show peripheral low, but malignancy should be considered if low is seen centrally and/or within solid areas. Additional indings suggesting malignancy include isoechoic branching structures within the lesion and invasion into adjacent organs.28 Struma ovarii is a teratoma composed entirely or predominantly of thyroid tissue. It occurs in 2% to 3% of teratomas. Color Doppler sonography detected central blood low in solid tissue in four reported cases of struma ovarii, compared with absent central blood low in benign cystic teratomas.173 his is likely caused by the highly vascularized thyroid tissue in struma ovarii, compared with the avascular fat and hair found in benign cystic teratomas. Although associated hormonal efects are rare, sonography may be valuable in identifying a pelvic lesion in a hyperthyroid patient when there is no evidence of a thyroid lesion in the neck.174 Immature teratoma is uncommon, representing less than 1% of all teratomas, and contains immature tissue from all three germ-cell layers. It is a rapidly growing malignant tumor that most oten occurs in the irst two decades of life. Sonographically,

the tumor usually presents as a solid mass, but cystic structures of varying size may also be seen.163 Calciications are typically present.

Dysgerminoma Dysgerminomas are malignant germ cell tumors that constitute 1% to 2% of primary ovarian neoplasms and 3% to 5% of ovarian malignancies.50 hey are composed of undiferentiated germ cells and are morphologically identical to the male testicular seminoma. Dysgerminomas are highly radiosensitive and have a 5-year survival of 75% to 90%. his tumor occurs predominantly in women younger than 30 years and is bilateral in approximately 15% of cases. Sonographically, they are solid masses that are predominantly echogenic but that may contain small anechoic areas caused by hemorrhage or necrosis163 (Fig. 16.20). CT and MRI have shown these solid masses to be lobulated with ibrovascular septa between the lobules.175 A report using color Doppler ultrasound in three dysgerminomas showed prominent arterial low within the ibrovascular septa of a multilobulated, solid, echogenic mass.176

U

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L U

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FIG. 16.20 Dysgerminomas in Three Young Women. (A) Transverse TAS shows large, solid pelvic mass (M) adjacent to the uterus (U). This appearance could be easily confused with a uterine ibroid. (B) TVS shows large solid ovarian mass with thin linear hyperechoic areas. (C) Transverse TAS shows large bilateral ovarian masses with increased vascularity seen in the right-sided tumor, which extends over the uterus (U). Note also the enlarged left ovary (L) due to tumor. See also Video 16.8.

CHAPTER 16 Yolk Sac Tumor his rare, rapidly growing tumor, also called endodermal sinus tumor, is the second most common malignant ovarian germ cell neoplasm ater dysgerminoma. Yolk sac tumor has a poor prognosis. It is thought to arise from the undiferentiated, multipotential embryonal carcinoma by selective diferentiation toward yolk sac or vitelline structures.50 It usually occurs in females under 20 years of age and is almost always unilateral. Increased levels of serum alpha-fetoprotein may be seen in association with endodermal sinus tumor. he sonographic appearance is similar to that of the dysgerminoma163 (see Video 16.8).

Sex Cord–Stromal Tumors Sex cord–stromal tumors arise from the sex cords of the embryonic gonad and from the ovarian stroma. he main tumors in this group include granulosa cell tumor, Sertoli-Leydig cell tumor (androblastoma), thecoma, and ibroma. his group accounts for 5% to 10% of all ovarian neoplasms and 2% of all ovarian malignancies.

Granulosa Cell Tumor Representing 1% to 2% of ovarian neoplasms, granulosa cell tumor has a low malignant potential. About 95% are of the adult type and occur predominantly in postmenopausal women; almost all are unilateral. Granulosa cell tumors are the most common estrogenically active ovarian tumor,50 and clinical signs of estrogen production can occur, including development of endometrial carcinoma (in 10%-15%). he juvenile type makes up 5% of granulosa cell tumors, occurring mainly in patients younger than 30 years. Granulosa cell tumors have a variable appearance, ranging from small solid masses to tumors with variable degrees of hemorrhage or ibrotic changes, to multilocular cystic lesions.177 Sertoli-Leydig Cell Tumor his rare tumor, also called androblastoma and arrhenoblastoma, constitutes less than 0.5% of ovarian neoplasms. It generally occurs in women younger than 30 years of age; almost all are unilateral. Malignancy occurs in 10% to 20% of these tumors. he malignant tumors tend to recur relatively soon ater initial diagnosis, with few recurrences ater 5 years.178 Clinically, signs and symptoms of virilization occur in about 30% of patients, although about half will have no endocrine manifestations.50 Occasionally, these tumors may be associated with estrogen production. Sonographically, Sertoli-Leydig cell tumors usually appear as solid hypoechoic masses or may be similar in appearance to granulosa cell tumors.178 Thecoma and Fibroma hecoma and ibroma arise from the ovarian stroma and may be diicult to distinguish from each other pathologically. Tumors with an abundance of thecal cells are classiied as thecomas, whereas those with fewer thecal cells and abundant ibrous tissue are classiied as thecoibromas and ibromas. hecomas constitute approximately 1% of all ovarian neoplasms, and 70% occur in postmenopausal females. hey are unilateral, almost always benign, and frequently show clinical signs of estrogen production.

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Fibromas represent about 4% of ovarian neoplasms, are benign, usually unilateral, and occur most oten in perimenopausal and postmenopausal women. Unlike thecomas, ibromas are rarely associated with estrogen production and therefore are frequently asymptomatic, despite reaching a large size. Ascites is present in up to 50% of patients with ibromas larger than 5 cm in diameter.179 Meigs syndrome (associated ascites and pleural efusion) occurs in 1% to 3% of patients with ovarian ibromas but is not speciic, having been reported in association with other ovarian neoplasms as well. Fibromas also occur in approximately 17% of patients with the basal cell nevus (Gorlin) syndrome. In this condition the ibromas are usually bilateral, calciied, and occur in younger women (mean age, 30 years).178 Sonographically, these tumors have a characteristic appearance of a ibrous lesion (Fig. 16.21). A hypoechoic mass with marked posterior attenuation of the sound beam is seen.179 he main diferential diagnosis is a pedunculated uterine ibroid. Not all ibromas and thecomas show this characteristic appearance, and a variety of sonographic appearances have been noted, probably because edema and cystic degeneration tend to occur within these tumors.180

Metastatic Tumors About 5% to 10% of ovarian neoplasms are metastatic in origin. he most common primary sites of ovarian metastases are tumors of the breast and gastrointestinal tract. he term Krukenberg tumor should be reserved for those tumors containing the typical mucin-secreting “signet ring” cells, usually of gastric or colonic origin. Endometrial carcinoma frequently metastasizes to the ovary, but it may be diicult to distinguish from primary endometrioid carcinoma, as discussed earlier. Sonographically, ovarian metastases are usually bilateral solid masses (Fig. 16.22A-C), but they may become necrotic and may have a complex, predominantly cystic appearance that simulates primary cystadenocarcinoma181,182 Testa et al.183 found that almost all ovarian metastases from primary tumors of the breast, stomach, and uterus were solid, whereas those from the colon and rectum were more heterogeneous, most being multicystic with irregular borders. Ascites may be seen in either primary or metastatic tumors. Lymphoma may involve the ovary, usually in a difuse, disseminated form that is frequently bilateral. he sonographic appearance is that of a solid hypoechoic mass similar to lymphoma elsewhere in the body (Fig. 16.22D-F).

FALLOPIAN TUBE With careful TVS examination, a normal fallopian tube may be identiied as an undulating structure measuring less than 10 mm in thickness that extends from the uterine cornu posterolaterally to the ipsilateral ovary. his assessment is not included as part of a routine pelvic sonogram. Identiication becomes easier when the fallopian tube is dilated or surrounded by luid. he contour of the lumen is not seen unless it is obstructed and luid-illed184 (Fig. 16.23). Diagnosis of an asymptomatic hydrosalpinx is important because it allows for what might otherwise be considered to be a concerning adnexal cyst to be ignored rather than followed (Videos 16.9 and 16.10). Developmental

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FIG. 16.21 Ovarian Fibroma. (A) and (B) TVS gray-scale and spectral Doppler images. (A) Hypoechoic mass with some posterior attenuation. (B) Spectral Doppler evaluation of the mass demonstrates internal low conirming a solid mass. (C) Pathologic specimen shows the homogeneous, solid nature of a ibroma. (A and B courtesy of Mindy Horrow MD, Einstein Medical Center.)

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FIG. 16.22 Solid Malignant Adnexal Masses in Two Patients: Metastatic Disease and Lymphoma. (A)-(C) Bilateral solid ovarian masses or Krukenberg tumors in young woman with colon cancer (A and B, right ovary; C, left ovary). (D)-(F) Bilateral predominantly solid masses in young woman with lymphoma (D and E, right ovary; F, left ovary).

CHAPTER 16

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FIG. 16.23 Hydrosalpinx. TVS images show tubular luid-illed structures with sonographic characteristics of the fallopian tube. (A) Incomplete septation related to the folding of the tube (arrows). (B) A waist sign also associated with tubal folds (arrows) and endosalpingeal folds forming surface nodularities. See also Videos 16.9 and 16.10.

abnormalities of the fallopian tube are rare. Abnormalities of the tube include pregnancy, infection, torsion, and neoplasm as well as scarring and obstruction due to other causes.

TABLE 16.2 Sonographic Findings of Pelvic Inlammatory Disease

Pelvic Inlammatory Disease

Endometritis

PID is a common condition that is increasing in frequency. It consists of inlammation of the endometrium, fallopian tubes, pelvic peritoneum, and adjacent structures. Typically, the primary infection is a sexually transmitted disease most oten associated with gonorrhea and chlamydia, although with previous disruption of endometrial and tubal tissue due to prior infection, or postsurgical or postpartum changes, the patient can be infected by her own vaginal lora. he infection typically spreads by ascent from the cervix and endometrium. he disease is manifested by tuboovarian complexes, peritonitis, and abscess formation and is usually bilateral. Long-term sequelae include chronic pelvic pain, infertility, and increased risk of ectopic pregnancy. Less common causes include direct extension from appendiceal, diverticular, or postsurgical abscesses that have ruptured into the pelvis, as well as puerperal and postabortion complications. Hematogenous spread is rare but can occur from tuberculosis. When caused by direct extension of an adjacent inlammatory process, it is most oten unilateral. he presence of an intrauterine device (IUD) increases the risk of PID, although only during a period of a few weeks following its placement. PID may be unilateral in patients with IUDs. Patients usually present clinically with pain, fever, cervical motion tenderness, and vaginal discharge. A pelvic mass may be palpated. TVS with color or power Doppler is highly speciic in the diagnosis of the disease process.185 However, because the success of the technique is dependent on the level of operator expertise and also because early changes can be subtle, TVS usually only detects complications of the disease. he sonographic indings may be normal early in the course of PID.186 Increased echogenicity of peritoneal fat and indistinctness of the uterus may be seen early in the disease process but may be diicult to appreciate. Sonographic indings of the fallopian tubes are the most speciic and conspicuous indicators of PID (Table 16.2).

Purulent material in cul-de-sac Periovarian inlammation Salpingitis

Tubo-ovarian complex Tubo-ovarian abscess

Endometrial thickening Intracavitary luid Fluid containing low-level echoes Enlarged ovaries with multiple cysts and indistinct margins Fluid-illed fallopian tube with (pyosalpinx) or without (hydrosalpinx) internal echoes Increased echogenicity of peritoneal fat Indistinctness of the uterus Fusion of inlamed, luid-distended tube and ovary Multiloculated mass with variable septations, irregular margins, and low-level internal echoes

When imaging a normal appearing fallopian tube, hypervascularity with color Doppler low within the tubal wall is a valuable early inding. As the disease progresses, a spectrum of indings may occur (Fig. 16.24). With inlammation, the tube swells and endosalpingeal folds thicken. With progressive inlammation and distal occlusion of the lumen, the tube ills with purulent echogenic luid, becoming a pyosalpinx. In the presence of a luid-distended fallopian tube, common indings include wall thickness greater than 5 mm, incomplete septa seen as the tube folds back on itself, and thickening of endosalpingeal folds (cogwheel sign).187,188 Color or power Doppler allows for detection of hyperemia in the walls and incomplete septi associated with fallopian tube inlammation (Fig. 16.24B).189 On TAS, dilated tubes appear as complex, predominantly cystic masses that are oten indistinguishable from other adnexal masses. However, TVS allows for depiction of the luid-illed tube with a tubular shape, somewhat

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FIG. 16.24 Progression of Pelvic Inlammatory Disease. (A) TVS gray-scale and (B) color Doppler images show a normal appearing left fallopian tube by gray-scale imaging but markedly increased associated vascularity using color Doppler, consistent with salpingitis. (C) TVS image of a tubo-ovarian complex, a complex mass of fallopian tube and ovary that can still be identiied as separate structures. (D) TVS color Doppler image of a tubo-ovarian abscess, a cystic, vascular mass containing thick septations in which the fallopian tube and ovary are no longer identiiable. See also Video 16.11.

folded coniguration, and well-deined walls.190 he dilated tube can be distinguished from a luid-illed bowel loop by the lack of peristalsis. A luid-pus level may occasionally be seen (Fig. 16.24A). Anechoic luid within the tube indicates hydrosalpinx. In assessing 14 acute and 60 chronic cases of PID, Timor-Tritsch et al.188 described three appearances of tubal wall structure: (1) cogwheel sign, an anechoic cogwheel-shaped structure visible in the cross section of the tube with thick walls, seen mainly in acute disease; (2) “beads on a string” sign, hyperechoic mural nodules measuring 2 to 3 mm on cross section of the luid-illed distended tube, caused by degenerated and lattened endosalpingeal fold remnants and seen only in chronic disease; and (3) incomplete septa, hyperechoic septa that originate as a triangular protrusion from one of the walls, but do not reach the opposite wall, seen frequently in both acute and chronic disease and not discriminatory. Patel et al.191 found that the presence of a tubular luid-illed mass with diametrically opposed indentations in the wall (“waist sign”) had the highest likelihood ratio in discriminating hydrosalpinx from other adnexal masses (Fig. 16.23B).191

Other indings include thick tubal walls and bilateral adnexal masses appearing as small solid masses or thick-walled cystic masses.192 Nonspeciic indings of PID include luid in the endometrial cavity and/or cul-de-sac, and ill-deined ovarian enlargement oten. Endometrial thickening or luid may indicate endometritis. Fluid containing low-level echoes may be demonstrated in the cul-de-sac consistent with purulent material. With progression of disease, there is exudation of pus from the distal fallopian tube, periovarian adhesions may form, with fusion of the inlamed dilated tube and ovary, forming an inlammatory tubo-ovarian complex (Fig. 16.24C, Video 16.11). he ovary is still recognizable but cannot be separated from the tube by applied pressure using the vaginal transducer.186 Further progression results in complete breakdown of tubal and ovarian architecture so that separate structures are no longer identiied and there is obscuration of the posterior and lateral margins of the uterus resulting in a tubo-ovarian abscess (Fig. 16.24D). Sonographically, this appears as a multiloculated mass with incomplete septations, irregular margins, and low-level internal

CHAPTER 16 echoes. here is usually posterior acoustic enhancement, and a luid-debris level or gas may occasionally be seen within the mass. he sonographic appearance may be indistinguishable from other benign and malignant adnexal masses. Clinical correlation is necessary to suggest the correct diagnosis. Regions of identiiable ovarian tissue may be seen within the inlammatory mass by TVS since the ovaries are relatively resistant to infection.3 Both TAS and TVS are useful in making the initial diagnosis in patients with PID and determining management. he TAS approach is helpful in assessing the extent of the disease, whereas the TVS approach is more sensitive in detecting dilated tubes, periovarian inlammatory change, and the internal characteristics of tubo-ovarian abscesses.186,193 However, because of cervical motion tenderness, it may be quite diicult to perform a good quality TVS examination. Although the use of outpatient antibiotic therapy has become the standard of care for mild to moderate cases of PID, according to guidelines from the Centers for Disease Control and Prevention,185 hospitalization for intravenous antibiotic therapy would be prompted by the presence of a tubo-ovarian abscess. By making this diagnosis, TVS is pivotal in determining management. Sonography is also used to follow the disease process following antibiotic therapy. If antibiotic therapy fails, sonographically guided drainage of tubo-ovarian abscesses in combination with antibiotics has been shown to be highly successful.194 his initial approach allows for decreased need for surgical intervention.

Tubal Torsion Tubal torsion is usually seen in conjunction with ovarian torsion, but isolated torsion of the fallopian tube is an infrequent inding. his may be seen in cases of paratubal cysts but also can be seen in association with chronic hydrosalpinx.195 he patient usually presents with sudden onset of severe pelvic pain. Hydrosalpinx and tubal torsion have also been reported as late complications in patients who have undergone tubal ligation.196

Fallopian Tube Carcinoma he fallopian tube is now thought to be the location for the initial development of high-grade serous cystadenocarcinomas.

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hus whereas fallopian tube cancer used to be considered a rare inding, it is now managed similarly to ovarian cancer. Serous tubal intraepithelial carcinoma, a lesion too small to visualize using imaging modalities, represents the acknowledged precursor of these neoplasms.154 A minority of patients have a profuse watery discharge, known as hydrops tubae proluens. he tumor usually involves the distal end, but it may involve the entire length of the tube. Sonographically, carcinoma of the fallopian tube has been described as a sausage-shaped, solid, or cystic mass with papillary projections.197-200 Patlas et al.201 stated that this diagnosis should be considered when a solid vascular mass corresponding to the expected location of the fallopian tube is seen in association with normal ovaries, especially if the mass is mobile.201

VASCULAR ABNORMALITIES IN THE ADNEXA Ovarian Vein Thrombosis or Thrombophlebitis Ovarian vein thrombosis or thrombophlebitis is an uncommon condition that is usually seen 48 to 96 hours postpartum (Fig. 16.25). Symptoms include fever, lower abdominal pain, and a palpable mass. he underlying cause is venous stasis and spread of bacterial infection from endometritis. he right ovarian vein is involved in 90% of cases. Retrograde venous low occurs in the let ovarian vein during the puerperium, which protects this side from bacterial spread from the uterus.50 he condition may be diagnosed by sonography although CT and MRI usually perform better in this diagnosis.202,203 Sonography may demonstrate an inlammatory mass lateral to the uterus and anterior to the psoas muscle. he ovarian vein may be seen as a tubular structure directed cephalad from the mass and containing echogenic thrombus. he thrombus usually afects the most cephalic portion of the right ovarian vein and can be demonstrated sonographically at the junction of the right ovarian vein with the inferior vena cava, sometimes extending into the inferior vena cava.204 Doppler ultrasound will demonstrate complete or

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FIG. 16.25 Ovarian Vein Thrombophlebitis. (A) Transverse gray-scale and (B) color Doppler images of the right ovarian vein containing echogenic material representing thrombus. Color Doppler image shows Doppler signal surrounding the thrombus.

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FIG. 16.26 Pelvic Congestion Syndrome. Transverse TVS images, (A) without and (B) with color Doppler, of the left adnexa demonstrating multiple large vascular structures consistent with varices.

partial absence of low in these veins.205 Most patients respond to anticoagulant and antibiotic therapy, and follow-up sonography may show resolution of the thrombus and normal low by duplex and color Doppler imaging.

Pelvic Congestion Syndrome Pelvic congestion syndrome is a condition that consists of dilatation of pelvic veins (pelvic varices) and reduced venous return causing dull chronic pain that is exacerbated by prolonged standing and relieved by lying down and elevating the legs. Although venography remains the reference standard for diagnosis, sonography can demonstrate an ovarian vein diameter of greater than 5 to 10 mm with relux, uterine vein engorgement, congestion of ovarian plexuses (tortuous and dilated pelvic venous plexuses in the adnexa with individual varices measuring greater than 5 mm in diameter, Fig. 16.26), illing of the pelvic veins across the midline, or illing of vulvovaginal and thigh varicosities.206 Dilated arcuate veins may also be seen crossing the myometrium. Spectral Doppler evaluation of ovarian veins may demonstrate reversed caudal low.

SONOGRAPHIC EVALUATION OF AN ADNEXAL MASS IN ADULT WOMEN Sonography in the setting of certain clinical features is oten used to evaluate an ovarian/adnexal mass. Clinical features to be considered when evaluating an adnexal mass include symptoms, patient age, menstrual status, and family history. Comparison with previous examinations, if available, is oten critical and may save the patient a surgical intervention, since many of these masses are hormonally driven and will resolve. A prior study will also demonstrate if there has been any change in size or internal characteristics. When a mass is found by sonography, it should be characterized by the following: • Location (intraovarian or extraovarian) • Size

• External contour (thin or thick walled and regularity of borders) • Internal consistency (cystic unilocular or multilocular with or without solid components, predominantly solid, or solid) Generally, ovarian masses are predominantly cystic, whereas uterine masses are usually solid tumors, benign leiomyomas. Even solid adnexal masses are usually exophytic or interligamentous leiomyomas. Demonstrating a uterine origin by grayscale and color Doppler is diagnostic and excludes a solid ovarian tumor. Occasionally, it may be diicult to determine the exact origin of the mass by sonography in which case MRI may be a problem-solving tool. In 2010 the Society of Radiologists in Ultrasound published results of a consensus conference regarding the reporting and follow-up needed for asymptomatic adnexal cysts (Table 16.3). Use of these guidelines allows for decreased need for follow-up of benign adnexal cysts.207,208 he vast majority of ovarian masses are functional in nature. Ovarian masses that are simple cysts are almost always benign. In premenopausal asymptomatic women, simple cysts or typical hemorrhagic cysts less than 5 cm can be considered functional. he simple adnexal cyst less than or equal to 1 cm in a postmenopausal woman is also very likely benign. hese indings should be considered of no clinical signiicance in asymptomatic women and do not require follow-up. Simple cysts greater than 5 cm in premenopausal women are also likely functional, but resolution should be conirmed with a follow-up examination. In postmenopausal women, simple cysts greater than 1 cm are most oten benign cystadenomas or hydrosalpinges or paraovarian/paratubal cysts that demonstrate no signiicant malignant potential. Cysts that are greater than 7 cm cannot be adequately evaluated sonographically for mural nodules, so MRI or surgical evaluation is recommended.28 Larger masses, especially those greater than 10 cm, and those with solid components have a higher incidence of malignancy. Solid ovarian masses that are not classic for ibromas are typically surgically removed because of association with malignancy. Cystic

CHAPTER 16

TABLE 16.3 Society of Radiologists in Ultrasound Recommendations for Follow-Up of Asymptomatic Adnexal Cysts Patient Population

Description in Report

Recommended Follow-Up

Premenopausal women

Simple or hemorrhagic cysts 3-5 cm

Simple or hemorrhagic cysts > 5 cm, 6 weeks to document resolution Yearly

Postmenopausal Cysts > 1 cm women Any age Hydrosalpinx No follow-up needed Any age Dermoid, Yearly endometrioma With permission from Levine D, Brown DL, Andreotti RF, et al. Management of asymptomatic ovarian and other adnexal cysts imaged at US: Society of Radiologists in Ultrasound Consensus Conference Statement. Radiology. 2010;256(3):943-954.28

masses with solid components may be either benign or malignant and should be further assessed for wall contour, septations, and mural nodules. Irregular borders, thick irregular septations, papillary projections, and echogenic solid nodules favor malignancy. Color and spectral Doppler ultrasound may demonstrate vascularity within the septa or nodules. Although ascites may be associated with benign masses such as the mucinous cystadenoma or ibroma, it is more commonly seen with malignant disease. Malignant ascites oten contains echogenic particulate matter. If a pelvic mass is suspected of being malignant, the abdomen should also be evaluated for evidence of ascites and peritoneal implants, obstructive uropathy, lymphadenopathy, and hepatic and splenic metastases. Hepatic and splenic metastases are uncommon in ovarian carcinoma, but when they occur, they are usually peripheral on the surface of the liver or spleen as a result of peritoneal implantation. Hematogenous metastases within the liver or splenic parenchyma may occur late in the course of the disease. Attempts have been made to standardize reporting of adnexal features and preoperatively classify these masses. he largest study to date analyzing features of ovarian and adnexal masses has been performed by the International Ovarian Tumor Analysis (IOTA) group.209 Timmerman et al.210 used these ultrasound-based features to develop simple rules that can correctly classify the majority of masses as benign or malignant (Table 16.4). If one or more of the malignant (M) rules or one or more of the benign (B) rules are present, the mass is classiied as benign or malignant. If both M and B rules are present or no rules are present, the mass cannot be classiied.

NONGYNECOLOGIC ADNEXAL MASSES Pelvic masses and pseudomasses may not be of gynecologic origin. To make this diagnosis, it is important to visualize the

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TABLE 16.4 Ten Simple Rules for Identifying a Benign or Malignant Tumor Rules for Predicting a Malignant Tumor (M-Rules)

Rules for Predicting a Benign Tumor (B-Rules)

M1 Irregular solid tumor M2 Presence of ascites

B1 Unilocular B2 Presence of solid components where the largest solid component has a largest diameter 100 ms) is detected within the hepatic parenchyma (Fig. 18.10). Within the hilum, no arterial low is demonstrated, or if periportal arterial collaterals are present, a tardus-parvus waveform may be detected. herefore demonstration of arterial low in the hepatic parenchyma does not exclude the presence of hepatic arterial thrombosis, and meticulous inspection of the parenchymal waveform is warranted29,30 (see Fig. 18.10). Occasionally, a false-positive diagnosis of hepatic artery thrombosis can occur with severe hepatic edema, systemic hypotension, and high-grade hepatic artery stenosis.8 In situations with poor visibility of the porta hepatis because of abdominal girth or overlying bowel gas, lack of detectable low within the hepatic artery should be viewed with caution and conirmed on computed tomography angiography (CTA).

Hepatic Artery Stenosis Hepatic artery stenosis has been reported in up to 11% of transplant recipients and most oten occurs at or within a few centimeters of the surgical anastomosis. Risk factors for development of stenosis include faulty surgical technique, clamp injury, rejection, and intimal trauma caused by perfusion catheters.27 Clinically, patients have biliary ischemia and/or abnormal LFT values. Doppler ultrasound can provide direct and indirect evidence of hepatic artery stenosis. Direct evidence involves identifying and localizing a hemodynamically signiicant narrowing within the vessel. he porta hepatis should be initially screened with color Doppler ultrasound to detect a focal region of color aliasing within the hepatic artery, which indicates high-velocity turbulent low produced by the stenotic segment. If the stenosis is hemodynamically signiicant, spectral tracing will reveal peak systolic velocity (PSV) of greater than 2 to 3 m/sec, with associated turbulent low distally. Indirect evidence of hepatic artery stenosis includes a tardus-parvus waveform anywhere within the hepatic artery (RI < 0.5; AT > 100 ms). his waveform suggests the presence of a more proximally located stenotic region.27 Indirect evidence of stenosis is much more common in clinical practice than documentation of the stenosis itself (Figs. 18.11 and 18.12). he presence of an intraparenchymal tardus-parvus waveform indicates alterations in the intrahepatic arterial bed from impaired arterial perfusion of the liver. Although it is detected most oten in patients with hepatic artery stenosis, tardus-parvus waveform may also result from collateral vessels arising from hepatic artery thrombosis or, less frequently, from severe aortoiliac atherosclerosis. herefore an intraparenchymal tardus-parvus waveform cannot distinguish between hepatic artery stenosis and thrombosis if the hepatic arterial trunk is not visualized and meticulously investigated.31 Mild degrees of hepatic artery narrowing may also be present without Doppler abnormalities. herefore if clinical suspicion is high, a normal Doppler study should not preclude further

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FIG. 18.9 Bile Duct: Stones. (A) Sonogram and (B) correlative noncontrast-enhanced CT show the presence of a large obstructing stone (arrow) in the common hepatic duct. (C) Transverse sonogram shows an echogenic focus (arrow) consistent with an intraductal calculus in this patient with recurrent primary sclerosing cholangitis. (D) Corresponding axial SPGR (spoiled gradient echo) T1-weighted pregadolinium-enhanced magnetic resonance image shows intraductal high-frequency signal (arrow) consistent with a stone. (E) Transverse sonogram at level of the common hepatic duct shows a nonshadowing echogenic focus (arrow) in the duct, consistent with a soft stone. (F) Corresponding T2-weighted magnetic resonance image shows a well-deined illing defect (arrow), conirming the presence of a calculus within the proximal common duct.

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FIG. 18.10 Hepatic Artery: Thrombosis in Three Patients. Patient 1: (A) Transverse sonogram shows a right lobe infarct appearing as a solid-cystic region (arrows), resulting from hepatic arterial thrombosis. (B) Corresponding CT scan shows the infarct as a low-attenuating wedgeshaped region. (C) On spectral Doppler, no low could be detected in the main hepatic artery. A tardus-parvus waveform detected within the liver indicates an upstream hepatic arterial problem—in this case, hepatic artery thrombosis with collateral arterial vessels supplying the hepatic tissue. Patient 2: (D) Transverse sonogram shows a greatly distended bile duct (arrows) with echogenic material within the lumen secondary to sloughed mucosa and blood. (E) Corresponding CT scan shows dramatically dilated intrahepatic bile ducts (arrows). The biliary necrosis is less well appreciated on CT. (F) Percutaneous cholangiogram shows contrast illing shaggy, intrahepatic ducts with multiple illing defects. The illing defects correspond to the sloughed biliary mucosa. Patient 3: (G) Transverse sonogram demonstrates multiple collateral vessels (arrow) at the porta hepatis. (H) Spectral Doppler sonogram within the liver shows a tardus-parvus waveform. (I) CT angiogram shows occlusion of the hepatic artery (arrow) caused by acute thrombosis. Multiple arterial collateral vessels (arrowheads) are identiied, as seen on (G).

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C FIG. 18.11 Hepatic Artery Stenosis: Doppler Features. (A) Intrahepatic spectral waveform and (B) hepatic artery waveform at porta hepatis show a prolonged acceleration time and low resistance, a tardus-parvus waveform, suggesting an upstream problem. (C) Spectral waveform at the anastomosis shows high-velocity low greater than 400 cm/sec. The corresponding color Doppler sonogram shows aliasing as turquoise and yellow between the red and blue at the stenosis, with turbulence beyond.

investigation with other cross-sectional techniques, although the stenosis, if detected, may be mild in these patients. Although detection of a tardus-parvus waveform should incite further assessment, false-positive diagnoses can occur, particularly in the early postoperative period (within 48 hour of surgery), possibly because of postoperative edema. In one study, approximately 30% of false-positive tardus-parvus waveforms were idiopathic and not associated with any causative factors.32

Elevated Hepatic Arterial Resistive Index In the early postoperative period, a normal hepatic artery may display a high-resistance arterial low (RI > 0.8) or a complete lack of low in diastole (RI = 1.0) on Doppler interrogation. In these patients the low within the hepatic artery usually returns to normal in a few days. he cause of this waveform is uncertain, although it may be related to older donor age or prolonged cold ischemic time of the grat. RIs may also be higher in normal grats with an infrarenal aortohepatic anastomosis compared with those grats with an end-to-end anastomosis. hus a high RI of the hepatic artery on Doppler assessment frequently has no clinical relevance and should not be misinterpreted as a sign of a hepatic artery abnormality.33,34 Hepatic Artery Pseudoaneurysms Hepatic artery pseudoaneurysms are uncommon complications of transplantation (1%) and occur most frequently at the vascular anastomosis or as a result of prior angioplasty. Intrahepatic pseudoaneurysms are rare, usually peripherally located, and associated with percutaneous needle biopsies, infection, or biliary

procedures. Intrahepatic aneurysms are oten asymptomatic but can cause life-threatening arterial hemorrhage or, in mycotic pseudoaneurysms, produce istulas between the aneurysm and the biliary tree or portal veins.8 Extrahepatic pseudoaneurysms occur at the donor-recipient arterial anastomosis and may be caused by infection or technical failure. Gray-scale ultrasound of hepatic artery pseudoaneurysms shows a hypoechoic structure (at times simulating a cyst), typically following the course of the hepatic artery, with intense swirling low on color Doppler and a disorganized spectral waveform (Fig. 18.13). Management options are dictated by the location of the pseudoaneurysm. Extrahepatic pseudoaneurysms can be treated by surgery, transcatheter embolization, or stent insertion, whereas intrahepatic pseudoaneurysms are oten treated with endovascular coil embolization.

Celiac Artery Stenosis Celiac artery stenosis may be caused by atheromatous disease or impingement of the celiac axis by the median arcuate ligament of the diaphragm. If severe, celiac stenosis can result in decreased arterial low to the allograt. Patients are oten asymptomatic before transplantation, presumably because of rich collateral networks, usually through the pancreaticoduodenal arcade. Ater transplantation, patients may become symptomatic, with evidence of biliary ischemia and abnormalities in serum LFT values, a result of the greater low demand imposed on the celiac artery by the newly transplanted liver. Doppler ultrasound may be normal or may reveal a lowresistance tardus-parvus waveform in the transplanted hepatic

CHAPTER 18

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FIG. 18.12 Hepatic Artery Stenosis in Two Patients. Patient 1: (A) Intraparenchymal spectral Doppler ultrasound shows a low-resistance waveform (resistive index [RI] = 0.4). (B) Corresponding contrast-enhanced CT angiogram shows subtle stenosis of the proximal hepatic artery (arrow). Patient 2: (C) Intraparenchymal spectral Doppler shows a tardus-parvus, low-resistance waveform with a delayed acceleration time of 120 ms. (D) Corresponding CT angiogram shows long stenosis of the hepatic artery (between arrows).

artery and high-velocity jet across the celiac stenosis. Patients are treated with division of the median arcuate ligament or, in the case of atheromatous disease, an aortohepatic interposition bypass grat35,36 (Fig. 18.14).

Portal Vein Complications Portal vein stenosis or thrombosis is uncommon, with a reported incidence of 1% to 13%.30,37,38 Risk factors include faulty surgical technique, misalignment of vessels, excessive vessel length, hypercoagulable states, and previous portal vein surgery.30

Factors extrinsic to the portal vein may also contribute, such as increased downstream resistance caused by a suprahepatic stricture of the IVC or diminished portal venous blood low. Clinical presentations include hepatic failure and signs of portal hypertension (gastrointestinal hemorrhage from varices or massive ascites). Gray-scale ultrasound of portal vein stenosis may show narrowing of the vessel lumen, usually at the anastomosis. Doppler interrogation shows a focal region of color aliasing, relecting turbulent, high-velocity low, with a threefold to fourfold velocity

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FIG. 18.13 Hepatic Artery Pseudoaneurysms in Two Patients. Patient 1: (A) Gray-scale sonogram shows a small cystic mass close to the porta hepatis (arrowheads). (B) Color Doppler ultrasound conirms vascularity within the pseudoaneurysm (arrowheads) arising from the hepatic artery (arrow). (C) Corresponding enhanced CT conirms the pseudoaneurysm arising at the hepatic artery anastomosis. Patient 2: (D) Transverse and (E) sagittal sonograms show a midline oval mass (arrows). (F) On color and spectral Doppler ultrasound, disorganized low is identiied in a portion of the mass, representing a partially thrombosed pseudoaneurysm. Arrows mark the thrombosed portion of the pseudoaneurysm. (A-C with permission from Crossin JD, Muradali D, Wilson SR. US of liver transplants: normal and abnormal. Radiographics. 2003;23[5]:1093-1114.5)

increase at the site of stenosis relative to the prestenotic segment on spectral interrogation (Fig. 18.15). Chong and colleagues39 showed that the presence of elevated portal vein anastomotic velocities greater than 125 cm/sec, or a velocity ratio of 3 : 1 at the anastomosis, was greater than 95% speciic for portal vein stenosis. True portal vein stenosis must be distinguished from a pseudostenosis of the portal vein. his entity is seen when the recipient portal vein is larger than the donor portal vein and no associated diferential gradient exists across the site of narrowing. Portal vein thrombosis manifests as echogenic solid material within the portal vein lumen (Figs. 18.16 and 18.17). In the acute state the thrombus may be anechoic, making detection diicult on gray-scale ultrasound and emphasizing the necessity for careful Doppler assessment of the entire portal venous system. As with portal vein thrombosis in the native liver, the thrombus may decrease in size and eventually recanalize, showing multiple venous low channels within the thrombus. Treatment options for portal vein thrombosis or stenosis include thrombectomy,

segmental portal vein resection, percutaneous thrombolysis, stent placement, and balloon angioplasty.

Inferior Vena Cava Complications Stenosis of the IVC is a rare complication of liver transplantation and may occur at the suprahepatic or infrahepatic anastomosis. IVC stenosis occurs more frequently in pediatric recipients and patients undergoing retransplantation.40 Causes of IVC stenosis include anastomotic discrepancy, IVC kinking, ibrosis, or neointimal hyperplasia. On gray-scale ultrasound, the IVC may show obvious narrowing at the site of anastomosis, associated with a focal region of aliasing on color Doppler. On spectral interrogation, a threefold to fourfold greater velocity gradient is observed across the stenosis compared with the prestenotic segment. he hepatic veins may show reversal of low or may lose their normal phasicity, with a monophasic waveform8 (Figs. 18.18 and 18.19). hrombosis of the IVC has been reported in less than 3% of recipients and is caused by technical diiculties at surgery, hypercoagulable states, or compression from adjacent luid

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collections.26,40 Gray-scale ultrasound shows echogenic thrombus within the IVC that may continue into the hepatic veins. In cases of recurrent HCC, tumor thrombus may extend from the hepatic veins into the IVC (Fig. 18.20).

Hepatic Vein Stenosis Hepatic vein stenosis occurs with a frequency of 1% in orthotopic liver transplant and 2% to 5% in living donor transplants. his discrepancy in frequency is primarily related to diferent surgical techniques. In orthotopic liver transplants, an anastomosis is performed between the donor and recipient IVC without touching the hepatic veins. In living donor transplants, however, the donor hepatic vein is anastomosed to either the hepatic vein stump or the IVC of the recipient. his results in the hepatic veins being rigidly ixed in position, such that any movement of the grat produces a buckling and narrowing of the hepatic veins. In addition, progressive growth of partial liver grats ater surgery may result in stretching or twisting of the hepatic veins, further contributing to narrowing of the venous outlet.41,42

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FIG. 18.14 Celiac Artery Stenosis: Impingement by Median Arcuate Ligament. (A) Transverse sonogram shows narrowing of the celiac artery secondary to impingement by the median arcuate ligament (arrow). (B) Spectral trace of the region of narrowing shows elevated peak systolic velocities of 412 cm/sec. (C) Spectral trace of left lobe intrahepatic arterial branch shows low-resistance tardus-parvus waveform. After surgical ligation of the median arcuate ligament, the spectral waveforms returned to normal.

Clinically, hepatic vein stenosis manifests with liver congestion, hepatomegaly, ascites, and/or pleural efusions. Hepatic venous obstruction in the early postoperative state is a surgical emergency, and reoperation is usually necessary for correction or for retransplantation, if substantial hepatic necrosis has occurred. Late-onset hepatic venous obstruction may be associated with a more insidious deterioration in liver function. hese patients may beneit from metallic stent insertion or balloon venoplasty, because surgical correction is oten diicult as a result of ibrotic changes around the anastomotic sites.41,42 Direct signs of hepatic vein stenosis include focal narrowing on gray-scale ultrasound associated with turbulent low on color and spectral Doppler interrogation (Fig. 18.21). A persistent, monophasic spectral waveform is suggestive of, but not diagnostic of, hepatic vein stenosis; monophasic waveforms may also be present in normal, nonobstructed hepatic veins. However, the presence of a triphasic or biphasic waveform rules out clinically important hepatic vein stenosis.42

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53.0 cm/s

F 120.1 cm/s

E 156.0 cm/s

D 32.8 cm/s

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FIG. 18.15 Portal Vein Stenosis: Anastomotic Stricture. (A) Gray-scale sonogram of main portal vein shows narrowing at the anastomosis (arrowhead). (B) Color Doppler shows aliasing at the region of stenosis caused by high-velocity turbulent low. (C) Spectral Doppler shows velocities of 32.8 cm/sec proximal to the stenosis. (D) Velocities at the stenosis are elevated at 156 cm/sec. (E) Poststenotic high-velocity turbulent low is identiied, measuring 120.1 cm/sec. (F) Beyond the turbulent low, velocities of 53 cm/sec are obtained. This represents a threefold increased velocity gradient across the anastomosis, indicating that the stenosis is hemodynamically signiicant.

Extrahepatic Fluid Collections Perihepatic luid collections and ascites are frequently observed ater transplantation. In the early postoperative period a small amount of free luid or a right pleural efusion may be observed, but these usually resolve in a few weeks. Fluid collections and hematomas are common in the areas of vascular anastomosis (hepatic hilum and adjacent to IVC) and biliary anastomosis, in the lesser sac, and in the perihepatic and subhepatic spaces.7 Because the peritoneal relections surrounding the liver are ligated at transplantation, luid collections can occur around the bare area of the liver, a location for luid that is not encountered in the preoperative liver5 (Fig. 18.22). Ultrasound is highly sensitive in detecting these luid collections, although it lacks speciicity with regard to etiology because bile, blood, pus, and lymphatic luid can all have a similar sonographic appearance. he presence of internal echoes in a luid collection suggests blood or infection. Particulate ascites may also be observed in peritoneal carcinomatosis, although this would seem less likely in the transplant recipient population.5

Adrenal Hemorrhage Right-sided adrenal hemorrhage may be observed in the immediate postoperative period and results from (1) venous engorgement caused by ligation of the right adrenal vein during the removal of a portion of the IVC or (2) a coagulopathy caused by the

patient’s preexisting liver disease.26 On ultrasound, adrenal hemorrhage may be seen as a hypoechoic nodular structure or as a luid collection in the right suprarenal region (Fig. 18.23).

Intrahepatic Fluid Collections Sterile postoperative luid collections are oten located along the falciform ligament and ligamentum venosum, usually appearing as luid-illed anechoic collections surrounding the echogenic ligaments (Fig. 18.24). Bilomas may manifest as a hypoechoic or complex cyst. Intraparenchymal hematomas may result from the transplant surgery or percutaneous biopsy or may be a sequela of donor trauma (e.g., motor vehicle crash).

Abscess Versus Infarct In the early stages it may be diicult to diferentiate a liver abscess from an infarct. Initially, both abscesses and infarcts may appear as a subtle hypoechoic region, associated with a localized coarsening of the parenchymal echotexture. Infarcts may subsequently organize into avascular round or wedge-shaped lesions, which can eventually develop central hypoechoic areas relecting liquefaction and necrosis. A focal liver infarct should be diagnosed with accompanying Doppler evidence of hepatic arterial compromise. As with infarcts, the ultrasound appearance of a liver abscess also varies with its maturation. he classic appearance of a mature transplant liver abscess is a complex, cystic structure with thick,

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FIG. 18.16 Portal Vein: Bland Thrombus in Two Patients. Patient 1: (A) Transverse sonogram and (B) corresponding contrast-enhanced CT show nonocclusive thrombus in the main portal vein (arrows). Patient 2: (C) Transverse sonogram and (D) corresponding contrast-enhanced CT scan show nonocclusive thrombus in the ascending ramus of the left portal vein (arrows).

irregular walls and particulate internal luid, with or without associated septations. Both infarcts and abscesses may contain bubbles of air, visualized as bright echogenic foci with or without posterior acoustic shadowing (Fig. 18.25). Occasionally, bubbles of air within the lumen of an intraparenchymal abscess can be confused with benign pneumobilia or may be mistaken for air outside the liver within the gastrointestinal tract. A high index of suspicion is critical in patients at risk for either abscess or infarct to avoid these misinterpretations.

Intrahepatic Solid Masses he diferential diagnosis of a solitary mass in the transplanted liver is similar to that in the native liver. For example, benign lesions, such as hemangiomas and cysts, are relatively common

in the transplanted liver, with the same range of appearances as described for the native liver. However, several pathologies unique to the transplanted liver may also appear as a solid or complex mass on gray-scale ultrasound, including infarcts (Fig. 18.26), abscesses, hematomas, recurrent or metastatic HCC, and posttransplant lymphoproliferative disorder (PTLD). Recurrent hepatocellular carcinoma is a serious complication that can potentially develop ater transplantation in patients with a preoperative history of end-stage cirrhosis with known or occult hepatomas. he most common site of recurrent HCC is the lung, presumably caused by embolization with tumor cells through the hepatic veins before or during transplantation. he second most common location of recurrent hepatomas is within the allograt, followed by regional or distant lymph nodes. Early detection of recurrent hepatomas in the transplanted liver is

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FIG. 18.17 Portal Vein: Malignant Thrombus in Two Patients. Patient 1: (A) Transverse sonogram of malignant thrombus (arrows) in right portal vein with (B) extension into main portal vein (arrow). (C) Triphasic CT of the liver shows the recurrent hepatocellular carcinoma (arrows) that accounts for the portal vein thrombus. Patient 2: (D) Transverse sonogram demonstrates malignant thrombus in the main portal vein (arrows). The background liver is extremely abnormal, with a large echogenic mass (arrowheads). (E) Portal venous phase of a triphasic CT scan conirms recurrent hepatocellular carcinoma (arrowheads) accompanied by expansile, enhancing malignant thrombus in the main portal vein (arrows). (A and B with permission from Crossin JD, Muradali D, Wilson SR. US of liver transplants: normal and abnormal. Radiographics. 2003;23[5]:1093-1114.5)

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FIG. 18.18 Inferior Vena Cava (IVC) Infrahepatic Anastomosis: Normal and Abnormal in Two Patients. Sagittal sonograms of IVC show (A) a normal caliber at the anastomosis (arrows) and (B) narrowing at the anastomosis (arrows).

FIG. 18.19 Inferior Vena Cava (IVC) Suprahepatic Anastomotic Stricture. Sagittal color Doppler sonogram of a stenosed segment of the IVC shows aliasing produced by high-velocity turbulent low in both the IVC and the hepatic vein. Spectral tracing shows a greater than threefold velocity increase at the stenotic region (left arrow).

dialysis. he only contraindications to transplantation are unsuitability for general anesthesia or surgery, preexisting infection or malignancy, and a risk of recurrent renal disease (e.g., active vasculitis or oxalosis). Before transplantation, a suitable donor must be obtained with appropriate human lymphocyte antigen (HLA) matching with the recipient.44 As the number of patients with CRF continues to rise, the major limitation for expanding transplant programs is the shortage of suitable donor kidneys. his organ shortage has resulted in an increasing number of renal transplantations from living related donors. hese donors may include family members or close friends with a long-standing relationship with the recipient. he average life expectancy for a cadaveric allograt is 7 to 10 years, whereas that for a live donor allograt is 15 to 20 years.44 Regardless of whether a cadaveric or live donor allograt is used, the cost-beneit ratio of a functioning successful transplant far outweighs that of a patient with persistent CRF, so multiple health care resources are targeted to ensure high rates of success. Ultrasound is the most valuable noninvasive imaging modality in monitoring the renal transplant.

Surgical Technique essential to facilitate early resection, ablation, or chemotherapy26,43 (Fig. 18.27). As in the general population, transplant recipients can develop any type of primary or secondary neoplasm within the liver.

RENAL TRANSPLANTATION Transplantation is the treatment of choice for many patients with chronic renal failure (CRF) severe enough to warrant

Detailed sonography of the renal transplant requires knowledge of the surgical procedure used in most institutions as well as the postsurgical anatomic relationships. he right or let lower quadrant is selected for the incision, based on the patient’s prior surgical history and the surgeon’s preference. Usually, the right lower quadrant is selected because the right iliac vein is more supericial and horizontal on this side of the pelvis, facilitating creation of a vascular anastomosis.45,46 he type of arterial anastomosis used depends on whether the allograt is cadaveric or living related and on the number

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FIG. 18.20 Inferior Vena Cava (IVC) Thrombosis in Three Patients. (A) Transverse and (B) sagittal sonograms show malignant IVC and hepatic vein thrombus (arrows) in a patient with recurrent hepatocellular carcinoma after transplantation. (C) Transverse sonogram of the hepatic veins and (D) sagittal sonogram of IVC show bland thrombus (arrows) in each. (E) Sagittal sonogram and (F) corresponding contrast-enhanced CT show bland thrombus in the IVC (arrows). A, Ascites. (A and B with permission from Crossin JD, Muradali D, Wilson SR. US of liver transplants: normal and abnormal. Radiographics. 2003;23[5]:1093-1114.5)

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and size of donor renal arteries. In patients with cadaveric transplants, the donor artery, along with a portion of the aorta (Carrel patch) are anastomosed end to side to the external iliac artery. In patients with living donor transplants, the donor renal artery is anastomosed to either the internal iliac artery (end to end) or the external iliac artery (end to side) of the recipient. Multiple donor arteries of similar size may be joined together with a side-to-side anastomosis to form a common ostium. Alternatively, multiple arteries may be anastomosed as a Carrel patch, or anastomosed separately to the external iliac artery.45,46 he donor renal vein is almost always anastomosed end to side to the external iliac vein. In the case of multiple renal veins,

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FIG. 18.21 Hepatic Vein Stenosis. (A) Color Doppler and (B) correlative CT show focal narrowing (arrow) of the right hepatic vein at junction with IVC. (C) Spectral Doppler shows monophasic low in the right hepatic vein.

the smaller veins are usually ligated, resulting in a single donor vein.46 he ureter is usually anastomosed to the superolateral wall of the urinary bladder through a neocystostomy. Several techniques are used to create a neocystostomy, but the basic procedure involves tunneling the ureter through the bladder wall to prevent relux to the transplant. For patients undergoing repeat surgery on the collecting system and those with complex surgeries, the recipient’s ureter may be used as a conduit to the bladder45 (Fig. 18.28). Because of the chronic shortage of donor organs, paired cadaveric kidneys from young (1.0) with reversal of low in diastole. This is seen with severely increased vascular resistance in the kidney from rejection or renal vein thrombosis.

Gas can be observed within the collecting system in emphysematous pyelonephritis, appearing as a bright echogenic focus with distal dirty shadowing. Milk of calcium cysts can produce dirty shadowing, mimicking an intrarenal abscess. Scanning the patient in a decubitus position allows for diferentiation; gas

Prerenal Vascular Complications Arterial Thrombosis Renal artery thrombosis occurs in less than 1% of transplants, usually within the irst month of surgery, and is oten initially asymptomatic. he most common cause is hyperacute or acute rejection, which results in occlusion of the intraparenchymal arterioles with retrograde main renal artery thrombosis. Other predisposing factors include a young pediatric donor kidney, atherosclerotic emboli, acquired renal artery stenosis, hypotension, vascular kinking, cyclosporine, hypercoagulable states, intraoperative vascular trauma, and poor intimal anastomosis.58 Global infarction of the allograt occurs when there is occlusive thrombosis of the main renal artery, with no perfusion to the renal parenchyma. On gray-scale ultrasound, the kidney may appear difusely hypoechoic and enlarged. On color and spectral Doppler ultrasound, complete absence of arterial and venous low distal to the occlusion, within both the hilar and the intraparenchymal vessels, is observed. Although surgical thrombectomy with arterial repair is oten attempted, nephrectomy is frequently indicated in these patients.46 Segmental infarction of the allograt may occur in transplants with a single main renal artery with thrombosis of a major arterial branch (Fig. 18.40), in transplants with multiple renal arteries where a single artery is thrombosed, and in patients with systemic vasculitis. On gray-scale sonography, a segmental infarct may appear as a poorly deined hypoechoic region, a hypoechoic mass, or a hypoechoic mass with a well-deined echogenic wall.

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FIG. 18.36 Chronic Renal Failure in Six Patients. (A) and (B) Cortical thinning. (A) Sagittal scan shows moderate cortical thinning with abundant renal sinus fat. (B) With progression, the kidney (arrows) becomes smaller and the cortex thinner. (C)-(F) Dystrophic calciications. Sagittal sonograms show (C) a few punctuate peripheral cortical calciications (arrows); (D) multiple peripheral and central cortical calciications (arrows); and (E) linear calciications that extend from the peripheral to deep cortex (arrows). (F) The end-stage kidney becomes calciied, appearing as an echogenic interface (arrow) associated with dirty shadowing (arrowheads). The kidney is frequently not identiied on sonography at this stage.

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FIG. 18.37 Renal Transplant-Related Infections. (A) Uroepithelial thickening. Sagittal sonogram shows mild uroepithelial thickening (arrowheads). (B) Sagittal scan shows mild uroepithelial thickening (arrows) surrounding a mildly dilated collecting system with internal echoes, secondary to early pyonephrosis. (C) Transverse sonogram shows moderate to severe uroepithelial thickening (arrow), which can be misinterpreted as a mass in the renal pelvis. (D)-(F) Focal pyelonephritis. (D) Sagittal sonogram shows subtle, focal echogenic region in the upper-pole cortex (arrowheads). (E) Intraparenchymal phlegmon appearing as a hypoechoic mass within the renal cortex (arrows). (F) On color Doppler, the phlegmon seen in image (E) is vascular. (G) and (H) Diffuse pyelonephritis. (G) Transverse sonogram shows a generous kidney with echogenic granular renal cortex, surrounded by inlamed echogenic perinephric fat (F). (H) Corresponding CT shows inlamed fat (F) as perinephric streaking. (I) Emphysematous pyelonephritis. Sagittal sonogram shows air (arrows) within collecting system, appearing as bright, echogenic linear foci with distal dirty shadowing.

On Doppler sonography, the infarcted region appears as a wedgeshaped area devoid of low on color or spectral interrogation.57 Interpretation of the gray-scale and Doppler indings should not be inluenced by urine output of the allograt or laboratory data, because segmental infarction may occur in the presence of preserved renal function. he absence of blood low on Doppler interrogation in the kidney parenchyma may be observed in conditions other than arterial thrombosis, including hyperacute rejection and renal vein thrombosis. In these conditions, however, the main renal

artery is patent on spectral Doppler ultrasound and may exhibit reversal of diastolic low.44

Renal Artery Stenosis Renal artery stenosis, the most common vascular complication of transplantation, occurs in up to 10% of patients within the irst year, is more frequent in living donor allograts compared with cadaveric allograts, and should be suspected in cases of severe hypertension refractory to medical therapy. Transplants with multiple renal arteries are now being used more frequently

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FIG. 18.38 Renal Transplant-Related Infections. (A) Perirenal Candida abscess. Transabdominal sagittal scan shows abscess (A) abutting the lower pole of the transplant kidney. (B) and (C) Subcapsular abscess on ultrasound and CT. Note the heterogeneous abscess (A) with gas (arrow) compressing the kidney (K). (D) and (E) Ureteritis. Sagittal sonograms of proximal (D) and midline (E) ureter show inlamed echogenic periureteral fat (arrows) secondary to an infected ureteral stent (arrowhead). (F) Cystitis. Transverse sonogram shows internal echoes and luid-debris level (arrow) in urinary bladder, secondary to cystitis. Arrowheads show thickened bladder wall.

and show a very slightly higher rate of renal artery stenosis compared with those renal allograts with a single artery. Stenosis may occur in one of three regions of the transplanted artery: the donor portion (Fig. 18.41), most frequently observed in end-to-side anastomoses and thought to arise from either rejection or diicult surgical technique; the recipient portion (Fig. 18.42), which is more uncommon and usually the result of intraoperative clamp injury or intrinsic atherosclerotic disease; and the anastomosis (Fig. 18.43), which is more frequent in end-to-end anastomoses and is directly related to surgical technique or may be secondary to rejection.54,58-60 Initially, color Doppler ultrasound should be used to determine the location of the anastomosis, as well as to document focal regions of aliasing, which would indicate the presence of highvelocity turbulent low and serve as a guide for meticulous spectral interrogation. A spectral tracing should then be obtained at the anastomosis and in any area where color aliasing is detected to determine the PSV in that region. he upper limit of normal for arterial PSV is unclear. Assigning a PSV upper limit of 200 cm/sec for diagnosing renal artery stenosis may result in a relatively high false-positive rate. hus some authors have suggested using an arterial threshold PSV of 250 cm/sec for the diagnosis of renal artery stenosis.54,61

However, high velocities in the renal artery may be secondary to changes in the external iliac artery. herefore the renal artery–external iliac artery PSV ratio can be calculated to determine if renal artery velocity measurements are a result of narrowing or high low rates from the external iliac artery. A renal artery–external iliac artery PSV ratio greater than 1.8:1 is suggestive of renal artery stenosis.54,62 In addition, within the renal parenchyma, a tardus-parvus spectral waveform can be observed in the intraparenchymal arteries in patients with renal artery stenosis.46,57 If no low abnormality is detected within the main renal artery ater color and spectral Doppler interrogation, signiicant stenosis can be excluded.63

Doppler Criteria for Renal Artery Stenosis Color aliasing at the stenotic segment Distal turbulent low Peak systolic velocity > 250 cm/sec Velocity gradient between the renal artery and external iliac artery greater than 1.8:1

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FIG. 18.39 Mimicker of Emphysematous Pyelonephritis. (A) Emphysematous pyelonephritis. Transverse scan shows air in collecting system (arrow). (B) Milk of calcium cyst. Supine sonogram shows layering of the calciication (arrowheads) in the cyst, producing dirty shadowing. (C) Scanning this patient in a decubitus position changes the orientation of the layering of calcium to the most dependent portion of the cyst, allowing for differentiation from an air-illed collection.

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FIG. 18.40 Renal Artery Thrombosis. (A) Sagittal sonogram shows normal gray-scale ultrasound on postoperative day 1. (B) However, power Doppler shows no low in the lower pole because of thrombosis of a segmental artery. (C) Three months later, there is secondary scarring of the entire lower pole (arrow).

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C FIG. 18.41 Renal Artery Stenosis: Donor Portion. (A) Color Doppler ultrasound of donor renal artery anastomosis shows focal area of aliasing (arrow). (B) Power Doppler shows area of narrowing in this region (arrow). (C) Spectral Doppler shows elevated angle-corrected velocities at the site of the arrow, greater than 400 cm/sec.

Intraparenchymal arterial stenosis may be observed in chronic rejection as a result of scarring in the tissues surrounding the involved vessels. On spectral Doppler ultrasound, a prolonged AT may be observed in the segmental and interlobar arteries, with a normal main renal artery waveform.45 Treatment options for renal artery stenosis include percutaneous transluminal angioplasty, endovascular stent placement, and surgery. Surgical management of these transplants involves resection and revision of the stenosis with insertion of a patch grat at the stenotic segment.46 A false-positive Doppler diagnosis of renal artery stenosis can occur if there is an abrupt turn in the main renal artery, if the artery is severely tortuous, or if there are errors in Doppler technique (Fig. 18.44). Inadvertent compression of the main renal artery by the sonographer while performing spectral interrogation may also produce transient narrowing of the artery and elevated PSV readings. Turning the patient in a decubitus position such that the anterior abdominal or pelvic wall tissues are displaced from lying over the transplant can reduce external pressure on the allograt during scanning.

Venous Thrombosis Occlusive renal vein thrombosis is slightly more common than arterial thrombosis, occurring in up to 4% of transplants, and is associated with acute pain, swelling of the allograt, and an abrupt cessation of renal function between the third and eighth postoperative day. Risk factors include technical diiculties at surgery, hypovolemia, propagation of femoral or iliac thrombosis, and compression by luid collections.58,64

On gray-scale ultrasound, the allograt may appear enlarged, and in rare cases intraluminal thrombus may be detected in a dilated main renal vein or within the intraparenchymal venous system. Spectral and color Doppler ultrasound will show a lack of venous low in the renal parenchyma, absence of low in the main renal vein, and reversal of diastolic low in the main renal artery, as well as sometimes in the intraparenchymal arteries65,66 (Fig. 18.45). he sonographer should be aware that reversal of low in diastole in the main renal artery or the intraparenchymal arterial branches is highly suggestive of renal vein thrombosis only in the absence of venous low in the renal parenchyma and main renal vein. Reversed diastolic arterial low, with preservation of venous low, is a nonspeciic inding indicating extremely high vascular resistance in the small intrarenal vessels or main hilar vessels. he outcome for these patients is generally poor, with allograt loss rates of 33% to 55%. Potential causes of reversed diastolic low include acute rejection, ATN, peritransplant hematomas (compressing renal grat or hilar vessels), and glomerulosclerosis.67

Renal Vein Stenosis Renal vein stenosis most oten occurs from perivascular ibrosis or external compression by adjacent luid collections. he renal cortex appears either normal or hypoechoic, and on color Doppler, aliasing is identiied at the stenotic region because of focal, high-velocity turbulent low. On spectral Doppler sonography, a threefold to fourfold increase in velocity across the region of

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FIG. 18.42 Renal Artery Stenosis: Recipient Portion. (A) Color Doppler ultrasound shows focal area of aliasing (arrow) proximal to the renal artery anastomosis. (B) Spectral Doppler of the region of aliasing seen in image (A) shows angle-corrected peak velocities of 400 cm/sec. (C) Angiography shows a focal area of stenosis (arrow) arising from the external iliac artery. (D) Angiogram performed after angioplasty shows resolution of the stenotic region (arrow).

narrowing indicates a hemodynamically signiicant stenosis63 (Fig. 18.46).

Postrenal Collecting System Obstruction Collecting system obstruction is unusual in renal transplants, occurring in less than 5% of patients.45,63 Because the allograt is denervated, the collecting system dilates without clinical signs of pain or discomfort. he diagnosis is oten made as an incidental inding on routine screening sonography or in the workup of

the transplant patient for asymptomatic deterioration of renal function parameters. he most common cause of ureteral obstruction is from ischemic strictures, usually involving the terminal ureter at the ureterovesical junction. he transplanted ureter is particularly susceptible to ischemic events because of its limited vascular supply from the renal artery. he ureterovesical junction is usually the region of most pronounced involvement because it is farthest anatomically from the renal

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FIG. 18.43 Renal Artery Stenosis: Anastomosis. (A) Color Doppler ultrasound shows focal area of narrowing and aliasing at the anastomosis (arrows). (B) Spectral Doppler at the anastomosis shows elevated angle-corrected velocity of 775.4 cm/sec. (C) Renal arterial angiogram conirms stenosis at the anastomosis (arrow). (D) Angiogram performed after angioplasty shows resolution of the anastomotic stenosis.

hilum, where the ureteral branch originates.46 Other causes of ureteral obstruction include strictures from iatrogenic injury, intraluminal lesions (e.g., stones, blood clots, sloughed papillae), perigrat ibrosis, and ureteral kinking (Figs. 18.47 and 18.48). Extrinsic compression of the ureter from peritransplant collections can also result in collecting system obstruction. Patients with renal transplants are at higher risk for stone development compared with the general population. In approximately 15% of these patients, the stone development is related

to hypercalcemia. Because the transplant is denervated, patients with stone-related collecting system obstruction may not have typical symptoms of renal colic.54 Evaluation of the collecting system with fundamental grayscale imaging may be diicult because of side-lobe and scatter artifact, which can potentially obscure optimal evaluation of the calyceal system and ureter. Harmonic imaging, however, uses a narrower ultrasound beam with smaller side lobes and is less susceptible to scatter artifact. hese parameters make harmonic imaging ideal for evaluating anechoic structures,

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FIG. 18.44 Mimickers of Renal Artery Stenosis. (A) Abrupt turn in renal artery. On color Doppler ultrasound, aliasing is identiied in this region (arrow), with peak systolic velocities of 429 cm/sec on spectral Doppler. (B)-(D) Misaligned angle correction. (B) Initial spectral Doppler shows elevated renal artery anastomotic velocity of 298 cm/sec. This elevated velocity reading is artifactual because the spectral angle correction is not aligned with the direction of the renal artery. (C) Follow-up spectral Doppler ultrasound shows a normal renal artery velocity of 189 cm/sec, with appropriate angle correction in the direction of the artery. (D) Renal angiogram conirms a normal renal artery (arrows) with no evidence of stenosis.

such as the renal collecting system for regions of subtle dilation, and the presence of small intraluminal stones (Fig. 18.49). Mild pelvicaliectasis may be secondary to nonobstructive causes such as overhydration, decreased ureteric tone (from denervation of transplant), and ureteric-vesical relux or can occur transiently in the immediate postoperative period from perianastomotic edema.45,68 In addition, multiple parapelvic cysts can mimic a dilated collecting system (Fig. 18.50).

Arteriovenous Malformations and Pseudoaneurysms Intraparenchymal arteriovenous malformations (AVMs) result from vascular trauma to both artery and vein during percutaneous biopsies and are usually asymptomatic with few clinical sequelae. Because most of these are small and resolve spontaneously, the incidence of posttransplant AVMs is unknown, although rates of 1% to 18% have been reported. In rare cases, large AVMs may manifest with bleeding, high-output cardiac failure, or decreased

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FIG. 18.45 Renal Vein Thrombosis. (A) Sagittal sonogram shows increased cortical echogenicity with a coarse echotexture. (B)-(D) Spectral Doppler ultrasound images of (B) cortical arteries, (C) renal sinus arterial branches, and (D) main renal artery show reversal of low in diastole. No venous low was detected in the transplant.

renal perfusion caused by the large shunt. In these patients, treatment usually involves percutaneous embolization therapy.44 Gray-scale ultrasound may not reveal small AVMs. Color Doppler sonography shows a focal region of aliasing with myriad intense colors, oten associated with a prominent feeding artery or draining vein. Turbulent low within the AVM produces vibration of the perivascular tissues, resulting in these tissues being assigned a color signal outside the borders of the renal vasculature. Spectral Doppler ultrasound is typical of that for all AVMs, with low-resistance, high-velocity low and diiculty diferentiating between artery and vein within the malformation.

If a dominant draining vein is detected, the waveform may be pulsatile or arterialized58,68-70 (Fig. 18.51, Video 18.3). On color Doppler ultrasound, focal regions of cortical dystrophic calciications or small stones can mimic an AVM by producing an intense color signal known as a twinkling artifact.71 hese artifacts can be diferentiated from a true AVM on spectral tracing because both calciications and stones produce characteristic linear bands on spectral interrogation. In our clinical experience, we have also observed a linear band of color posterior to these regions of calcium that extend to the limits of the color box. We have not observed this phenomenon with AVMs and

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FIG. 18.46 Renal Vein Stenosis. Color Doppler of renal vein anastomosis shows focal area of aliasing (white arrow). Spectral interrogation in region of aliasing shows velocities of 200 cm/sec. Spectral interrogation proximal to aliasing shows velocities of 40 cm/sec (yellow arrow), indicating a hemodynamically signiicant stenosis of the renal vein.

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FIG. 18.47 Ureteral Strictures. (A) Sagittal sonogram and (B) percutaneous nephrostogram show grade 3 pelvocaliectasis secondary to a stricture at the ureteropelvic junction (arrow). (C) Sagittal sonogram shows grade 4 pelvocaliectasis. The distal ureter was not seen on ultrasound. (D) Percutaneous nephrostogram shows a stricture at the ureterovesicular junction (arrow). (E) Sagittal sonogram shows grade 3 pelvocaliectasis, produced by (F) a stricture at the ureterovesicular junction (arrows). arrowheads, Tiny nonobstructing stone; B, bladder; U, ureter.

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FIG. 18.48 Multiple Obstructing Ureteral Stones. (A) Sagittal sonogram of the kidney shows grade 3 pelvocaliectasis. (B) Sagittal sonogram of the distal ureter (U) shows multiple obstructing stones (arrows). (C) Coronal CT shows multiple obstructing ureteral stones (arrows). B, Bladder; K, kidney.

have found it a useful tool in diferentiating vascular malformations from focal calciications (Fig. 18.52). Pseudoaneurysms result from vascular trauma to the arterial system during percutaneous biopsy or, more frequently, occur at the site of the vascular anastomosis. hey may be intrarenal or extrarenal (Figs. 18.53 and 18.54,Video 18.4). Pseuodaneurysms located in the renal hilum are somewhat more concerning than intrarenal pseudoaneurysms owing to their increased risk of rupture. On gray-scale sonography, pseudoaneurysms can mimic a simple or complex cyst. On color Doppler ultrasound, low

can easily be obtained in the lumen of patent pseudoaneurysms, oten with a swirling pattern, whereas on spectral Doppler, a central to-and-fro waveform or a disorganized arterial tracing may be obtained.45,54 Presumed cysts in the renal parenchyma or in the region of the hilum should be assessed with color Doppler to exclude the possibility of a pseudoaneurysm.

Fluid Collections Perinephric collections are demonstrated in up to 50% of transplant recipients.72,73 he most common collections include

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FIG. 18.49 Harmonic Imaging in Two Patients. (A) Sagittal fundamental image shows barely detectable stones (arrows) and a dilated collecting system. (B) Harmonic image shows improved resolution of stones (arrows), now seen associated with distal acoustic shadowing, within anechoic dilated collecting system. (C) Fundamental image shows cortical cyst (arrowhead) with internal echoes and minimal through transmission. (D) Harmonic image shows cyst (arrowhead) to be anechoic and simple, now associated with an appropriate amount of through transmission.

hematoma, urinoma, lymphocele, and abscess. he ultrasound appearances of these peritransplant collections are oten nonspeciic, and clinical indings are warranted to determine their cause. However, the presence of air within a perirenal collection, without a history of recent percutaneous intervention, is highly suggestive of an abscess. he size and location of each collection should be documented on baseline scans because an increase in size may indicate the need for surgical intervention. Postoperative hematomas are variable in size but are oten small, perirenal in location, and insigniicant clinically and oten resolve spontaneously.68 heir ultrasound appearance depends on the age of the collection. An acute hematoma will appear as an echogenic heterogeneous solid mass. With time the hematoma will liquefy, becoming a complex luid collection with internal echoes, strands, or pseudoseptations. Postbiopsy hematomas have

a morphology similar to that of their postoperative counterparts (Figs. 18.55 and 18.56). Urine leaks, or urinomas, have been reported in up to 6% of renal transplants and occur within the irst 2 weeks ater surgery.44 hey are usually secondary to either anastomotic leaks or ureteric ischemia. Rarely, urinomas can result from high-grade collecting system obstruction (Fig. 18.57). On sonography, urinomas are well deined and anechoic, may be associated with hydronephrosis, and in some cases can increase rapidly in size.57 Large urine leaks may result in widespread extravasation and gross intraperitoneal urinary ascites. Lymphoceles result from surgical disruption of the iliac lymphatics and have been reported in up to 20% of patients. hey most oten occur 4 to 8 weeks ater surgery but may develop years ater transplantation. Although most are discovered

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FIG. 18.50 Parapelvic Cysts Versus Pelvocaliectasis in Two Patients. Patient 1: Parapelvic cysts. (A) Transverse and (B) sagittal sonograms show multiple parapelvic cysts mimicking pelvocaliectasis. Patient 2: Grade 3 pelvocaliectasis mimicking parapelvic cysts. (C) Sagittal sonogram shows multiple anechoic structures in the central aspect of the kidney, initially interpreted as multiple parapelvic cysts. (D) Contrast-enhanced magnetic resonance image shows contrast illing grossly dilated calyces (*). A single parapelvic cyst (arrow) is present.

incidentally and are asymptomatic, lymphoceles are the most common luid collection to result in ureteric obstruction. Lymphoceles can become infected or can obstruct venous drainage, resulting in edema of the lower limb, scrotum, or labia.45 Symptomatic collections are drained (surgically or percutaneously) or undergo marsupialization. On sonography, lymphoceles are well-deined collections that are anechoic or that may contain ine internal strands (Figs. 18.58 and 18.59).

PANCREAS TRANSPLANTATION Pancreatic transplantation is performed in select patients who have major complications related to type 1 diabetes. Pancreas transplant represents the only form of self-regulating endocrine

replacement therapy, with more than 80% of recipients becoming free of exogenous insulin requirements within 1 year of surgery. Since 1988 in the United States, more than 15,000 kidney-pancreas transplants and 6000 pancreas transplants have been performed, with 1-year patient survival greater than 90%.3,74 Pancreatic transplantation aims to restore an adequate functioning beta cell mass and therefore to regain physiologic normoglycemic function, typically in the setting of insulin dependent diabetes. Recipients are typically type 1 diabetics in end-stage renal failure with other sequelae of long-term diabetes including neuropathy and atherosclerotic disease. Improvement in glycemic control diminishes the risk of long-term complications in diabetic patients.75 In particular, simultaneous pancreas

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FIG. 18.51 Arteriovenous Malformations (AVMs). (A) Gray-scale ultrasound; AVM not detectable. (B) Corresponding color Doppler image shows large AVM. (C) Sagittal sonogram shows lower-pole AVM. (D) Spectral Doppler of AVM in image (C) shows high-velocity, low-resistance waveform. (E) Sagittal sonogram shows AVM with feeding vessel (arrow). (F) Sagittal scan shows lower-pole AVM with surrounding tissue vibration. See also Video 18.3.

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FIG. 18.52 Arteriovenous Malformation: Mimicker. (A)-(C) Sagittal sonograms show twinkling artifact produced by (A) lower-pole dystrophic cortical calciication (arrow); (B) upper-pole stone; and (C) lower-pole stone. (D)-(F) Differentiation from AVM. On (D) color Doppler and (E) power Doppler, color artifact (arrows) may be seen posterior to border of kidney. Size of twinkling artifact varies with size of the color box. (F) On spectral Doppler ultrasound, the twinkling artifact shows linear bands as on these three spectral traces.

transplant in the setting of kidney transplants has been known to improve long-term patient survival.

Surgical Technique he simultaneous pancreas-kidney transplant is the most common form of pancreas transplantation in the United States and accounts of 80% of all pancreatic transplant procedures. To achieve optimum functioning beta cell mass, the procedure is a wholeorgan pancreas transplant performed in conjunction with a kidney transplant. Best results are achieved if the procedure is performed before the need for dialysis. his approach allows serum creatinine to be used not only as a marker of renal rejection, but also as a surrogate marker of pancreatic grat rejection. his is particularly important because serum amylase and lipase are not sensitive or speciic markers of pancreatic rejection. Serum amylase has only 50% sensitivity for detection of rejection, and lipase may be elevated in both rejection and pancreatitis. he ultimate diagnosis of grat dysfunction is oten made on biopsy. here are several further strategies for pancreas transplantation. A pancreas transplant can be performed as a second step following a successful renal transplant. he latter will typically be a living donor kidney and is usually advised for diabetic patients younger than age 5 with ongoing severe complications. he most severe complication is hypoglycemic unawareness wherein a patient

may be wholly lacking the normal stigmata or warning signs of a low glucose level (such as trembling, sweating, and tachycardia).76 his is the second most common mode of pancreatic transplant and contributes about 25% of all transplants in the United States. Finally, pancreas-only transplantation can be performed in diabetic patients who have no evidence of diabetic nephropathy. Only a minority of diabetic patients are eligible for this approach because it is limited to patients whose hypoglycemic awareness is challenging to manage medically. here are two well-established techniques for pancreas transplantation. Use of the bladder for exocrine drainage (duodenocystostomy) and use of the iliac vessels for arterial and venous supply were considered safer with regard to postoperative infection. his more traditional surgery, exocrine bladder drainage, involved anastomosing the donor duodenum to the urinary bladder and the donor portal vein to the recipient external iliac vein (systemic venous-endocrine drainage)77 (Fig. 18.60). In this circumstance the pancreas grat is placed in the right hemipelvis and the renal grat on the let. he chronic loss of pancreatic secretions into the bladder can result in problems with dehydration, metabolic acidosis, and allograt pancreatitis.3 here is also a higher risk of chemical cystitis secondary to the high amylase and lipase levels of pancreatic secretions. his can result in

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FIG. 18.53 Intrarenal Pseudoaneurysms in Two Patients. Patient 1: (A) Sagittal sonogram shows lower-pole anechoic structure, mimicking a simple cyst. (B) On color Doppler ultrasound, however, swirling low is identiied in this structure, indicating that it represents a pseudoaneurysm. (C) Spectral Doppler ultrasound shows disorganized swirling low within the pseudoaneurysm identiied on image B. Patient 2: (D) Sagittal sonogram shows upper-pole anechoic structure. (E) On color Doppler ultrasound, swirling low is identiied in the anechoic structure identiied on image (D) (arrow). This is adjacent to a large central arteriovenous malformation (AVM). (F) Spectral Doppler ultrasound shows disorganized low in the pseudoaneurysm (yellow arrow) and low-resistance high-velocity low in the central AVM (white arrow).

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FIG. 18.54 Extrarenal Pseudoaneurysm of Renal Artery. (A) Transverse sonogram shows anechoic structure adjacent to renal hilum. (B) Color Doppler ultrasound shows that this structure contains swirling low and represents a pseudoaneurysm. (C) Spectral Doppler ultrasound shows disorganized internal low within pseudoaneurysm. (D) CT shows pseudoaneurysm arising from site of renal artery anastomosis. (E) and (F) In another patient, color Doppler images show a partially thrombosed pseudoaneurysm (arrows). See also Video 18.4.

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FIG. 18.55 Renal Transplant Subcapsular Hematoma Secondary to Biopsy. (A) Sagittal sonogram shows acute hematoma appearing as solid heterogeneous structure. (B) After 1 week, cystic regions have developed within the hematoma. (C) After 1 month, hematoma has liqueied and is larger because of a hyperosmolar effect. Arrows mark the junction of the renal cortex and hematoma.

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FIG. 18.56 Hematomas in Three Patients. Patient 1: (A) Transverse sonogram shows an intraparenchymal hematoma appearing as an anechoic cyst with mildly irregular walls (arrow). (B) Eight months later, the cyst has resolved. Patient 2: (C) Sagittal sonogram shows a hypoechoic solidappearing mass (arrows) abutting the upper pole of the transplant kidney (K). Patient 3: (D)-(F) Postoperative perirenal hematoma. (D) Sagittal sonogram shows hematoma 1 day after surgery, appearing as a solid echogenic heterogeneous mass. (E) Four weeks later, hematoma has begun to liquefy, with interspersed solid components. (F) Six weeks later, hematoma is almost completely liqueied; arrows mark the junction of the hematoma and renal cortex.

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recurrent urinary tract infections and hematuria. In male patients there is a higher risk of urethral infections and balanitis, which in turn may lead to urethral strictures. hese complication risks have resulted in a move toward the intestinal or enteric-based drainage procedure whereby a duodenojejunostomy is created for exocrine drainage of pancreatic secretions. his is performed as either a side-to-side anastomosis or a Roux-en-Y anastomosis. he endocrine drainage is either systemic (anastomosis of donor portal vein to right common iliac vein or distal IVC) or portal venous (anastomosis of donor portal vein to SMV) (Fig. 18.61). his type of surgery provides a more physiologic transplant than the more traditional techniques and is not associated with dehydration or metabolic acidosis. In addition, it provides more appropriate glycemic control, with lower fasting insulin levels, and may be associated with a lower incidence of transplant rejection than the more traditional systemic venous-bladder drainage allograts.3,78 Table 18.1 shows the major diferences between two types of pancreatic transplants (exocrine bladder drainage and exocrine enteric drainage).

FIG. 18.57 Urinoma Secondary to High-Grade Ureterovesical Junction Obstruction. (A) Sagittal sonogram shows dilation of upper-pole calyx (arrow). (B) Dilation eventually ruptures through the adjacent cortex (arrow). (C) Obstruction forms a cortical defect (arrow) and subsequently a perinephric urinoma (U).

Venous Drainage he two methods for venous drainage can be categorized as systemic, wherein the transplanted portal vein is anastomosed to an iliac vein or vena cava, or alternately as using the portal technique, whereby it drains into the SMV of the recipient. he latter technique has over time been shown to confer no additional advantage in terms of outcome compared with the systemic technique.

Arterial Supply In both techniques (systemic and portal venous drainage) the arterial blood supply to the grat is via the donor common iliac artery being attached to the common or external iliac artery of the recipient. Most commonly at our institution, an arterial Y grat of the donor common iliac artery and external and internal iliac artery is anastomosed end to end with two separate anastomoses to the donor superior mesenteric and splenic arteries. here are some alternate methods, however, which include forming a single donor iliac arterial conduit (comprising either the common iliac and either the external or internal iliac artery),

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FIG. 18.58 Sterile Lymphoceles in Four Patients. (A) Sagittal sonogram shows large, simple lymphocele abutting the transplant. (B) Sagittal scan shows small lymphocele (L) adjacent to the external iliac artery and vein. (C) Anechoic lymphocele (L) causes obstruction of the midureter (arrow) and dilation of the calyceal system (C). (D) Transverse sonogram shows septated perinephric lymphocele.

TABLE 18.1 Surgical Techniques for Pancreatic Transplantation Systemic Venous-Bladder Drainage

Portal Venous-Enteric Drainage

Venous drainage

Right lower quadrant Head caudad Y-shaped donor arterial graft anastomosed to recipient common iliac artery Donor portal vein is attached to external iliac vein

Endocrine drainage Exocrine drainage

Systemic venous En bloc donor duodenal stump to recipient bladder

Right upper quadrant Tail caudad Donor splenic artery to recipient common iliac artery Donor portal vein anastomosed to superior mesenteric vein Portal venous Duodenal segment anastomosed to Roux-en-Y loop of jejunum

Location Pancreatic orientation Arterial supply

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FIG. 18.59 Infected Lymphoceles in Five Patients. Sagittal sonograms show infected lymphoceles with (A) a few thin internal strands; (B) multiple internal strands; (C) internal strands, draining to the skin through a cutaneous istula (arrow); (D) thick septations and internal echoes; and (E) internal echoes and punctate wall calciications (arrows). A, Ascites; K, kidney; L, lymphocele.

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FIG. 18.60 Pancreas Transplant: Systemic Venous-Bladder Drainage (Traditional Surgery). (A) Donor portal vein (purple) is anastomosed to the external iliac vein, and donor artery Y graft (coral arrow) to the external iliac artery. Duodenal stump (D) is anastomosed to the bladder (B). (B) Sagittal sonogram shows duodenal stump anastomosed to the bladder (B). P, Pancreas.

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FIG. 18.61 Pancreas Transplant: Portal Venous-Enteric Drainage (New Technique). (A) Donor portal vein (purple) is anastomosed to the superior mesenteric vein (blue), and donor artery (arrow) is anastomosed to the common iliac artery. Duodenal stump (D) is anastomosed to a Roux-en-Y (Y). (B) Transverse sonogram shows pancreas transplant (P) with luid-illed duodenal stump (D).

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which is then anastomosed in an end-to-end fashion to the donor superior mesenteric artery (SMA) and end donor splenic artery to side donor iliac artery anastomosis. If the grat is portally drained, the arterial conduit is much longer than in a systemically drained grat.

Normal Pancreas Transplant Ultrasound To perform an ultrasound assessment of a transplanted pancreas, the sonographer should be aware of the surgical technique used, the position of the allograt in the abdomen at surgery, and the sites of vascular anastomosis. his oten entails a detailed review of the intraoperative surgical notes or discussion with the surgeon before scanning the patient. With the systemic venous technique, the pancreatic head is placed in the iliac fossa, with the body and tail placed obliquely in the midabdomen. he pancreatic tail is therefore positioned superior to the head. With the portal venous technique, the orientation of the grat is such that the pancreatic head lies superiorly and the body and tail lie inferiorly. he grat is positioned within the right side of the abdomen within the inferior mesocolic space. his allows the recipient’s SMV to be anastomosed to the portal vein of the grat. In some instances the grat may be oriented in the transverse midline such that the recipient SMV is sagittally oriented to the transplant portal vein. he normal allograt retains the normal gray-scale morphology of a native pancreas with well-deined margins; a homogeneous echotexture, isoechoic or minimally echogenic to liver; and a thin, nondilated pancreatic duct (Fig. 18.62, Video 18.5 and Video 18.6). he peripancreatic fat shows a normal echogenicity. Occasionally a trace amount of peripancreatic luid may be observed and usually resolves without complication. Color Doppler ultrasound is useful for locating the mesenteric vessels, particularly when the grat is poorly visualized because of overlying bowel gas. Spectral Doppler sonography of the normal grat shows continuous monophasic venous low and low-resistance arterial waveforms.

FIG. 18.62 Normal Pancreas Transplant. Gray-scale ultrasound of pancreas transplant shows normal echogenicity and echotexture of allograft, with nondilated pancreatic duct (arrowheads). See also Video 18.5 and Video 18.6.

If patient habitus is slim and the grat lies in a relatively supericial location within the right iliac fossa, a high-frequency linear probe in the range of 5 to 12 MHz can be used for interrogation. Probe compression as well as placement of the patient in a right anterior oblique position will help to displace overlying bowel gas. Color and power Doppler ultrasound are useful for locating the parenchymal and grat vessels, particularly when the grat is poorly visualized because of overlying bowel gas. Spectral Doppler sonography of the normal grat shows continuous monophasic venous low and low-resistance arterial waveforms, with a rapid systolic upstroke and continuous diastolic low.

Role of Contrast-Enhanced Ultrasound CT and MRI are oten used for problem solving in the setting of postoperative complications; however, in the setting of associated renal impairment in this vulnerable patient group, the impact of iodinated contrast agents must be considered. Similarly, the potential risk of nephrogenic systemic ibrosis needs to be weighed against any possible diagnostic beneit when performing contrastenhanced MRI, particularly in patients with elevated creatinine. Contrast-enhanced ultrasound (CEUS) circumvents any underlying issues with renal impairment and facilitates the conspicuity of the grat relative to the surrounding tissues. It also allows assessment of areas of hypoperfusion. Its other inherent advantages have been well described and include safety, patient tolerance, and lack of ionizing radiation. Because the grat pancreas is highly vascularized, CEUS allows for visualization of areas of reduced or absent microcirculation. he contrast agent remains entirely intravascular, so focal areas of diminished perfusion or necrosis can be seen, and biopsy readily performed under ultrasound guidance. CEUS may also potentially allow an earlier diagnosis of grat rejection.79

Abnormal Pancreas Transplant he grat vasculature consists of the following: 1. he iliac arterial grat is connected to the donor SMA and splenic artery. A Doppler arterial waveform is usually obtained from the SMA, the proximal and distal splenic artery, the intrapancreatic arcade, and the transverse vessels. he waveform is assessed for peak systolic low velocity as well as being evaluated for vascular resistance within the grat. A normal grat should have arterial low with a sharp systolic upstroke and continuous antegrade diastolic low. his is seen in conjunction with an RI of 0.5 to 0.7, which implies a relatively low intragrat vascular resistance. Because there is no capsule enveloping the grat pancreas, normal resistance may be seen in a transplanted pancreas with edema (in the setting of either pancreatitis or rejection). his is in contradistinction to the grat kidney, wherein intrarenal edema results in elevation of vascular resistance. 2. he grat splenic vein and SMV join together to form the donor portal vein. his can be anastomosed to the recipient iliac vein, vena cava (systemic drainage), or SMV (portal drainage). Cardiac phasicity can be seen in the venous waveform when there is systemic venous drainage. Relative lattening of the venous waveform at the site of the donor portal vein

CHAPTER 18 anastomosis to the recipient iliac or SMV is not an uncommon inding and is related to mild narrowing at this site. he most common complications are venous thrombosis and arterial pseudoaneurysm. Potential symptoms of grat thrombosis include unexplained hyperglycemia, grat tenderness, and, in the context of systemicbladder drainage technique, hematuria and diminished urinary amylase levels. Potential complications of grat thrombosis include grat dysfunction and necrosis, pancreatitis, leakage of pancreatic secretions, and sepsis.

Thrombosis Grat thrombosis, including both venous and arterial thrombosis, occurs in 2% to 19% of patients and is the second leading cause of transplant loss, ater rejection. Pancreatic transplants are more vulnerable to grat thrombosis than renal transplants because the rate of blood low in the transplanted pancreas is slower than that in a transplanted kidney.80,81 Although the clinical signs and symptoms of grat thrombosis are nonspeciic, detection of vascular thrombosis is imperative for both salvaging the transplant and preventing life-threatening sequelae, such as sepsis and cardiovascular collapse. Venous thrombosis, which occurs with an estimated incidence of 5%, is a particular concern because of the increased risk of hemorrhagic pancreatitis, tissue necrosis, infection, thrombus propagation, and pulmonary embolism.81 Grat thrombosis can be categorized as early or late, depending on the time of diagnosis ater surgery. Early grat thrombosis occurs within 1 month of transplantation and is secondary to either microvascular injury during preservation of the grat or technical error during surgery. Late grat thrombosis occurs 1 month ater transplant surgery and is usually caused by alloimmune arteritis, in which gradual occlusion of the small blood vessels eventually culminates in complete proximal vessel occlusion.80 Other technical factors predisposing to grat thrombosis include coagulopathies, long preservation time, poor donor vessels, let-sided grat placement resulting in a deeper anastomosis, and the use of a venous extension grat.81 Prompt surgical intervention may be required depending on the severity of the thrombosis. hrombosis of the grat splenic artery and vein results in infarction of the grat pancreatic body and tail. If there is thrombosis of the grat SMA and SMV, it may result in infarction of the pancreatic head and transplanted duodenum. In the context of acute thrombosis the grat may appear enlarged, whereas in more chronic thrombosis the grat appears difusely atrophic. Venous thrombosis is far more common than arterial thrombosis and is either completely or partially occlusive. It can be localized to the SMV, the splenic vein, or both vessels. A venous thrombosis may form owing to a phlebitis related to an underlying pancreatitis. Alternate mechanisms include stasis caused by a perianastomotic luid collection or a torque on the venous anastomosis related to a shit in position of the grat resulting in stretching or twisting. Stasis in a stump of the SMV distal to the pancreaticoduodenal vessels may be a nidus for venous thrombosis. Venous thrombi within the pancreatic grat may remain localized and not propagate into the portal vein, the iliac vein,

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or the IVC (systemic venous drainage) or the SMV (portal venous drainage). Normal grat function can therefore be maintained.82 However, the potential for propagation of venous thrombi always exists, and if not well seen on ultrasound may need to be imaged dynamically in the venous phase on multiphase computed tomography (CT) or magnetic resonance imaging (MRI). Splenic vein thrombosis results in reversal of arterial diastolic low and absence of splenic venous low on Doppler ultrasound. Difuse narrowing of the transplanted portal vein can be visualized with either technique and is typically seen in association with elevation of venous pressure within the grat. A combination of systemic anticoagulation and/or thrombolytic therapy may be necessary to treat complete splenic vein occlusion.83 Endovascular thrombectomy may also be performed for partial or occlusive thrombus, provided there is no underlying pancreatitis or extrinsic vascular compression.84 Pseudoaneurysms occur at anastomotic sites or elsewhere as a result of pancreatitis or underlying infections or abscess. hey can also occur secondary to biopsy or surgical trauma. he iatrogenic pseudoaneurysms may be seen in association with arteriovenous istulas. Similar to the stump venous thrombi described earlier, stasis in low-low surgically created vascular stumps can occur in peripheral superior mesenteric and splenic arterial segments and contributes to formation of stump thrombi. Arterial thrombosis involves the grat SMA, the grat splenic artery, or the donor Y construct. he pancreas has a smaller microcirculatory blood low in comparison with other grat types, and this increases its risk for thrombosis. It is usually mitigated by the formation of intrapancreatic arterial collaterals, which means that patency of only one allograt artery (SMA or splenic artery) is suicient for grat survival and function. hese collaterals are oten better appreciated on a modality such as CT owing to the relatively diminutive caliber of the vessels. hrombosis is least common in the simultaneous pancreaskidney transplant as compared with the other techniques, as well as being less likely when the systemic-bladder drainage technique is used as compared with the portal-enteric drainage technique. However, kinking of the Y grat is more likely in the portal enteric technique and is related to the length of the vessel (the grat is placed higher in the abdomen). Many of these arterial complications can be managed via endovascular intervention, including coil embolization and covered stents. Surgical resection of aneurysms and grating are usually reserved for patients who have infected grats and pseudoaneurysms in the setting of abscesses in the transplant bed. On ultrasound, occlusive or nonocclusive thrombus may be visualized within the lumen of the transplanted arteries or veins (Fig. 18.63). We have also observed several cases of thrombus occurring at the suture line of blind-ending arteries or veins (Fig. 18.64). On spectral Doppler, no arterial low is detected in transplants with occlusive arterial thrombus. In grats with occlusive venous thrombus, a lack of venous low is detected on spectral tracing, with high-resistance arterial low showing either no low in diastole (RI = 1) or reversal of diastolic low.81 Surgically ligated arteries containing thrombus may show a cyclic pattern of low adjacent to the thrombus, which we presume is secondary

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FIG. 18.63 Graft Thrombosis in Different Patients. (A) Transverse sonogram, (B) sagittal sonogram, and (C) color Doppler image show nonocclusive venous thrombus (arrows). (D) Gray-scale ultrasound (arrow) and (E) correlative CT (arrows) show nonocclusive venous thrombus. (F) Sagittal sonogram shows occlusive arterial thrombus (arrows). (G) Sagittal sonogram, (H) transverse sonogram, and (I) color Doppler image show nonocclusive venous (arrowhead) and arterial (arrow) thrombus in the same transplant.

to local eddy currents, with a normal arterial waveform more proximally.

Arteriovenous Fistula and Pseudoaneurysms Arteriovenous istulas and pseudoaneurysms are rare complications of pancreatic transplants and may be related to the blind ligation of mesenteric vessels along the inferior border of the pancreas during retrieval. In some patients, mycotic pseudoaneurysms may occur in the setting of grat infection.85 On gray-scale ultrasound, arterial malformations may not be detectable. On color Doppler sonography, however, a mosaic of intense colors may be identiied, produced by the tangle of vessels within the malformation and adjacent tissue vibration.

Spectral Doppler ultrasound reveals high-velocity, low-resistance low within the lesion, which is typical of arteriovenous shunting (Fig. 18.65). On gray-scale ultrasound, pseudoaneurysms usually appear as anechoic spherical structures, although mural-based intraluminal thrombus may be detected. On spectral Doppler ultrasound, the classic to-and-fro pattern may be observed.

Rejection Rejection is the most common cause of pancreatic grat loss ater transplantation. his condition afects up to 40% of grats and can be hyperacute, acute, or chronic.77 Early recognition of transplant rejection remains a challenge because clinical

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he usefulness of arterial RIs as an indicator of rejection is controversial. It has been shown that RIs of the arteries supplying the pancreatic transplant cannot diferentiate allograts with mild or moderate rejection from normal transplants without rejection.90 he reason may be that the pancreatic transplant does not contain a discrete investing capsule, and therefore swelling from transplant rejection may not necessarily result in increased parenchymal pressures or elevated vascular resistance.91 Grossly elevated RIs greater than 0.8 have been observed in pancreatic allograts with biopsy-proven acute severe rejection. Although these elevated RIs may be sensitive, they are not speciic in the detection of severe pancreatic transplant rejection.90 Similarly, grat enlargement and heterogeneity may be seen in acute pancreatitis and ischemia. In a small series of patients, CEUS played a useful role in the surveillance of pancreatic grats and in particular helped in the earlier diagnosis of rejection. Time-intensity curves in patients during rejection showed a signiicantly slower ascent and diminished maximum intensity. Overall, there was a signiicantly reduced maximum intensity and time to reach peak intensity. Ater successful treatment of the episode of rejection, these parameters near normalized to initial values. Ultimately, image-guided biopsy is the reference standard for conirming and grading the severity of rejection. FIG. 18.64 Thrombus Adjacent to Suture Line. Echogenic thrombus (arrowhead) at suture line (small arrows) of blind-ending ligated artery. Spectral trace adjacent to thrombus shows to-and-fro waveform (bottom), whereas spectral trace (top) more distally is normal.

parameters used to evaluate pancreas grat dysfunction have low sensitivity and speciicity in detection of rejection. In particular, there is no individual biochemical marker that would permit acute rejection to be distinguished from vascular thrombosis or pancreatitis. Although current advances in immunosuppressives have had an impact on acute rejection rates, chronic rejection remains one of the major causes of long-term grat failure. Hyperacute rejection is rare and occurs in the immediate postsurgical period, usually as a result of preformed circulating cytotoxic antibodies in the recipient’s blood. hrombosis and immediate grat loss occur with this condition. Acute rejection occurs as a result of an autoimmune vasculitis and develops 1 week to 3 months ater transplantation. here is small vessel occlusion, which results in diminished perfusion and long-term infarction if not treated early.86 Recurrent episodes of inadequately treated or unrecognized rejection result in chronic rejection, with progressive endarteritis of small vessels with acinar atrophy, and eventually with ibrosis and parenchymal atrophy. Chronic rejection occurs in 4% to 10% of patients and is seen as gradual decline in exocrine and then endocrine function. On gray-scale ultrasound, the allograt may appear hypoechoic or may contain multiple anechoic regions, and the parenchymal echotexture may be patchy and heterogeneous87,88 (Fig. 18.66). In addition, there may be abnormal grat size, typically enlargement in acute rejection and atrophy in chronic rejection. Pancreatic enlargement in acute rejection has a sensitivity of 58% and a speciicity of 100%.89

Pancreatitis Almost all patients develop symptoms of pancreatitis immediately ater surgery, presumably caused by reperfusion injury and ischemia.91 his typically involves the entire grat. A temporary elevation of serum amylase 48 to 96 hours posttransplantation is therefore common and usually of no clinical consequence. here is also a mild transient elevation in amylase. Focal edema of the donor mesenteric fat attached to the arterial stump of the SMA should not be misdiagnosed as a focal pancreatitis. his inding is related to ligation of the donor’s lymphatic vessels. Other causes of pancreatitis include partial or complete occlusion of the pancreatic duct, poor perfusion of the allograt, and, in patients with systemic venous-bladder drainage, reluxrelated pancreatitis.87 Long term, grat pancreatitis is seen in up to 35% of transplants. Underlying predisposing factors include prolonged warm ischemia time, grat handling, and reperfusion injury. he major diferential diagnoses to consider include grat rejection and ischemia. he ultrasound appearance of pancreatitis in the allograt is similar to that of pancreatitis in the native gland (Fig. 18.67). Gray-scale indings include a normal-sized or bulky edematous pancreas, poorly deined margins, increased echogenicity of the peripancreatic fat secondary to surrounding inlammation, peripancreatic luid, and thickening of the adjacent gut wall. In cases of pancreatitis resulting from ductal obstruction, a dilated pancreatic duct may be observed.87,91 In nonacute cases of pancreatitis, pseudocysts adjacent to or distal from the transplant may be identiied, usually appearing as a well-circumscribed luid collection with minimal adjacent inlammatory changes. Needle aspiration of this structure typically demonstrates luid with high amylase content. Pancreatitis may be seen in association with vascular sequelae such as a focal arterial aneurysm or venous thrombosis. Similarly,

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FIG. 18.65 Pancreas Transplant Vascular Malformations. (A) and (B) Parenchymal arteriovenous malformation (AVM). Transverse gray-scale ultrasound shows no abnormality. (B) Color Doppler ultrasound, however, shows an intense mosaic of color within the pancreas, secondary to a parenchymal AVM. (C)-(F) Transplant-related arteriovenous istula (AVF). Gray-scale (C) and color Doppler (D) show dilated vessels with arterial (E) and mixed atrial and venous (F) waveforms.

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FIG. 18.66 Pancreas Transplant Rejection. (A) Transverse sonogram shows hypoechoic pancreas (arrows). The pancreatic parenchyma is also atrophied. (B) Oblique sonogram shows dilated pancreatic duct (D) secondary to surrounding parenchymal atrophy.

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FIG. 18.67 Pancreatitis. (A) Transverse and (B) oblique images show bulky, edematous allograft. (C) Oblique ultrasound shows echogenic inlamed peripancreatic fat (arrow). (D) This appears as “stranding” in the peripancreatic fat on CT (arrow). P, Pancreas transplant.

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severe grat pancreatitis is associated with a range of complications akin to those seen in a native pancreas such as pancreatic hemorrhage and necrosis, peripancreatic luid collections, pseudocysts, abscesses, and pseudoaneurysms. Ultrasound can be used to guide aspiration of potential luid collections and help discriminate pseudocysts from abscesses or seromas. If infection is demonstrated at the time of ultrasoundguided aspiration, CT is oten performed to assess the grat in its entirety and in particular to evaluate for areas of duct disruption as well as to demonstrate the location of luid collections in relation to the duodenal C loop and duodenojejunostomy. Early luid collections are oten surgically managed.

Fluid Collections Peripancreatic transplant-related luid collections are associated with an increased likelihood of loss of allograt function and overall increased mortality and morbidity. Early diagnosis and characterization of these collections are imperative, because treatment in the acute stages is associated with improved grat function and decreased recipient morbidity.92 In the immediate postoperative period, peritransplant luid may be caused by leakage of pancreatic luid from transected ductules and lymphatics, an inlammatory exudate, blood, or urine (Fig. 18.68). hese collections may require either close serial imaging follow-up or drainage, depending on the clinical status of the patient. Duodenal leaks in systemic venous-bladder drainage transplants occur from dehiscence of the duodenal-bladder anastomosis and result in the formation of urinomas, frequently at the medial aspect of the transplant. Urinomas may also result from infection or necrosis of the grat.92 Duodenal leaks in portal venous-enteric drainage transplants occur at the blind end of the donor duodenum or from the anastomosis with the recipient Roux-en-Y loop. On ultrasound, gross ascites, duodenal wall thickening, or free intraperitoneal air may be observed in patients with breakdown of the duodenal anastomoses. hese leaks may result in overwhelming sepsis and can be life-threatening. Furthermore, the presence of digestive enzymes in contact with the grat may lead to substantial tissue necrosis.91 Patients with pancreatic transplants are also susceptible to infection because of their immunosuppressive therapy, as well as their underlying diabetes mellitus. Abscesses are occasionally identiied and are oten associated with hematomas, urinary tract infections, and pancreatitis. Although gas within a luid collection may indicate the presence of a gas-forming organism, bubbles of air within a collection may also result from the presence of a istula or tissue necrosis in cases of vascular thrombosis. On sonography these collections may demonstrate a thick irregular wall with peripheral hyperemia on Doppler interrogation. If gas is present, it typically is seen as echogenic foci with posterior reverberation artifact. Adjacent changes in the fat include increased echogenicity and luid. In the posttransplant period, the development of a new collection or change in the sonographic morphology of the collection may result from a variety of causes, including infection; malfunction of the pancreatic duct, stent, or external drain; hemorrhage; or associated tissue infarction.92

Miscellaneous Complications Other complications of pancreatic transplants include intussusception of the Roux-en-Y loop, small bowel obstruction from adhesions, internal hernias (due to the surgically created mesenteric defect), and volvulus along the long axis of the grat. Because the patient is immunocompromised, there is a higher incidence of entities such as typhlitis or Clostridium diicile colitis.

POST TRANSPLANT LYMPHOPROLIFERATIVE DISORDER he global improvement in survival ater transplantation can be attributed to a parallel improvement in immunosuppressant regimens. he depressed immune response to oncoviruses such as the Epstein-Barr virus (EBV) results in increased vulnerability of these patients to malignancies that are mediated by such oncoviruses. his contributes to a threefold to eightfold increased malignancy risk in transplant patients as compared with the baseline population.93-95 PTLD is the second most common malignancy in adult transplant patients, following skin malignancy (nonmelanoma).96 PTLD encompasses myriad disease processes ranging from lymphoid hyperplasia to poorly diferentiated lymphoma. Biopsy is required to discriminate among the various subtypes. Many patients are asymptomatic or have vague symptomatology, resulting in a delayed diagnosis. It can be hard to discriminate PTLD from infection or allograt rejection. Imaging is therefore important in establishing the diagnosis, enabling tissue sampling, and monitoring response to treatment. EBV infection is relatively prevalent, with 90% to 95% of adults being seropositive; however, most immunocompetent hosts can eradicate B cells that display EBV antigens by using T cells. However, in immunocompromised patients as well as a small group of immunocompetent hosts, a small number of EBVinfected B cells escape and survive with resultant latent EBV infection.97 Ater solid organ transplantation, cytotoxic EBV-speciic T cells may be completely lost within 6 months of transplantation as a result of immunosuppressive medication.98 Latently infected B cells have the potential to proliferate, resulting in PTLD.99 A variety of genetic mutations (including p53, NRAS) can result in PTLD. hese genes are involved in the division, proliferation, and death of cells. Overproduction of cytokines such as interleukin-6 has also been implicated in the genesis of PTLD. Similarly, CMV-seronegative patients have a higher risk of developing PTLD ater solid organ transplantation.100 he incidence of PTLD is thought to be related to the degree of immunosuppression and the type of allograt. he aggressive immunosuppressive therapy required to prevent heart-lung transplant rejection has resulted in a reported incidence of PTLD as high as 4.6%. However, the milder immunosuppression used in patients with liver transplant or renal transplant has resulted in a lower incidence of PTLD, reported as 2.2% and 1%, respectively.101,102 In addition, the numbers of lymphoid aggregates are higher in intestinal and lung transplants, both of which are associated with some of the highest incidences of PTLD.103 It is therefore

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FIG. 18.68 Fluid Collections. (A)-(C) Hematoma. (A) Sagittal and (B) transverse sonograms show complex collection with internal echoes and strands. (C) Correlative CT shows hematoma in left upper quadrant that extends to pancreas (P). (D)-(I) Pseudocysts in three patients. Patient 1: (D) Sagittal sonogram shows complex epigastric cyst with internal septation. Patient 2: (E) Sagittal sonogram shows complex collection adjacent to pancreas (arrowheads). (F) Correlative CT scan shows collection extending into pancreatic head (P) and associated with free luid (arrows). Patient 3: (G) Sagittal sonogram shows large pseudocyst with internal echoes surrounding pancreatic tail (P). (H) and (I) Seroma. Transverse sonogram and correlative CT scan show large, anechoic cystic structure surrounding pancreatic body (P). The wall enhanced on CT scan. The collection was sterile on aspiration.

not surprising that agents that suppress T-cell activity are associated with a higher risk of PTLD. By the same token, a larger total number of immunosuppressant agents used by a patient may result in an increased risk of PTLD.104 he incidence of PTLD is bimodal, with the initial peak in the irst year ater transplantation and the second peak approximately 4 to 5 years ater transplantation.105 Biologically, the two peaks have a very diferent clinical course. he early-onset disease has a more favorable course, is pleomorphic in subtype, and has a positive response to reducing the level of immunosuppression.

Late-onset disease is more commonly seen in conjunction with EBV infection, a monomorphic subtype, and an aggressive disease course. here is a higher mortality, and the disease is oten resistant to chemotherapy.106 PTLD can be categorized depending on its primary location into either nodal disease (22%) or extranodal disease (81%). Nodal disease is either mediastinal or retroperitoneal in location. he involved lymph nodes have an abnormal appearance, showing a hypoechoic thickened cortex with an absent or lattened fatty hilum (Figs. 18.69 to 18.72). Extranodal disease

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FIG. 18.69 Renal Posttransplant Lymphoproliferative Disorder in Two Patients. Patient 1: (A) Sagittal sonogram shows iniltrative mass (arrows) in renal hilum. (B) Six months later, the mass (arrowheads) has iniltrated into the renal cortex. (C) Correlative CT shows hilar mass iniltrating into renal cortex. Patient 2: (D) Sagittal and (E) transverse sonograms show a hypoechoic to anechoic structure with low-level echoes (arrows) in the renal hilum that could be interpreted as a complex cyst. (F) Contrast-enhanced MRI shows that this structure represents a solid mass (arrows).

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FIG. 18.70 Renal Posttransplant Lymphoproliferative Disorder (PTLD): Extrarenal Manifestations in Two Patients. Patient 1: (A) Sagittal sonogram shows a hypoechoic renal hilar mass (arrows). (B) Sagittal and (C) transverse sonograms of the spleen show a mass in the hilum (arrows) as well as an intraparenchymal mass (arrowheads). Patient 2: (D) Sagittal sonogram shows hilar mass (arrows). (E) Transverse sonogram shows that mass (arrows) encases transplanted renal artery. (F) Correlative magnetic resonance image shows hilar mass (arrows) encasing renal vessels. (G) Transverse sonogram shows malignant-appearing hepatic nodule (arrow). (H) Sagittal sonogram shows malignant lymphadenopathy. (I) CT shows tonsillar adenopathy in Waldeyer ring (arrows) secondary to PTLD.

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FIG. 18.71 Renal Posttransplant Lymphoproliferative Disorder (PTLD): Mimicker. (A) Sagittal and (B) transverse sonograms show a poorly deined, hypoechoic region in the renal sinus (arrows), potentially representing an iniltrative mass. (C) Correlative magnetic resonance scan shows that the hypoechoic region represents sinus fat. K, Kidney.

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G FIG. 18.72 Hepatic Posttransplant Lymphoproliferative Disorder (PTLD) in Three Patients. Patient 1: (A) Oblique sonogram shows malignant mass (arrows) encasing and narrowing main portal vein. (B) Correlative CT shows mass iniltrating liver. Patient 2: (C) Transverse and (D) sagittal color Doppler sonograms show avascular solid nodules (arrow). (E) Correlative CT scan shows solid hypovascular masses (arrows). Patient 3: (F) Transverse sonogram shows thick-walled gut (white arrow) adjacent to inlamed echogenic fat (black arrows). (G) Correlative CT scan shows thick-walled loop of small bowel (arrows).

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by deinition involves three main sites—the central nervous system, solid organs, or the gastrointestinal tract. he liver is the most common site of intraabdominal involvement, occurring in 30% to 45% of patients with PTLD. In rare cases, intraosseous lesions may be present, with imaging features on CT and MRI similar to those of metastatic disease, infection, or primary bone lymphoma. Overall, PTLD should be considered in the diferential diagnosis of any transplant patient with lymphadenopathy or a new lesion within a solid viscus or the skeletal system.107-110 When the solid organs are involved, there are four main patterns of disease: 1. Iniltrative pattern: here is an ill-deined mass or masses that are extrinsic to the hilum and can result in secondary mass efect and/or vascular compromise. For instance, within the liver it may cause biliary obstruction and obstruction of blood low within the periportal space. In renal involvement the mass typically is located extrinsic to the renal pelvis with resultant mass efect and obstruction of the vessels and the collecting system. In both instances the mass is usually relatively hypoenhancing but luorodeoxyglucose (FDG) avid on positron emission tomography (PET) imaging. 2. Parenchymal pattern: his is characterized by multiple lesions that are disseminated throughout the afected organ. hese also tend to be hypoenhancing. In the lung they are typically solid and may rarely cavitate. here may also be ill-deined alveolar iniltrates. 3. Solitary mass: A solitary mass in the afected organ is seen on ultrasound as a hypoechoic lesion with no Doppler signal on color Doppler imaging. Calciication is unusual but seen in the context of posttreatment changes or tumor necrosis. 4. Iniltrative lesion: his lesion involves the organ in question but also extends to involve regional structures such as the chest, abdominal wall, and adjacent solid organs. As a secondary manifestation, there may be dysfunction of the other organ(s) that are involved. Pancreatic PTLD tends to produce difuse glandular enlargement, with an appearance that is indistinguishable from pancreatitis or rejection.111 Gastrointestinal disease can involve either bowel or the peritoneal cavity. When there is peritoneal disease, it can be nodular or difusely iniltrating.112 PTLD involving the gastrointestinal tract is seen in association with mural thickening, aneurysmal dilatation, ulceration, intussusception, and polypoidal lesions. Perforation is a rare manifestation of intestinal PTLD; the decline in perforation rates has been attributed to improved diagnosis and treatment of PTLD. As with any other lymphomatous-type lesions of the gut, obstruction of the bowel segments is rare.

Treatment Options Stratiication and patient management are determined by the subtype of PTLD, the distribution of disease, and the type of allograt. Potential management options include modiication of immunosuppression, chemotherapy, radiation, and rituximab therapy as well as surgical resection of isolated lesions. Rituximab

is a monoclonal antibody against B cell receptors, has a low toxicity proile, and has a response rate on the order of 60%. Preservation of grat function is an important goal of management while treating the PTLD.113,114 PET-CT has a pivotal role to play in monitoring response to therapy, particularly in patients in whom there are persistent focal lesions. In this scenario, FDG uptake allows discrimination between residual tumor and ibrosis. REFERENCES 1. Takemoto S, Terasaki PI, Cecka JM, et al. Survival of nationally shared, HLA-matched kidney transplants from cadaveric donors. he UNOS Scientiic Renal Transplant Registry. N Engl J Med. 1992;327(12):834-839. 2. Berthoux FC, Jones EH, Mehls O, Valderrabano F. Transplantation report. 1: Renal transplantation in recipients aged 60 years or older at time of grating. he EDTA-ERA Registry. European Dialysis and Transplant Association–European Renal Association. Nephrol Dial Transplant. 1996;11(Suppl. 1):37-40. 3. Cattral MS, Bigam DL, Hemming AW, et al. Portal venous and enteric exocrine drainage versus systemic venous and bladder exocrine drainage of pancreas grats: clinical outcome of 40 consecutive transplant recipients. Ann Surg. 2000;232(5):688-695. 4. United Network for Organ Sharing. National data. Transplants by organ type January 1, 1988–June 30, 2016. Available from: https://www.unos.org/ data. Accessed 2016 July 18. 5. Crossin JD, Muradali D, Wilson SR. US of liver transplants: normal and abnormal. Radiographics. 2003;23(5):1093-1114. 6. Mazzaferro V, Regalia E, Doci R, et al. Liver transplantation for the treatment of small hepatocellular carcinomas in patients with cirrhosis. N Engl J Med. 1996;334(11):693-699. 7. Quiroga S, Sebastia MC, Margarit C, et al. Complications of orthotopic liver transplantation: spectrum of indings with helical CT. Radiographics. 2001;21(5):1085-1102. 8. Nghiem HV. Imaging of hepatic transplantation. Radiol Clin North Am. 1998;36(2):429-443. 9. Kamel IR, Kruskal JB, Raptopoulos V. Imaging for right lobe living donor liver transplantation. Semin Liver Dis. 2001;21(2):271-282. 10. Wolfsen HC, Porayko MK, Hughes RH, et al. Role of endoscopic retrograde cholangiopancreatography ater orthotopic liver transplantation. Am J Gastroenterol. 1992;87(8):955-960. 11. Keogan MT, McDermott VG, Price SK, et al. he role of imaging in the diagnosis and management of biliary complications ater liver transplantation. AJR Am J Roentgenol. 1999;173(1):215-219. 12. Letourneau JG, Castaneda-Zuniga WR. he role of radiology in the diagnosis and treatment of biliary complications ater liver transplantation. Cardiovasc Intervent Radiol. 1990;13(4):278-282. 13. Barton P, Maier A, Steininger R, et al. Biliary sludge ater liver transplantation: 1. Imaging indings and eicacy of various imaging procedures. AJR Am J Roentgenol. 1995;164(4):859-864. 14. Miller WJ, Campbell WL, Zajko AB, et al. Obstructive dilatation of extrahepatic recipient and donor bile ducts complicating orthotopic liver transplantation: imaging and laboratory indings. AJR Am J Roentgenol. 1991;157(1):29-32. 15. Zajko AB, Campbell WL, Bron KM, et al. Cholangiography and interventional biliary radiology in adult liver transplantation. AJR Am J Roentgenol. 1985;144(1):127-133. 16. Sheng R, Zajko AB, Campbell WL, Abu-Elmagd K. Biliary strictures in hepatic transplants: prevalence and types in patients with primary sclerosing cholangitis vs those with other liver diseases. AJR Am J Roentgenol. 1993;161(2):297-300. 17. Ward EM, Wiesner RH, Hughes RW, Krom RA. Persistent bile leak ater liver transplantation: biloma drainage and endoscopic retrograde cholangiopancreatographic sphincterotomy. Radiology. 1991;179(3):719720. 18. McDonald V, Matalon TA, Patel SK, et al. Biliary strictures in hepatic transplantation. J Vasc Interv Radiol. 1991;2(4):533-538.

CHAPTER 18 19. Yeh BM, Coakley FV, Westphalen AC, et al. Predicting biliary complications in right lobe liver transplant recipients according to distance between donor’s bile duct and corresponding hepatic artery. Radiology. 2007;242(1): 144-151. 20. Sheng R, Sammon JK, Zajko AB, Campbell WL. Bile leak ater hepatic transplantation: cholangiographic features, prevalence, and clinical outcome. Radiology. 1994;192(2):413-416. 21. Gow PJ, Chapman RW. Liver transplantation for primary sclerosing cholangitis. Liver. 2000;20(2):97-103. 22. Chen LY, Goldberg HI. Sclerosing cholangitis: broad spectrum of radiographic features. Gastrointest Radiol. 1984;9(1):39-47. 23. Ciaccia D, Branch MS. Disorders of the biliary tree related to liver transplantation. In: DiMarino AJBS, editor. Gastrointestinal diseases: an endoscopic approach. Boston: Blackwell Scientiic; 1997. p. 918-927. 24. Zajko AB, Campbell WL, Bron KM, et al. Diagnostic and interventional radiology in liver transplantation. Gastroenterol Clin North Am. 1988;17(1):105-143. 25. Starzl TE, Putnam CW, Hansbrough JF, et al. Biliary complications ater liver transplantation: with special reference to the biliary cast syndrome and techniques of secondary duct repair. Surgery. 1977;81(2):212-221. 26. Ito K, Siegelman ES, Stolpen AH, Mitchell DG. MR imaging of complications ater liver transplantation. AJR Am J Roentgenol. 2000;175(4):11451149. 27. Dodd GD 3rd, Memel DS, Zajko AB, et al. Hepatic artery stenosis and thrombosis in transplant recipients: Doppler diagnosis with resistive index and systolic acceleration time. Radiology. 1994;192(3):657-661. 28. Horrow MM, Blumenthal BM, Reich DJ, Manzarbeitia C. Sonographic diagnosis and outcome of hepatic artery thrombosis ater orthotopic liver transplantation in adults. AJR Am J Roentgenol. 2007;189(2):346-351. 29. Gunsar F, Rolando N, Pastacaldi S, et al. Late hepatic artery thrombosis ater orthotopic liver transplantation. Liver Transpl. 2003;9(6):605-611. 30. Wozney P, Zajko AB, Bron KM, et al. Vascular complications ater liver transplantation: a 5-year experience. AJR Am J Roentgenol. 1986;147(4): 657-663. 31. De Gaetano AM, Cotroneo AR, Maresca G, et al. Color Doppler sonography in the diagnosis and monitoring of arterial complications ater liver transplantation. J Clin Ultrasound. 2000;28(8):373-380. 32. Park YS, Kim KW, Lee SJ, et al. Hepatic arterial stenosis assessed with Doppler US ater liver transplantation: frequent false-positive diagnoses with tardus parvus waveform and value of adding optimal peak systolic velocity cutof. Radiology. 2011;260(3):884-891. 33. Garcia-Criado A, Gilabert R, Salmeron JM, et al. Signiicance of and contributing factors for a high resistive index on Doppler sonography of the hepatic artery immediately ater surgery: prognostic implications for liver transplant recipients. AJR Am J Roentgenol. 2003;181(3): 831-838. 34. De Candia A, Como G, Tedeschi L, et al. Color Doppler sonography of hepatic artery reconstruction in liver transplantation. J Clin Ultrasound. 2002;30(1):12-17. 35. Dravid VS, Shapiro MJ, Needleman L, et al. Arterial abnormalities following orthotopic liver transplantation: arteriographic indings and correlation with Doppler sonographic indings. AJR Am J Roentgenol. 1994;163(3): 585-589. 36. Fukuzawa K, Schwartz ME, Katz E, et al. he arcuate ligament syndrome in liver transplantation. Transplantation. 1993;56(1):223-224. 37. Langnas AN, Marujo W, Stratta RJ, et al. Hepatic allograt rescue following arterial thrombosis. Role of urgent revascularization. Transplantation. 1991;51(1):86-90. 38. Raby N, Karani J, homas S, et al. Stenoses of vascular anastomoses ater hepatic transplantation: treatment with balloon angioplasty. AJR Am J Roentgenol. 1991;157(1):167-171. 39. Chong WK, Beland JC, Weeks SM. Sonographic evaluation of venous obstruction in liver transplants. AJR Am J Roentgenol. 2007;188(6): W515-W521. 40. Pfammatter T, Williams DM, Lane KL, et al. Suprahepatic caval anastomotic stenosis complicating orthotopic liver transplantation: treatment with percutaneous transluminal angioplasty, Wallstent placement, or both. AJR Am J Roentgenol. 1997;168(2):477-480.

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41. Kubo T, Shibata T, Itoh K, et al. Outcome of percutaneous transhepatic venoplasty for hepatic venous outlow obstruction ater living donor liver transplantation. Radiology. 2006;239(1):285-290. 42. Ko EY, Kim TK, Kim PN, et al. Hepatic vein stenosis ater living donor liver transplantation: evaluation with Doppler US. Radiology. 2003;229(3): 806-810. 43. Ferris JV, Baron RL, Marsh Jr JW, et al. Recurrent hepatocellular carcinoma ater liver transplantation: spectrum of CT indings and recurrence patterns. Radiology. 1996;198(1):233-238. 44. Baxter GM. Ultrasound of renal transplantation. Clin Radiol. 2001; 56(10):802-818. 45. Brown ED, Chen MY, Wolfman NT, et al. Complications of renal transplantation: evaluation with US and radionuclide imaging. Radiographics. 2000;20(3):607-622. 46. Kobayashi K, Censullo ML, Rossman LL, et al. Interventional radiologic management of renal transplant dysfunction: indications, limitations, and technical considerations. Radiographics. 2007;27:1109-1130. 47. Memel DS, Dodd GD 3rd, Shah AN, et al. Imaging of en bloc renal transplants: normal and abnormal postoperative indings. AJR Am J Roentgenol. 1993;160(1):75-81. 48. O’Neill WC, Baumgarten DA. Ultrasonography in renal transplantation. Am J Kidney Dis. 2002;39(4):663-678. 49. Lachance SL, Adamson D, Barry JM. Ultrasonically determined kidney transplant hypertrophy. J Urol. 1988;139(3):497-498. 50. Babcock DS, Slovis TL, Han BK, et al. Renal transplants in children: long-term follow-up using sonography. Radiology. 1985;156(1):165-167. 51. Absy M, Metreweli C, Matthews C, Al Khader A. Changes in transplanted kidney volume measured by ultrasound. Br J Radiol. 1987;60(714): 525-529. 52. American College of Radiology (ACR), Society for Pediatric Radiology (SPR), Society of Radiologists in Ultrasound (SRU), American Institute of Ultrasound in Medicine (AIUM). AIUM practice guideline for the performance of an ultrasound examination of solid-organ transplants. J Ultrasound Med. 2014;33(7):1309-1320. 53. Tublin ME, Bude RO, Platt JF. Review. he resistive index in renal Doppler sonography: where do we stand? AJR Am J Roentgenol. 2003;180(4): 885-892. 54. Weber TM, Lockhart ME. Renal transplant complications. Abdom Imaging. 2013;38(5):1144-1154. 55. Rigg KM. Renal transplantation: current status, complications and prevention. J Antimicrob Chemother. 1995;36(Suppl. B):51-57. 56. Pirsch JD, Ploeg RJ, Gange S, et al. Determinants of grat survival ater renal transplantation. Transplantation. 1996;61(11):1581-1586. 57. Akbar SA, Jafri SZ, Amendola MA, et al. Complications of renal transplantation. Radiographics. 2005;25(5):1335-1356. 58. Dodd GD 3rd, Tublin ME, Shah A, Zajko AB. Imaging of vascular complications associated with renal transplants. AJR Am J Roentgenol. 1991;157(3): 449-459. 59. Jordan ML, Cook GT, Cardella CJ. Ten years of experience with vascular complications in renal transplantation. J Urol. 1982;128(4):689-692. 60. Hanto DW, Simmons RL. Renal transplantation: clinical considerations. Radiol Clin North Am. 1987;25(2):239-248. 61. Baxter GM, Ireland H, Moss JG, et al. Colour Doppler ultrasound in renal transplant artery stenosis: which Doppler index? Clin Radiol. 1995;50(9): 618-622. 62. de Morais RH, Muglia VF, Mamere AE, et al. Duplex Doppler sonography of transplant renal artery stenosis. J Clin Ultrasound. 2003;31(3): 135-141. 63. Tublin ME, Dodd GD 3rd. Sonography of renal transplantation. Radiol Clin North Am. 1995;33(3):447-459. 64. Penny MJ, Nankivell BJ, Disney AP, et al. Renal grat thrombosis. A survey of 134 consecutive cases. Transplantation. 1994;58(5):565-569. 65. Baxter GM, Morley P, Dall B. Acute renal vein thrombosis in renal allograts: new Doppler ultrasonic indings. Clin Radiol. 1991;43(2): 125-127. 66. Reuther G, Wanjura D, Bauer H. Acute renal vein thrombosis in renal allograts: detection with duplex Doppler US. Radiology. 1989;170(2): 557-558.

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67. Lockhart ME, Wells CG, Morgan DE, et al. Reversed diastolic low in the renal transplant: perioperative implications versus transplants older than 1 month. AJR Am J Roentgenol. 2008;190(3):650-655. 68. Pozniak MA, Dodd GD 3rd, Kelcz F. Ultrasonographic evaluation of renal transplantation. Radiol Clin North Am. 1992;30(5):1053-1066. 69. Middleton WD, Kellman GM, Melson GL, Madrazo BL. Postbiopsy renal transplant arteriovenous istulas: color Doppler US characteristics. Radiology. 1989;171(1):253-257. 70. Huang MW, Muradali D, hurston WA, et al. Uterine arteriovenous malformations: gray-scale and Doppler US features with MR imaging correlation. Radiology. 1998;206(1):115-123. 71. Rahmouni A, Bargoin R, Herment A, et al. Color Doppler twinkling artifact in hyperechoic regions. Radiology. 1996;199(1):269-271. 72. Letourneau JG, Day DL, Ascher NL, Castaneda-Zuniga WR. Imaging of renal transplants. AJR Am J Roentgenol. 1988;150(4):833-838. 73. Silver TM, Campbell D, Wicks JD, et al. Peritransplant luid collections. Ultrasound evaluation and clinical signiicance. Radiology. 1981;138(1): 145-151. 74. Data from the Organ Procurement and Transplantation Network and the U.S. Scientiic Registry of Transplant Recipients. In United Network for Organ Sharing and Scientiic Registry Data, 2008. Available from: https:// optn.transplant.hrsa.gov/data/view-data-reports/national-data/#. 75. White SA, Shaw JA, Sutherland DE. Pancreas transplantation. Lancet. 2009;373(9677):1808-1817. 76. Hariharan S, Pirsch JD, Lu CY, et al. Pancreas ater kidney transplantation. J Am Soc Nephrol. 2002;13(4):1109-1118. 77. Pozniak MA, Propeck PA, Kelcz F, Sollinger H. Imaging of pancreas transplants. Radiol Clin North Am. 1995;33(3):581-594. 78. Freund MC, Steurer W, Gassner EM, et al. Spectrum of imaging indings ater pancreas transplantation with enteric exocrine drainage: Part 1, posttransplantation anatomy. AJR Am J Roentgenol. 2004;182(4):911-917. 79. Kersting S, Ludwig S, Ehehalt F, et al. Contrast-enhanced ultrasonography in pancreas transplantation. Transplantation. 2013;95(1):209-214. 80. Krebs TL, Daly B, Wong JJ, et al. Vascular complications of pancreatic transplantation: MR evaluation. Radiology. 1995;196(3):793-798. 81. Foshager MC, Hedlund LJ, Troppmann C, et al. Venous thrombosis of pancreatic transplants: diagnosis by duplex sonography. AJR Am J Roentgenol. 1997;169(5):1269-1273. 82. Vandermeer FQ, Manning MA, Frazier AA, Wong-You-Cheong JJ. Imaging of whole-organ pancreas transplants. Radiographics. 2012;32(2): 411-435. 83. Stockland AH, Willingham DL, Paz-Fumagalli R, et al. Pancreas transplant venous thrombosis: role of endovascular interventions for grat salvage. Cardiovasc Intervent Radiol. 2009;32(2):279-283. 84. Barth MM, Khwaja K, Faintuch S, Rabkin D. Transarterial and transvenous embolotherapy of arteriovenous istulas in the transplanted pancreas. J Vasc Interv Radiol. 2008;19(8):1231-1235. 85. Hagspiel KD, Nandalur K, Burkholder B, et al. Contrast-enhanced MR angiography ater pancreas transplantation: normal appearance and vascular complications. AJR Am J Roentgenol. 2005;184(2):465-473. 86. Drachenberg CB, Papadimitriou JC. Spectrum of histopathological changes in pancreas allograt biopsies and relationship to grat loss. Transplant Proc. 2007;39(7):2326-2328. 87. Patel B, Markivee CR, Mahanta B, et al. Pancreatic transplantation: scintigraphy, US, and CT. Radiology. 1988;167(3):685-687. 88. Yuh WT, Wiese JA, Abu-Yousef MM, et al. Pancreatic transplant imaging. Radiology. 1988;167(3):679-683. 89. Wong JJ, Krebs TL, Klassen DK, et al. Sonographic evaluation of acute pancreatic transplant rejection: morphology—Doppler analysis versus guided percutaneous biopsy. AJR Am J Roentgenol. 1996;166(4):803-807. 90. Aideyan OA, Foshager MC, Benedetti E, et al. Correlation of the arterial resistive index in pancreas transplants of patients with transplant rejection. AJR Am J Roentgenol. 1997;168(6):1445-1447. 91. Heyneman LE, Keogan MT, Tuttle-Newhall JE, et al. Pancreatic transplantation using portal venous and enteric drainage: the postoperative appearance of a new surgical procedure. J Comput Assist Tomogr. 1999;23:283290.

92. Patel BK, Garvin PJ, Aridge DL, et al. Fluid collections developing ater pancreatic transplantation: radiologic evaluation and intervention. Radiology. 1991;181(1):215-220. 93. Howard RJ, Patton PR, Reed AI, et al. he changing causes of grat loss and death ater kidney transplantation. Transplantation. 2002;73(12): 1923-1928. 94. Briggs JD. Causes of death ater renal transplantation. Nephrol Dial Transplant. 2001;16(8):1545-1549. 95. Apel H, Walschburger-Zorn K, Haberle L, et al. De novo malignancies in renal transplant recipients: experience at a single center with 1882 transplant patients over 39 yr. Clin Transplant. 2013;27(1):E30-E36. 96. Penn I. Post-transplant malignancy: the role of immunosuppression. Drug Saf. 2000;23(2):101-113. 97. Parker A, Bowles K, Bradley JA, et al. Diagnosis of post-transplant lymphoproliferative disorder in solid organ transplant recipients—BCSH and BTS guidelines. Br J Haematol. 2010;149(5):675-692. 98. Haque T, Crawford DH. Role of donor versus recipient type Epstein-Barr virus in post-transplant lymphoproliferative disorders. Springer Semin Immunopathol. 1998;20(3-4):375-387. 99. Babcock GJ, Decker LL, Freeman RB, horley-Lawson DA. Epstein-Barr virus–infected resting memory B cells, not proliferating lymphoblasts, accumulate in the peripheral blood of immunosuppressed patients. J Exp Med. 1999;190(4):567-576. 100. Opelz G, Daniel V, Naujokat C, et al. Efect of cytomegalovirus prophylaxis with immunoglobulin or with antiviral drugs on post-transplant non-Hodgkin lymphoma: a multicentre retrospective analysis. Lancet Oncol. 2007;8(3): 212-218. 101. Nalesnik MA, Makowka L, Starzl TE. he diagnosis and treatment of posttransplant lymphoproliferative disorders. Curr Probl Surg. 1988;25(6): 367-472. 102. Vrachliotis TG, Vaswani KK, Davies EA, et al. CT indings in posttransplantation lymphoproliferative disorder of renal transplants. AJR Am J Roentgenol. 2000;175(1):183-188. 103. Tsao L, Hsi ED. he clinicopathologic spectrum of posttransplantation lymphoproliferative disorders. Arch Pathol Lab Med. 2007;131(8): 1209-1218. 104. Opelz G, Dohler B. Lymphomas ater solid organ transplantation: a collaborative transplant study report. Am J Transplant. 2004;4(2):222-230. 105. Vegso G, Hajdu M, Sebestyen A. Lymphoproliferative disorders ater solid organ transplantation—classiication, incidence, risk factors, early detection and treatment options. Pathol Oncol Res. 2011;17(3):443-454. 106. Dotti G, Fiocchi R, Motta T, et al. Epstein-Barr virus–negative lymphoproliferate disorders in long-term survivors ater heart, kidney, and liver transplant. Transplantation. 2000;69(5):827-833. 107. Donnelly LF, Frush DP, Marshall KW, White KS. Lymphoproliferative disorders: CT indings in immunocompromised children. AJR Am J Roentgenol. 1998;171(3):725-731. 108. Penn I. Cancers complicating organ transplantation. N Engl J Med. 1990;323(25):1767-1769. 109. Pickhardt PJ, Siegel MJ. Abdominal manifestations of posttransplantation lymphoproliferative disorder. AJR Am J Roentgenol. 1998;171(4): 1007-1013. 110. Kaushik S, Fulcher AS, Frable WJ, May DA. Posttransplantation lymphoproliferative disorder: osseous and hepatic involvement. AJR Am J Roentgenol. 2001;177(5):1057-1059. 111. Meador TL, Krebs TL, Cheong JJ, et al. Imaging features of posttransplantation lymphoproliferative disorder in pancreas transplant recipients. AJR Am J Roentgenol. 2000;174(1):121-124. 112. Pickhardt PJ, Siegel MJ. Posttransplantation lymphoproliferative disorder of the abdomen: CT evaluation in 51 patients. Radiology. 1999;213(1): 73-78. 113. Allen U, Hebert D, Moore D, et al. Epstein-Barr virus–related post-transplant lymphoproliferative disease in solid organ transplant recipients, 1988-97: a Canadian multi-centre experience. Pediatr Transplant. 2001;5(3): 198-203. 114. Swinnen LJ. Diagnosis and treatment of transplant-related lymphoma. Ann Oncol. 2000;11(Suppl. 1):45-48.

PART THREE: Small Parts, Carotid Artery, and Peripheral Vessel Sonography CHAPTER

19

The Thyroid Gland Luigi Solbiati, J. William Charboneau, Vito Cantisani, Carl Reading, and Giovanni Mauri

SUMMARY OF KEY POINTS • Ultrasound is the best imaging modality to study the thyroid gland for both diffuse and nodular disease. • The overwhelming majority of thyroid nodules are benign. Thyroid cancer is rare and accounts for less than 1% of all malignant neoplasms. • Approximately 80% of nodular thyroid disease is caused by hyperplasia. When hyperplasia leads to an overall increase in size or volume of the gland, the term “goiter” is used. • Most hyperplastic or adenomatous nodules are isoechoic compared with normal thyroid tissue, but may become hyperechoic because of the numerous interfaces between cells and colloid substance. • Hyperfunctioning (autonomous) nodules often exhibit an abundant perinodular and intranodular vascularity. • Purely anechoic areas are caused by serous or colloid luid. • Adenomas represent only 5% to 10% of all nodular disease of the thyroid and are seven times more common in women than men. In general, the cytologic features of follicular adenomas are indistinguishable from those of follicular carcinoma.

• Solid consistency, hypoechogenicity, microcalciications, taller-than-wide appearance, hypervascularity, irregular margins, invasion of adjacent structures, and presence of cervical lymph node metastases are suspicious signs of thyroid malignancy. • Ultrasound-guided ine-needle aspiration is the most effective method for diagnosing malignancy in a thyroid nodule. • After partial or near-total thyroidectomy for carcinoma, sonography is the preferred method for follow-up, by detecting residual, recurrent, or metastatic disease in the neck. • The Thyroid Imaging Reporting and Data System (TIRADS) can be used to stratify the risk of malignancy of a thyroid nodule according to its ultrasonographic characteristics. • Ultrasound-guided ablation with chemical agents (ethanol) or thermal energy (radiofrequency and laser ablation) can be used to treat thyroid adenoma, benign cold nodules, and even nodal metastases of thyroid cancers.

CHAPTER OUTLINE INSTRUMENTATION AND TECHNIQUE ANATOMY CONGENITAL THYROID ABNORMALITIES NODULAR THYROID DISEASE Pathologic Features and Sonographic Correlates Hyperplasia and Goiter Adenoma

B

Carcinoma Lymphoma Thyroid Metastases Fine-Needle Aspiration Biopsy Sonographic Applications Detection of Thyroid Masses Differentiation of Benign and Malignant Nodules Thyroid Imaging Reporting and Data System

ecause of the supericial location of the thyroid gland, highresolution real-time gray-scale and color Doppler sonography can demonstrate normal thyroid anatomy and pathologic conditions with remarkable clarity. As a result, ultrasound plays an increasingly important role in the diagnostic evaluation of thyroid disease, although it is only one of several diagnostic methods currently available. To use ultrasound efectively and economically, it is important to understand its current capabilities and limitations.

Contrast-Enhanced Ultrasound and Elastography Guidance for Needle Biopsy Guidance for Percutaneous Treatment The Incidentally Detected Nodule DIFFUSE THYROID DISEASE Acknowledgment

INSTRUMENTATION AND TECHNIQUE High-frequency transducers (7.5-15.0 MHz) currently provide both deep ultrasound penetration—up to 5 cm—and highdeinition images, with a resolution of 0.5 to 1.0 mm. No other clinically used imaging method can achieve this degree of spatial resolution. Linear array transducers with either rectangular or trapezoidal scan format are preferred to sector transducers because of the wider near ield of view and the capability to combine

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Submandibular gland Internal jugular vein

A

Carotid artery

Strap muscles

Trachea

Sternocleidomastoid muscle Clavicle

Thyroid gland Internal jugular vein

FIG. 19.1 Cervical “Map.” Such diagrams help communicate relationships of pathology to clinicians and serve as a reference for follow-up examinations.

VII Cervical vertebrae Common carotid artery Esophagus

high-frequency gray-scale and color Doppler images. he thyroid gland is one of the most vascular organs of the body. As a result, Doppler examination may provide useful diagnostic information in some thyroid diseases. Two newer techniques used for the sonographic study of the thyroid gland are contrast-enhanced sonography and elastography. Contrast-enhanced sonography using second-generation contrast agents and very low mechanical index can provide useful information for the diagnosis of select cases of nodular disease and for ultrasound-guided therapeutic procedures. Elastography is based on the principle that when body tissues are compressed, the soter parts deform more easily than the harder parts. he amount of displacement at various depths is determined by the ultrasound signals relected by tissues before and ater they are compressed, and the corresponding strains are calculated from these displacements and displayed visually. he patient is typically examined in the supine position, with the neck extended. A small pad may be placed under the shoulders to provide better exposure of the neck, particularly in patients with a short, stocky habitus. he thyroid gland must be examined thoroughly in both transverse and longitudinal planes. Imaging of the lower poles can be enhanced by asking the patient to swallow, which momentarily raises the thyroid gland in the neck. he entire gland, including the isthmus, must be examined. he examination must also be extended laterally to include the region of the carotid artery and jugular vein to identify enlarged jugular chain lymph nodes, superiorly to visualize submandibular adenopathy, and inferiorly to deine any pathologic supraclavicular lymph nodes. In addition to the images recorded during the examination, some operators include in the permanent record a diagrammatic representation of the neck showing the location(s) of any abnormal indings (Fig. 19.1). his cervical “map” helps to communicate the anatomic relationships of the pathology more clearly to the referring clinician and the patient. It also serves as a useful reference for the radiologist and sonographer for follow-up examinations.

FIG. 19.2 Normal Thyroid Gland. (A) Transverse sonogram made with 7.5-MHz linear array transducer. (B) Corresponding anatomic drawing. C, Common carotid artery; J, jugular vein; Tr, tracheal air shadow.

Longus colli muscle

B

ANATOMY he thyroid gland is located in the anteroinferior part of the neck (infrahyoid compartment) in a space outlined by muscle, trachea, esophagus, carotid arteries, and jugular veins (Fig. 19.2). he thyroid gland is made up of two lobes located along either side of the trachea and connected across the midline by the isthmus, a thin structure draping over the anterior tracheal wall at the level of the junction of the middle and lower thirds of the thyroid gland. From 10% to 40% of normal patients have a small thyroid (pyramidal) lobe arising superiorly from the isthmus and lying in front of the thyroid cartilage.1 It can be regularly visualized in younger patients, but it undergoes progressive atrophy in adulthood and becomes invisible. he size and shape of the thyroid lobes vary widely in normal patients. In tall individuals the lateral lobes have a longitudinally elongated shape on the sagittal scans, whereas in shorter individuals the gland is more oval. In the newborn the thyroid gland is 18 to 20 mm long, with an anteroposterior (AP) diameter of 8 to 9 mm. By 1 year of age, the mean length is 25 mm and AP diameter is 12 to 15 mm.2 In adults the mean length is approximately 40 to 60 mm, with mean AP diameter of 13 to 18 mm. he mean thickness of the isthmus is 4 to 6 mm.3 Sonography is an accurate method for calculating thyroid volume. In about one-third of cases, the sonographic measurement of volume difers from the estimated physical size on examination.4 hyroid volume measurements may be useful for goiter size determination to assess the need for surgery, permit calculation of the dose of iodine-131 (131I) needed for treating thyrotoxicosis, and evaluate response to suppression treatments.5 hyroid volume can be calculated with linear parameters or more precisely with mathematical formulas. Among the linear

CHAPTER 19

A

The Thyroid Gland

693

B

C

D

FIG. 19.3 Volume Measurement of Thyroid Gland. (A) Transverse and (B) longitudinal images show calipers at the boundaries of thyroid gland. C, Carotid artery; Tr, trachea air shadow. The calculated thyroid volume is based on the ellipsoid formula with a correction factor (length × width × thickness × 0.52 for each lobe). In this case, the volume is 10 mL (or grams), which is within normal limits for this female patient. (C) Images from real-time three-dimensional study of normal thyroid lobe, visualized simultaneously in axial (top left), longitudinal (top right), and coronal (bottom left) planes. (D) Volumetric reconstruction of gland.

parameters, the AP diameter is the most precise because it is relatively independent of possible dimensional asymmetry between the two lobes. When the AP diameter is more than 2 cm, the thyroid gland may be considered “enlarged.” he most common mathematical method to calculate thyroid volume is based on the ellipsoid formula with a correction factor (length × width × thickness × 0.529 for each lobe)6 (Fig. 19.3A-B). With use of this method, the mean estimated error is approximately 15%. he most precise mathematical method is the integration of the cross-sectional areas of the thyroid gland, achieved through evenly spaced sonographic scans.7 With this method the mean estimated error is 5% to 10%.8 Modern threedimensional (3-D) ultrasound technology allows one to simultaneously obtain the three orthogonal planes of thyroid lobes and then to calculate the volume either automatically or manually9 (Fig. 19.3C-D). In neonates, thyroid volume ranges from 0.40 to 1.40 mL, increasing by 1.0 to 1.3 mL for each 10 kg of body weight, up to a normal volume in adults of 10 to 11 ± 3 mL.7 In general, thyroid volume is larger in patients living in regions with iodine deiciency and in patients who have acute hepatitis or chronic

renal failure. Volume is smaller in patients who have chronic hepatitis or have been treated with thyroxine or radioactive iodine.5,7 Normal thyroid parenchyma has a homogeneous, medium- to high-level echogenicity that makes detection of focal cystic or hypoechoic thyroid lesions relatively easy in most cases. he thin, hyperechoic line around the thyroid lobes is the capsule, which is oten identiiable on ultrasound. It may become calciied in patients who have uremia or disorders of calcium metabolism. With currently available high-sensitivity Doppler instruments, the rich vascularity of the gland can be seen homogeneously distributed throughout the entire parenchyma (Fig. 19.4). he superior thyroid artery and vein are found at the upper pole of each lobe. he inferior thyroid vein is found at the lower pole (Fig. 19.5), and the inferior thyroid artery is located posterior to the lower third of each lobe. he mean diameter of the arteries is 1 to 2 mm; the lower veins can be up to 8 mm in diameter. Normally, peak systolic velocities reach 20 to 40 cm/ sec in the major thyroid arteries and 15 to 30 cm/sec in intraparenchymal arteries. hese are the highest velocities found in blood vessels supplying supericial organs.

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he sternohyoid and omohyoid muscles (strap muscles) are seen as thin, hypoechoic bands anterior to the thyroid gland (see Fig. 19.2). he sternocleidomastoid muscle is seen as a larger oval band that lies lateral to the thyroid gland. An important anatomic landmark is the longus colli muscle, located posterior to each thyroid lobe, in close contact with the prevertebral space.

he recurrent laryngeal nerve and the inferior thyroid artery pass in the angle among the trachea, esophagus, and thyroid lobe. On longitudinal scans, the recurrent laryngeal nerve and inferior thyroid artery may be seen between the thyroid lobe and esophagus on the let and between the thyroid lobe and longus colli muscle on the right. he esophagus, primarily a midline structure, may be found laterally and is usually on the let side. It is clearly identiied by the target appearance of bowel in the transverse plane and by its peristaltic movements when the patient swallows.

CONGENITAL THYROID ABNORMALITIES

FIG. 19.4 Normal Thyroid Vascularity on Power Doppler Ultrasound.

Congenital conditions of the thyroid gland include aplasia of one lobe or the whole gland, varying degrees of hypoplasia, and ectopia (Fig. 19.6). Sonography can be used to help establish the diagnosis of hypoplasia by demonstrating a diminutive gland. High-frequency ultrasound can also be used in the study of congenital hypothyroidism (CH), a relatively common disorder occurring in about 1 in 3000 to 4000 live births. Determining the cause of CH (dysgenesis, dyshormonogenesis, or pituitary or hypothalamic hypothyroidism) is clinically important because prognosis and therapy difer. Early initiation of therapy can prevent mental retardation and delayed bone development.10,11 Measurement of thyroid lobes can be used to diferentiate aplasia (absent gland) from goitrous hypothyroidism (gland enlargement). Radionuclide scans are more oten used to detect ectopic thyroid tissue (e.g., in a lingual or suprahyoid position).

NODULAR THYROID DISEASE FIG. 19.5 Normal Inferior Thyroid Vein. Longitudinal power Doppler image shows a large inferior thyroid vein with associated normal venous spectral waveform.

A

Many thyroid diseases can manifest clinically with one or more thyroid nodules. Such nodules represent common and controversial clinical problems. Epidemiologic studies estimate that

B

FIG. 19.6 Congenital Thyroid Abnormalities. (A) Hypoplasia of right thyroid lobe. C, Carotid artery; Tr, tracheal air shadow. (B) Ectopic (sublingual) thyroid gland. Transverse ultrasound image inferior to the base of the tongue shows a U-shaped parenchymal structure.

CHAPTER 19 4% to 7% of adults in the United States have palpable thyroid nodules, with women afected more frequently than men.12,13 Exposure to ionizing radiation increases the incidence of benign and malignant nodules, with 20% to 30% of a radiation-exposed population having palpable thyroid disease.14,15 Although nodular thyroid disease is relatively common, thyroid cancer is rare and accounts for less than 1% of all malignant neoplasms.16 he overwhelming majority of thyroid nodules are benign. he clinical challenge is to distinguish the few clinically signiicant malignant nodules from the many benign nodules and thus identify patients who need surgical excision. his task is complicated because nodular disease of the thyroid gland oten is clinically occult ( 1.5 cm

3 2 1 0

Mortality

1973 1976 1979 1982 1985 1988 1991 1994 1997 2000 Year FIG. 19.43 Thyroid Cancer: Incidence Versus Mortality. Although the rate of occurrence of thyroid cancer has more than doubled in the last 30 years, the mortality rate is unchanged over that period. (Adapted from Davies L, Welch HG. Increasing incidence of thyroid cancer in the United States, 1973-2002. JAMA. 2006;295[18]:2164-2167.138)

surgery for nodule excision based on positive, suspicious, or nondiagnostic results, and most of these nodules are benign.101,142,143 Of these surgical patients, only 15% to 32% have cancer.101,142 herefore the majority of patients who undergo surgery for thyroid nodule excision will have had an operation for clinically insigniicant, benign nodular disease. he potential cost of the FNA biopsy workup of these nodules must be considered. For discussion purposes, assume that 1 million of the estimated 300 million people in the United States undergo a high-frequency ultrasound thyroid examination, and that one or more thyroid nodules are detected in approximately 40%. herefore 400,000 people will have one or more thyroid nodules detected by ultrasound imaging. Assuming a cost of approximately $1500 for an ultrasound-guided FNA and cytologic analysis, $600 million could theoretically be spent to exclude or detect thyroid cancer in this group. If 18% of these FNA biopsies result in suspicious or nondiagnostic results, 72,000 procedures could occur at a cost of almost $20,000 each, for an additional cost of $1.44 billion. Finally, approximately 5%, or almost 3600 patients, could experience signiicant postsurgical morbidity, including hoarseness, hypoparathyroidism, and long-lasting pain.144 Clearly, this type of aggressive management of thyroid nodules would entail massive health care expenditures and could have an extremely negative clinical impact.145 4. Which incidentally discovered nodules should be pursued? Because of the many nodules detected on ultrasound, the therapeutic approach should allow most patients with clinically signiicant cancers to go on to further investigations. More important, it should allow most patients with benign lesions to avoid further costly, potentially harmful workup. With this goal in mind, many practices, including ours, have found that it is both impractical and imprudent to pursue the diagnosis for most of the small nodules detected incidentally on ultrasound. If technically possible, we usually obtain FNA biopsy of lesions that exhibit sonographic features strongly associated with malignancy, such as marked hypoechogenicity, taller-than-wide shape, and thick irregular margins, as well as lesions containing microcalciications.

Nodules that have malignant features (marked hypoechogenicity, taller-than-wide shape, thick irregular margins, and/or calciications or microcalciications)

DIFFUSE THYROID DISEASE Several thyroid diseases are characterized by difuse rather than focal involvement. his usually results in generalized enlargement of the gland (goiter) and no palpable nodules. Speciic conditions that produce such difuse enlargement include chronic autoimmune lymphocytic thyroiditis (Hashimoto thyroiditis), colloid or adenomatous goiter, and Graves disease. hese conditions are usually diagnosed on the basis of clinical and laboratory indings and occasionally FNA biopsy. Sonography is seldom indicated. However, high-resolution sonography can be helpful when the underlying difuse disease causes asymmetrical thyroid enlargement, which suggests a mass in the larger lobe. he sonographic inding of generalized parenchymal abnormality may alert the clinician to consider difuse thyroid disease as the underlying cause. FNA, with sonographic guidance if necessary, can be performed if a nodule is detected. Recognition of difuse thyroid enlargement on sonography can oten be facilitated by noting the thickness of the isthmus, normally a thin bridge of tissue measuring only a few millimeters in AP dimension. With difuse thyroid enlargement, the isthmus may be up to 1 cm or more in thickness.

Diffuse Thyroid Diseases Acute suppurative thyroiditis Subacute granulomatous thyroiditis Hashimoto thyroiditis (chronic lymphocytic thyroiditis) Adenomatous or colloid goiter Painless (silent) thyroiditis

Each type of thyroiditis, including acute suppurative thyroiditis, subacute granulomatous thyroiditis (de Quervain disease), and chronic lymphocytic thyroiditis (Hashimoto disease) has distinctive clinical and laboratory features.146 Acute suppurative thyroiditis is a rare inlammatory disease usually caused by bacterial

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infection and afecting children. Sonography can be useful in select patients to detect the development of a frank thyroid abscess. he infection usually begins in the perithyroidal sot tissues. On ultrasound images, an abscess is seen as a poorly deined, hypoechoic heterogeneous mass with internal debris, with or without septa and gas. Adjacent inlammatory nodes are oten present. Subacute granulomatous thyroiditis or De Quervain disease is a spontaneously remitting inlammatory disease probably caused by viral infection. he clinical indings include fever, enlargement of the gland, and pain on palpation. Sonographically, the gland may appear enlarged and hypoechoic, with normal or decreased vascularity caused by difuse edema of the gland, or the process may appear as focal hypoechoic regions147,148 (Fig. 19.44). Although usually not necessary, sonography can be used to assess evolution of de Quervain disease ater medical therapy. he most common type of thyroiditis is chronic autoimmune lymphocytic thyroiditis, or Hashimoto thyroiditis. It typically occurs as a painless, difuse enlargement of the thyroid gland in a young or middle-aged woman, oten associated with hypothyroidism. It is the most common cause of hypothyroidism in North America. Patients with this autoimmune disease develop antibodies to their own thyroglobulin as well as to the major

B

FIG. 19.44 Focal Areas of Subacute Thyroiditis. (A) Longitudinal power Doppler image of the thyroid gland shows two poorly deined hypoechoic areas (arrows) caused by subacute thyroiditis at ine-needle aspiration. (B) Longitudinal image of a different patient shows poorly deined hypoechoic area (arrows). (C) This area has returned to normal on follow-up examination 4 weeks later after medical therapy.

enzyme of thyroid hormonogenesis, thyroid peroxidase. he typical sonographic appearance of Hashimoto thyroiditis is difuse, coarsened, parenchymal echotexture, generally more hypoechoic than a normal thyroid144 (Fig. 19.45). In most cases the gland is enlarged. Multiple, discrete hypoechoic micronodules from 1 to 6 mm in diameter are strongly suggestive of chronic thyroiditis; this appearance has been called micronodulation (see Fig. 19.45, Video 19.7). Micronodulation is a highly sensitive sign of chronic thyroiditis, with a positive predictive value of 94.7%.149 Histologically, micronodules represent lobules of thyroid parenchyma that have been iniltrated by lymphocytes and plasma cells. hese lobules are surrounded by multiple linear echogenic ibrous septations (Fig. 19.46). hese ibrotic septations may give the parenchyma a “pseudolobulated” appearance. Both benign and malignant thyroid nodules may coexist with chronic lymphocytic thyroiditis, and FNA is oten necessary to establish the inal diagnosis150 (Figs. 19.47 to 19.49). As with other autoimmune disorders, there is an increased risk of malignancy, with a B-cell malignant lymphoma most oten arising within the gland. he vascularity on color Doppler imaging is normal or decreased in most patients with the diagnosis of Hashimoto thyroiditis (see Fig. 19.45). Occasionally, hypervascularity similar to the “thyroid inferno” of Graves disease occurs. One study

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E

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FIG. 19.45 Hashimoto Thyroiditis: Micronodularity. (A) Transverse and (B) longitudinal images of the left lobe demonstrate multiple small hypoechoic nodules that are lymphocyte iniltration of the parenchyma. (C) and (D) Longitudinal images of another patient show multiple tiny hypoechoic nodules and increased low on power Doppler. This increased low may indicate an acute phase of the thyroiditis. (E) and (F) Longitudinal images of a different patient show multiple tiny hypoechoic nodules and decreased low on color Doppler scan. The blood low is normal or diminished in most cases of Hashimoto thyroiditis.

suggested that hypervascularity occurs when hypothyroidism develops, perhaps related to stimulation from the associated high serum levels of thyrotropin (TSH).151 Oten, cervical lymphadenopathy is present, most evident near the lower pole of the thyroid gland (Fig. 19.50). he end stage of chronic thyroiditis is atrophy, when the thyroid gland is small, with poorly deined margins and heterogeneous texture caused by progressive ibrosis. Blood

low signals are absent. Occasionally, discrete nodules occur, and FNA biopsy is needed to establish the diagnosis.150 Painless (silent) thyroiditis has the typical histologic and sonographic pattern of chronic autoimmune thyroiditis (hypoechogenicity, micronodulation, and ibrosis), but clinical indings resemble classic subacute thyroiditis, with the exception of node tenderness. Moderate hyperthyroidism with thyroid

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FIG. 19.46 Hashimoto Thyroiditis: Coarse Septations. (A) Transverse dual image of the thyroid shows marked diffuse enlargement of both lobes and the isthmus. Multiple linear bright echoes throughout the hypoechoic parenchyma are caused by lymphocytic iniltration of the gland with coarse septations from ibrous bands. Tr, Tracheal air shadow. (B) Transverse and (C) longitudinal images of another patient demonstrate linear echogenic septations throughout the gland. (D) Longitudinal image of another patient shows thicker echogenic linear areas that separate hypoechoic regions.

FIG. 19.47 Hashimoto Thyroiditis: Nodule. Longitudinal image shows a discrete hypoechoic nodule (arrows) that proved to be Hashimoto thyroiditis at ine-needle aspiration biopsy.

FIG. 19.48 Hashimoto Thyroiditis With Papillary Thyroid Cancer. Longitudinal image shows classic Hashimoto thyroiditis (micronodularity) and a hypoechoic dominant nodule (arrow) in the upper pole caused by papillary thyroid carcinoma. A dominant nodule in Hashimoto thyroiditis should be considered “indeterminate” and ineneedle aspiration performed.

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FIG. 19.49 Lymphoma in Hashimoto Thyroiditis. Transverse image of the left lobe shows diffuse hypoechoic enlargement caused by lymphoma in a gland with Hashimoto thyroiditis. Tr, Tracheal air shadow.

B FIG. 19.51 Hyperthyroidism: Graves Disease. (A) Transverse dual image of the thyroid gland shows marked diffuse enlargement of both thyroid lobes and the isthmus. The gland is diffusely hypoechoic. (B) Transverse color Doppler image of the left lobe shows increased vascularity, indicating an acute stage of the Graves disease process. Tr, Trachea.

FIG. 19.50 Hashimoto Thyroiditis With Hyperplastic Enlarged Lymph Nodes. Longitudinal image shows micronodularity of Hashimoto thyroiditis and an enlarged lymph node (arrow) inferior to the lower pole.

enlargement usually occurs in the early phase, in some cases followed by hypothyroidism of variable degree. In postpartum thyroiditis the progression to hypothyroidism is more common. In most cases the disease spontaneously remits within 3 to 6 months, and the gland may return to a normal appearance. Although the appearance of difuse parenchymal inhomogeneity and micronodularity is typical of Hashimoto thyroiditis, other difuse thyroid diseases, most frequently multinodular or adenomatous goiter, may have a similar sonographic appearance. Most patients with adenomatous goiter have multiple discrete nodules separated by otherwise normal-appearing thyroid parenchyma (see Fig. 19.29); others have enlargement with rounding of the poles of the gland, difuse parenchymal inhomogeneity, and no recognizable normal tissue. Adenomatous goiter afects women three times more oten than men.

Graves disease is a common difuse abnormality of the thyroid gland and is usually biochemically characterized by hyperfunction (thyrotoxicosis). he echotexture may be more inhomogeneous than in difuse goiter, mainly because of numerous large, intraparenchymal vessels. Furthermore, especially in young patients, the parenchyma may be difusely hypoechoic because of the extensive lymphocytic iniltration or the predominantly cellular content of the parenchyma, which becomes almost devoid of colloid substance. Color Doppler sonography oten demonstrates a hypervascular pattern referred to as the thyroid inferno (Fig. 19.51). Spectral Doppler will oten demonstrate peak systolic velocities exceeding 70 cm/sec, which is the highest velocity found in thyroid disease. here is no correlation between the degree of thyroid hyperfunction assessed by laboratory studies and the extent of hypervascularity or blood low velocities. Previous studies have shown that Doppler analysis can be used to monitor therapeutic response in patients with Graves disease.152 A signiicant decrease in low velocities in the superior and inferior thyroid arteries ater medical treatment has been reported. he rarest type of inlammatory thyroid disease is invasive ibrous thyroiditis, also called Riedel struma.146 his disease primarily afects women and oten progresses to complete destruction of the gland. Some cases may be associated with

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B

C FIG. 19.52 Riedel Struma (Invasive Fibrous Thyroiditis). (A) Transverse dual-color Doppler ultrasound image of the thyroid shows a diffuse hypoechoic process in the right lobe extending around the common carotid artery (arrows). Tr, Trachea. (B) Longitudinal power Doppler image of the right common carotid artery shows a hypoechoic soft tissue mass (arrows) encasing the vessel. (C) Contrast-enhanced CT scan shows mild enlargement of the right thyroid lobe and soft tissue thickening (arrows) around the right common carotid artery. Incidentally noted is dilation of the air-illed esophagus (E).

mediastinal or retroperitoneal ibrosis or sclerosing cholangitis. In the few cases of invasive ibrous thyroiditis examined sonographically, the gland was difusely enlarged and had an inhomogeneous parenchymal echotexture. he primary reason for sonography is to check for extrathyroid extension of the inlammatory process, with encasement of the adjacent vessels (Fig. 19.52). Such information can be particularly useful in surgical planning. Open biopsy is generally required to distinguish this condition from anaplastic thyroid carcinoma. he sonographic indings in these two diseases may be identical.

Acknowledgment he authors would like to acknowledge the aid of Maija Radzina, MD, PhD, Institute of Diagnostic Radiology, Paula Stradins Clinical University Hospital, Riga, Latvia.

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78. Clark KJ, Cronan JJ, Scola FH. Color Doppler sonography: anatomic and physiologic assessment of the thyroid. J Clin Ultrasound. 1995;23(4): 215-223. 79. Shimamoto K, Endo T, Ishigaki T, et al. hyroid nodules: evaluation with color Doppler ultrasonography. J Ultrasound Med. 1993;12(11):673-678. 80. Frates MC, Benson CB, Doubilet PM, et al. Can color Doppler sonography aid in the prediction of malignancy of thyroid nodules? J Ultrasound Med. 2003;22(2):127-131. 81. Xie C, Cox P, Taylor N, LaPorte S. Ultrasonography of thyroid nodules: a pictorial review. Insights Imaging. 2016;7(1):77-86. 82. Horvath E, Majlis S, Rossi R, et al. An ultrasonogram reporting system for thyroid nodules stratifying cancer risk for clinical management. J Clin Endocrinol Metab. 2009;94(5):1748-1751. 83. Kwak JY, Han KH, Yoon JH, et al. hyroid imaging reporting and data system for US features of nodules: a step in establishing better stratiication of cancer risk. Radiology. 2011;260(3):892-899. 84. Cantisani V, Bertolotto M, Weskott HP, et al. Growing indications for CEUS: he kidney, testis, lymph nodes, thyroid, prostate, and small bowel. Eur J Radiol. 2015;84(9):1675-1684. 85. Yu D, Han Y, Chen T. Contrast-enhanced ultrasound for diferentiation of benign and malignant thyroid lesions: meta-analysis. Otolaryngol Head Neck Surg. 2014;151(6):909-915. 86. Rago T, Vitti P. Role of thyroid ultrasound in the diagnostic evaluation of thyroid nodules. Best Pract Res Clin Endocrinol Metab. 2008;22(6): 913-928. 87. Rubaltelli L, Corradin S, Dorigo A, et al. Diferential diagnosis of benign and malignant thyroid nodules at elastosonography. Ultraschall Med. 2009;30(2):175-179. 88. Cantisani V, Consorti F, Guerrisi A, et al. Prospective comparative evaluation of quantitative-elastosonography (Q-elastography) and contrast-enhanced ultrasound for the evaluation of thyroid nodules: preliminary experience. Eur J Radiol. 2013;82(11):1892-1898. 89. Cantisani V, Lodise P, Di Rocco G, et al. Diagnostic accuracy and interobserver agreement of quasistatic ultrasound elastography in the diagnosis of thyroid nodules. Ultraschall Med. 2015;36(2):162-167. 90. Cosgrove D, Piscaglia F, Bamber J, et al. EFSUMB guidelines and recommendations on the clinical use of ultrasound elastography. Part 2: Clinical applications. Ultraschall Med. 2013;34(3):238-253. 91. Liu BJ, Li DD, Xu HX, et al. Quantitative shear wave velocity measurement on acoustic radiation force impulse elastography for diferential diagnosis between benign and malignant thyroid nodules: a meta-analysis. Ultrasound Med Biol. 2015;41(12):3035-3043. 92. Nell S, Kist JW, Debray TP, et al. Qualitative elastography can replace thyroid nodule ine-needle aspiration in patients with sot thyroid nodules. A systematic review and meta-analysis. Eur J Radiol. 2015;84(4):652-661. 93. Razavi SA, Hadduck TA, Sadigh G, Dwamena BA. Comparative efectiveness of elastographic and B-mode ultrasound criteria for diagnostic discrimination of thyroid nodules: a meta-analysis. AJR Am J Roentgenol. 2013;200(6): 1317-1326. 94. Ueno E, Ito A. Diagnosis of breast cancer by elasticity imaging. Eizo Joho Med. 2004;36:2-6. 95. Ferrari FS, Megliola A, Scorzelli A, et al. Ultrasound examination using contrast agent and elastosonography in the evaluation of single thyroid nodules: preliminary results. J Ultrasound. 2008;11(2):47-54. 96. Hong Y, Liu X, Li Z, et al. Real-time ultrasound elastography in the diferential diagnosis of benign and malignant thyroid nodules. J Ultrasound Med. 2009;28(7):861-867. 97. Lyshchik A, Higashi T, Asato R, et al. hyroid gland tumor diagnosis at US elastography. Radiology. 2005;237(1):202-211. 98. Rago T, Santini F, Scutari M, et al. Elastography: new developments in ultrasound for predicting malignancy in thyroid nodules. J Clin Endocrinol Metab. 2007;92(8):2917-2922. 99. Quinn SF, Nelson HA, Demlow TA. hyroid biopsies: ine-needle aspiration biopsy versus spring-activated core biopsy needle in 102 patients. J Vasc Interv Radiol. 1994;5(4):619-623. 100. Taki S, Kakuda K, Kakuma K, et al. hyroid nodules: evaluation with US-guided core biopsy with an automated biopsy gun. Radiology. 1997;202(3): 874-877.

101. Goellner JR, Gharib H, Grant CS, Johnson DA. Fine needle aspiration cytology of the thyroid, 1980 to 1986. Acta Cytol. 1987;31(5):587-590. 102. Kuna SK, Bracic I, Tesic V, et al. Ultrasonographic diferentiation of benign from malignant neck lymphadenopathy in thyroid cancer. J Ultrasound Med. 2006;25(12):1531-1537. 103. Lyshchik A, Higashi T, Asato R, et al. Cervical lymph node metastases: diagnosis at sonoelastography—initial experience. Radiology. 2007;243(1): 258-267. 104. Snozek CL, Chambers EP, Reading CC, et al. Serum thyroglobulin, highresolution ultrasound, and lymph node thyroglobulin in diagnosis of differentiated thyroid carcinoma nodal metastases. J Clin Endocrinol Metab. 2007;92(11):4278-4281. 105. Miller JM, Hamburger JI, Taylor CI. Is needle aspiration of the cystic thyroid nodule efective and safe treatment? In: Hamburger JI, Miller JM, editors. Controversies in clinical thyroidology. New York: Springer-Verlag; 1981. 106. Verde G, Papini E, Pacella CM, et al. Ultrasound guided percutaneous ethanol injection in the treatment of cystic thyroid nodules. Clin Endocrinol (Oxf). 1994;41(6):719-724. 107. Yasuda K, Ozaki O, Sugino K, et al. Treatment of cystic lesions of the thyroid by ethanol instillation. World J Surg. 1992;16(5):958-961. 108. Antonelli A, Campatelli A, Di Vito A, et al. Comparison between ethanol sclerotherapy and emptying with injection of saline in treatment of thyroid cysts. Clin Investig. 1994;72(12):971-974. 109. Lee SJ, Ahn IM. Efectiveness of percutaneous ethanol injection therapy in benign nodular and cystic thyroid diseases: long-term follow-up experience. Endocr J. 2005;52(4):455-462. 110. Raggiunti B, Fiore G, Mongia A, et al. A 7-year follow-up of patients with thyroid cysts and pseudocysts treated with percutaneous ethanol injection: volume change and cost analysis. J Ultrasound. 2009;12(3):107-111. 111. Livraghi T, Paracchi A, Ferrari C, et al. Treatment of autonomous thyroid nodules with percutaneous ethanol injection: preliminary results. Work in progress. Radiology. 1990;175(3):827-829. 112. Cerbone G, Spiezia S, Colao A, et al. Percutaneous ethanol injection under power Doppler ultrasound assistance in the treatment of autonomously functioning thyroid nodules. J Endocrinol Invest. 1999;22(10):752-759. 113. Goletti O, Monzani F, Caraccio N, et al. Percutaneous ethanol injection treatment of autonomously functioning single thyroid nodules: optimization of treatment and short term outcome. World J Surg. 1992;16(4):784-789. 114. Livraghi T, Paracchi A, Ferrari C, et al. Treatment of autonomous thyroid nodules with percutaneous ethanol injection: 4-year experience. Radiology. 1994;190(2):529-533. 115. Ozdemir H, Ilgit ET, Yucel C, et al. Treatment of autonomous thyroid nodules: safety and eicacy of sonographically guided percutaneous injection of ethanol. AJR Am J Roentgenol. 1994;163(4):929-932. 116. Pacella CM, Papini E, Bizzarri G, et al. Assessment of the efect of percutaneous ethanol injection in autonomously functioning thyroid nodules by colour-coded duplex sonography. Eur J Radiol. 1995;5:395-400. 117. Baek JH, Moon WJ, Kim YS, et al. Radiofrequency ablation for the treatment of autonomously functioning thyroid nodules. World J Surg. 2009;33(9): 1971-1977. 118. Deandrea M, Limone P, Basso E, et al. US-guided percutaneous radiofrequency thermal ablation for the treatment of solid benign hyperfunctioning or compressive thyroid nodules. Ultrasound Med Biol. 2008;34(5): 784-791. 119. Chianelli M, Bizzarri G, Todino V, et al. Laser ablation and 131-iodine: a 24-month pilot study of combined treatment for large toxic nodular goiter. J Clin Endocrinol Metab. 2014;99(7):E1283-E1286. 120. Goletti O, Monzani F, Lenziardi M, et al. Cold thyroid nodules: a new application of percutaneous ethanol injection treatment. J Clin Ultrasound. 1994;22(3):175-178. 121. Dossing H, Bennedbaek FN, Karstrup S, Hegedus L. Benign solitary solid cold thyroid nodules: ultrasound-guided interstitial laser photocoagulation— initial experience. Radiology. 2002;225:53-57. 122. Pacella CM, Bizzarri G, Spiezia S, et al. hyroid tissue: US-guided percutaneous laser thermal ablation. Radiology. 2004;232(1):272-280. 123. Papini E, Guglielmi R, Bizzarri G, et al. Treatment of benign cold thyroid nodules: a randomized clinical trial of percutaneous laser ablation versus levothyroxine therapy or follow-up. hyroid. 2007;17(3):229-235.

CHAPTER 19 124. Pacella CM, Mauri G, Achille G, et al. Outcomes and risk factors for complications of laser ablation for thyroid nodules: a multicenter study on 1531 patients. J Clin Endocrinol Metab. 2015;100(10):3903-3910. 125. Jeong WK, Baek JH, Rhim H, et al. Radiofrequency ablation of benign thyroid nodules: safety and imaging follow-up in 236 patients. Eur Radiol. 2008;18(6):1244-1250. 126. Dupuy DE, Monchik JM, Decrea C, Pisharodi L. Radiofrequency ablation of regional recurrence from well-diferentiated thyroid malignancy. Surgery. 2001;130(6):971-977. 127. Lewis BD, Hay ID, Charboneau JW, et al. Percutaneous ethanol injection for treatment of cervical lymph node metastases in patients with papillary thyroid carcinoma. AJR Am J Roentgenol. 2002;178(3):699-704. 128. Fukunari N. PEI therapy for thyroid lesions. Biomed Pharmacother. 2002;56:79-82. 129. Kim BM, Kim MJ, Kim EK, et al. Controlling recurrent papillary thyroid carcinoma in the neck by ultrasonography-guided percutaneous ethanol injection. Eur Radiol. 2008;18(4):835-842. 130. Kim JH, Yoo WS, Park YJ, et al. Eicacy and safety of radiofrequency ablation for treatment of locally recurrent thyroid cancers smaller than 2 cm. Radiology. 2015;276(3):909-918. 131. Mauri G, Cova L, Tondolo T, et al. Percutaneous laser ablation of metastatic lymph nodes in the neck from papillary thyroid carcinoma: preliminary results. J Clin Endocrinol Metab. 2013;98(7):E1203-E1207. 132. Papini E, Bizzarri G, Bianchini A, et al. Percutaneous ultrasound-guided laser ablation is efective for treating selected nodal metastases in papillary thyroid cancer. J Clin Endocrinol Metab. 2013;98(1):E92-E97. 133. Mazzaferri EL. Managing small thyroid cancers. JAMA. 2006;295(18): 2179-2182. 134. Horlocker T, Hay I, James E. Prevalence of incidental nodular thyroid disease detected during high-resolution parathyroid ultrasonography. In: MedeirosNeto G, Gaitan E, editors. Frontiers in thyroidology. New York: New York: Plenum; 1986. p. 1209-1312. 135. Cronan JJ. hyroid nodules: is it time to turn of the US machines? Radiology. 2008;247(3):602-604. 136. Hay ID, Bergstralh EJ, Goellner JR, et al. Predicting outcome in papillary thyroid carcinoma: development of a reliable prognostic scoring system in a cohort of 1779 patients surgically treated at one institution during 1940 through 1989. Surgery. 1993;114(6):1050-1057.

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137. Harach HR, Franssila KO, Wasenius VM. Occult papillary carcinoma of the thyroid. A “normal” inding in Finland. A systematic autopsy study. Cancer. 1985;56(3):531-538. 138. Davies L, Welch HG. Increasing incidence of thyroid cancer in the United States, 1973-2002. JAMA. 2006;295(18):2164-2167. 139. Ross DS. Editorial: predicting thyroid malignancy. J Clin Endocrinol Metab. 2006;91(11):4253-4255. 140. Burch HB. Evaluation and management of the solid thyroid nodule. Endocrinol Metab Clin North Am. 1995;24(4):663-710. 141. Goellner J. Fine-needle aspiration of the thyroid gland. In: Erosan YS, Boniglio TA, editors. Fine-needle aspiration of subcutaneous organs and masses. Philadelphia: Lippincott-Raven; 1996. p. 81-98. 142. Haas S, Trujillo A, Kunstle J. Fine needle aspiration of thyroid nodules in a rural setting. Am J Med. 1993;94(4):357-361. 143. Spiliotis J, Scopa CD, Gatopoulou C, et al. Diagnosis of thyroid cancer in southwestern Greece. Bull Cancer. 1991;78(10):953-959. 144. Songun I, Kievit J, Wobbes T, et al. Extent of thyroidectomy in nodular thyroid disease. Eur J Surg. 1999;165(9):839-842. 145. Reading CC, Charboneau JW, Hay ID, Sebo TJ. Sonography of thyroid nodules: a “classic pattern” diagnostic approach. Ultrasound Q. 2005;21(3): 157-165. 146. Hay ID. hyroiditis: a clinical update. Mayo Clin Proc. 1985;60(12): 836-843. 147. Adams H, Jones MC. Ultrasound appearances of de Quervain’s thyroiditis. Clin Radiol. 1990;42(3):217-218. 148. Birchall IW, Chow CC, Metreweli C. Ultrasound appearances of de Quervain’s thyroiditis. Clin Radiol. 1990;41(1):57-59. 149. Yeh HC, Futterweit W, Gilbert P. Micronodulation: ultrasonographic sign of Hashimoto thyroiditis. J Ultrasound Med. 1996;15(12):813819. 150. Takashima S, Matsuzuka F, Nagareda T, et al. hyroid nodules associated with Hashimoto thyroiditis: assessment with US. Radiology. 1992;185(1): 125-130. 151. Lagalla R, Caruso G, Benza I, et al. [Echo-color Doppler in the study of hypothyroidism in the adult]. Radiol Med. 1993;86(3):281-283. 152. Castagnone D, Rivolta R, Rescalli S, et al. Color Doppler sonography in Graves’ disease: value in assessing activity of disease and predicting outcome. AJR Am J Roentgenol. 1996;166(1):203-207.

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The Parathyroid Glands Bonnie J. Huppert and Carl Reading

SUMMARY OF KEY POINTS • In the vast majority of cases, primary hyperparathyroidism is caused by hyperfunction of a single parathyroid gland due to adenoma, much less commonly due to multiple gland involvement. • Surgical removal of the abnormal gland is the only deinitive treatment for primary hyperparathyroidism, and selective, minimally invasive surgical techniques are most commonly used for irst-time surgery. • The role of parathyroid imaging is not in the diagnosis of primary hyperparathyroidism but rather to provide accurate adenoma localization to successfully direct selective surgical parathyroid resection. • When used by an experienced examiner, parathyroid sonography can provide high-resolution anatomic imaging

with good sensitivity and accuracy which is noninvasive, lacks radiation exposure, is relatively low cost, and has the added ability to assess for concomitant thyroid disease prior to surgery. • In persistent or recurrent hyperparathyroidism, liberal use of multimodality preoperative imaging is particularly beneicial prior to reoperation. • In selected cases, ultrasound can also be used to guide biopsy of suspected parathyroid adenomas to provide preoperative conirmation and to guide ablation of abnormal parathyroid glands in patients who are not surgical candidates.

CHAPTER OUTLINE EMBRYOLOGY AND ANATOMY PRIMARY HYPERPARATHYROIDISM Prevalence Diagnosis Pathology Treatment SONOGRAPHIC APPEARANCE Shape Echogenicity and Internal Architecture Vascularity Size Multiple Gland Disease Carcinoma

H

ADENOMA LOCALIZATION Sonographic Examination and Typical Locations Ectopic Locations Retrotracheal/Retroesophageal Adenoma Mediastinal Adenoma Intrathyroid Adenoma Carotid Sheath/Undescended Adenoma PERSISTENT OR RECURRENT HYPERPARATHYROIDISM SECONDARY HYPERPARATHYROIDISM

igh-frequency sonography is a well-established, noninvasive imaging method used in the evaluation and treatment of patients with parathyroid disease. Sonography is oten used for the preoperative localization of enlarged parathyroid glands or adenomas in patients with hyperparathyroidism. Ultrasound is also used to guide the percutaneous biopsy of suspected parathyroid adenomas or enlarged glands, particularly in patients with persistent or recurrent hyperparathyroidism, as well as in some patients with suspected ectopic glands. In select patients, sonography can be used to guide the percutaneous ethanol

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PITFALLS IN INTERPRETATION False-Positive Examination False-Negative Examination ACCURACY IN IMAGING Ultrasound Other Modalities Importance of Imaging in Primary Hyperparathyroidism INTRAOPERATIVE SONOGRAPHY PERCUTANEOUS BIOPSY ETHANOL ABLATION

ablation of parathyroid adenomas as an alternative to surgical treatment.

EMBRYOLOGY AND ANATOMY he paired superior and inferior parathyroid glands have diferent embryologic origins, and knowledge of their development aids in understanding their ultimate anatomic locations.1-3 he superior parathyroid glands arise from the paired fourth branchial pouches (clets), along with the lateral lobes of the

CHAPTER 20 thyroid gland. Minimal migration occurs during fetal development, and the superior parathyroids usually remain associated with the posterior aspect of the middle to upper portion of the thyroid gland. he majority of superior parathyroid glands (>80%) are found at autopsy within a 2-cm area located just superior to the crossing of the recurrent laryngeal nerve and the inferior thyroid artery.4 he inferior parathyroid glands arise from the paired third branchial pouches, along with the thymus.2 During fetal development, these “parathymus glands” migrate caudally along with the thymus in a more anterior plane than their superior counterparts, bypassing the superior glands to become the inferior parathyroid glands.3 Because of their greater caudal migration, the inferior parathyroid glands are more variable in location than the superior glands and can be found anywhere from the angle of the mandible to the pericardium. he majority of inferior parathyroid glands (>60%) come to rest at or just inferior to the posterior aspect of the lower pole of the thyroid4 (Fig. 20.1). A signiicant percentage of parathyroid glands lie in relatively or frankly ectopic locations in the neck or mediastinum. Symmetry to ixed landmarks occurs in 70% to 80%, so side-to-side comparisons can oten be made.3,4 he ectopic superior parathyroid gland usually lies posterior to the esophagus or in the

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tracheoesophageal groove, in the retropharyngeal space, or has continued its descent from the posterior neck into the posterosuperior mediastinum.5,6 Superior glands are less oten found higher in the neck, near the superior extent of the thyroid, or, in rare cases, surrounded by thyroid tissue within the thyroid capsule.4 he inferior parathyroid gland is more frequently ectopic than its superior counterpart.4,6 About 25% of the inferior glands fail to completely dissociate from the thymus and continue to migrate in an anterocaudal direction and are found in the low neck along the thyrothymic ligament or embedded within or adjacent to the thymus in the low neck and anterosuperior mediastinum. Less common ectopic positions of the inferior parathyroid glands include an undescended position high in the neck anterior to the carotid bifurcation associated with a remnant of thymus, and lower in the neck along or within the carotid sheath.7 In other rare cases, ectopic glands have also been reported in the mediastinum posterior to the esophagus or carina, in the aortopulmonic window, within the pericardium, or even far laterally within the posterior triangle of the neck. Most adults have four parathyroid glands, two superior and two inferior, each measuring about 5 × 3 × 1 mm and weighing on average 35 to 40 mg (range, 10-78 mg).3,8 Supernumerary glands (>4) may be present and result from the separation of parathyroid anlage when the glands pull away from the pouch structures during the embryologic branchial complex phase.9,10 hese supernumerary glands are oten associated with the thymus in the anterior mediastinum, suggesting a relationship in their development with the inferior parathyroid glands.11 Supernumerary glands have been reported in 13% of the population at autopsy studies3,4; however, many of these are small, rudimentary or split glands. “Proper” supernumerary glands (>5 mg and located well away from the other four glands) are found in 5% of cases. he presence of fewer than four parathyroid glands is rare clinically but has been reported in 3% at autopsy. Normal parathyroid glands vary from a yellow to a red-brown color, depending on the degree of vascularity and the relative content of yellow parenchymal fat and chief cells.8 he chief cells are the primary source for the production of parathyroid hormone (PTH, parathormone). he percentage of glandular fat typically increases with age or with disuse atrophy. Hyperfunctioning glands resulting from adenomas or hyperplasia contain relatively little fat and are vascular, thus more reddish. he glands are generally oval or bean shaped but may be spherical, lobular, elongated, or lattened. Although normal parathyroid glands are occasionally seen with high-frequency ultrasound,12,13 typically they are not visualized, likely because of their small size, deep location, and poor conspicuity related to increased glandular fat. Eutopic parathyroid glands typically derive their major blood supply from branches of the inferior thyroid artery, with a lesser and variable contribution to the superior glands from the superior thyroid artery.3,7

PRIMARY HYPERPARATHYROIDISM FIG. 20.1 Location of Parathyroid Glands. Frequency of the location of normal superior and inferior parathyroid glands. Anatomic drawing from 527 autopsies. T, Thymus. (Modiied from Gilmour JR. The gross anatomy of the parathyroid glands. J Pathol 1938;46:133-148.1)

Prevalence Primary hyperparathyroidism is a common endocrine disease, with prevalence in the United States of 1 to 2 per 1000

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population.14 Women are afected two to three times more frequently than men, particularly ater menopause. More than half of patients with primary hyperparathyroidism are older than 50 years, and cases are rare in those younger than age 20.

Diagnosis Primary hyperparathyroidism is usually suspected because an increased serum calcium level is detected on routine biochemical screening. Elevated ionized serum calcium level, hypophosphatasia, and hypercalciuria may be further biochemical clues to the disease. A serum PTH level that is “inappropriately high” for the corresponding serum calcium level conirms the diagnosis. Even when the PTH level is within the upper limits of the normal range in a hypercalcemic patient, the diagnosis of primary hyperparathyroidism should still be suspected, since hypercalcemia from other nonparathyroid causes (including malignancy) should suppress the glandular function and decrease the serum PTH level. Because of earlier detection by increasingly routine laboratory tests, the later “classic” signs of hyperparathyroidism, such as “painful bones, renal stones, abdominal groans, and psychic moans,” are oten not present. Many patients are diagnosed before severe manifestations of hyperparathyroidism, such as nephrolithiasis, osteopenia, subperiosteal resorption, and osteitis ibrosis cystica. In general, patients rarely have obvious symptoms unless their serum calcium level exceeds 12 mg/dL. However, subtle nonspeciic symptoms, such as muscle weakness, malaise, constipation, dyspepsia, polydipsia, and polyuria, may be elicited from these otherwise asymptomatic patients by more speciic questioning.

Pathology Primary hyperparathyroidism is caused by a single adenoma in 80% to 90% of cases, by multiple gland enlargement in 10% to 20%, and by carcinoma in less than 1%.6,15,16 A solitary adenoma may involve any one of the four glands. Multigland enlargement most oten results from primary parathyroid hyperplasia and less oten from multiple adenomas. Hyperplasia usually involves all four glands asymmetrically, whereas multiple adenomas may involve two or possibly three glands. An adenoma and hyperplasia cannot always be reliably distinguished histologically, and the sample may be referred to as “hypercellular parathyroid” tissue. Because of this inconsistent pattern of gland involvement, and because distinguishing hyperplasia from multiple adenomas is diicult pathologically, these two entities are oten histologically considered together as “multiple gland disease.”17

Causes of Primary Hyperparathyroidism Type of Disease

Percentage

Single adenoma Multiple gland disease Carcinoma

80%-90% 10%-20% 14 mg/dL). he diagnosis is oten made at operation when the surgeon discovers an enlarged, irm gland that is adherent to the surrounding tissues due to local invasion. A thick, ibrotic capsule is oten present. Treatment consists of en bloc resection without entering the capsule, to prevent tumor seeding. In many cases, cure may not be possible because of the invasive and metastatic nature of the disease. Generally, death occurs not from tumor spread but from complications associated with unrelenting hyperparathyroidism.

Treatment No efective deinitive medical therapies are available for the treatment of primary hyperparathyroidism. Medications utilized include short-term hypocalcemic agents such as calcitonin and calcimimetics (calcium-sensing receptor agonists) such as cinacalcet. he bisphosphonates aid in preventing bone mass loss. Synthetic vitamin D analogs such as paricalcitol are mainly used in the treatment of secondary hyperparathyroidism. Surgery is the only deinitive treatment for primary hyperparathyroidism. Studies demonstrate that surgical cure rates by an experienced surgeon are greater than 95%, and the morbidity and mortality rates are extremely low.24,25 herefore in symptomatic patients with primary hyperparathyroidism, the treatment of choice is surgical excision of the involved parathyroid gland or glands.

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FIG. 20.2 Typical Parathyroid Adenoma. (A) Transverse and (B) longitudinal sonograms of a typical adenoma (arrows) located adjacent to the posterior aspect of the thyroid (T). C, Common carotid artery; J, internal jugular vein; Tr, trachea.

However, since in current practice, most cases of primary hyperparathyroidism are discovered in the early stages of the disease, some controversy exists as to whether asymptomatic patients with minimal hypercalcemia should be treated surgically, or followed medically with frequent measurements of bone density, serum calcium levels, and urinary calcium excretion and monitoring for nephrolithiasis.26 Recommendations for the management of asymptomatic primary hyperparathyroidism have been outlined in various articles, many of which are based on International Workshop and National Institutes of Health (NIH) Consensus Conference statements and subsequent updates. his area continues to evolve, and approaches to treatment may difer slightly among clinical practices.24-31

SONOGRAPHIC APPEARANCE Shape Parathyroid adenomas are typically oval or bean shaped (Fig. 20.2). As parathyroid glands enlarge, they dissect between longitudinally oriented tissue planes in the neck and acquire a characteristic oblong shape. If this process is exaggerated, they can become tubular or lattened. here is oten asymmetry in the enlargement, and the cephalic and/or caudal end can be more bulbous, producing a triangular, tapering, teardrop or bilobed shape.19,32-34

Echogenicity and Internal Architecture he echogenicity of most parathyroid adenomas is substantially less than that of normal thyroid tissue (Fig. 20.3). he characteristic hypoechoic appearance of parathyroid adenomas is caused by the uniform hypercellularity of the gland with little fat content, which leaves few interfaces for relecting sound. Occasionally, adenomas have a heterogeneous appearance, with areas of increased and decreased echogenicity. he rare, functioning parathyroid lipoadenomas are more echogenic than the adjacent thyroid gland because of their high fat content35 (Fig. 20.3G). A great majority of parathyroid adenomas are homogeneously solid. About 2% have internal cystic components resulting from cystic degeneration (most oten) or true simple cysts (less oten)36-38 (Fig. 20.3E and F, Video 20.1). Adenomas may rarely contain internal calciication (Fig. 20.3H and I).

Vascularity Color low, spectral, and power Doppler sonography of an enlarged parathyroid gland may demonstrate a hypervascular pattern with prominent diastolic low (Fig. 20.4). An enlarged extrathyroidal artery, oten originating from branches of the inferior thyroidal artery, may be visualized supplying the adenoma with its insertion along the long-axis pole.39-44 A inding described in parathyroid adenomas is a vascular arc, which envelops 90 to 270 degrees of the mass. his vascular low pattern may increase the sensitivity of initial detection of parathyroid adenomas and aid in conirming the diagnosis by allowing for diferentiation from lymph nodes, which have a central hilar low pattern. Asymmetric increased vascular low may also be present in the thyroid gland adjacent to a parathyroid adenoma.

Size Most parathyroid adenomas are 0.8 to 1.5 cm long and weigh 500 to 1000 mg. he smallest adenomas can be minimally enlarged glands that appear virtually normal during surgery but are found to be hypercellular on pathologic examination (Fig. 20.5, Video 20.2). Large adenomas can be 5 cm or more in length and weigh more than 10 g. Preoperative serum calcium levels are usually higher in patients with larger adenomas.32

Multiple Gland Disease Multiple gland disease may be caused by difuse hyperplasia or multiple adenomas. Individually, these enlarged glands may have the same sonographic and gross appearance as other parathyroid adenomas (Fig. 20.6, Videos 20.3 and 20.4). However, the glands may be inconsistently and asymmetrically enlarged, and the diagnosis of multigland disease can be diicult to make sonographically. For example, if one gland is much larger than the others, the appearance may be misinterpreted as solitary adenomatous disease. Alternatively, if multiple glands are only minimally enlarged, the diagnosis may be missed altogether.

Carcinoma Carcinomas are usually larger than adenomas.45-47 Carcinomas oten measure more than 2 cm compared with about 1 cm for adenomas (Fig. 20.7). On ultrasound, carcinomas also frequently have a lobular contour, heterogeneous internal architecture, and internal cystic components. However, large adenomas may also

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FIG. 20.3 Spectrum of Echogenicity and Internal Architecture of Parathyroid Adenomas and Enlarged Hyperplastic Glands. Longitudinal sonograms. (A) Typical homogeneous hypoechoic appearance of a parathyroid adenoma (arrows) with respect to the overlying thyroid tissue. (B) Highly hypoechoic solid adenoma. (C) Mixed-geographic echogenicity. The adenoma is hyperechoic in its cranial portion and hypoechoic in its caudal portion. (D) An adenoma with diffusely heterogeneous echogenicity. (E) Partial cystic change. An ectopic adenoma posterior to the jugular vein (J) has both solid and cystic components. (F) Completely cystic 2-cm adenoma (calipers) near the lower pole of the thyroid (T). See also Video 20.1. (G) A lipoadenoma is more echogenic than the adjacent lower pole thyroid tissue. (H) Enlarged parathyroid gland with small, nonshadowing calciications in the setting of secondary hyperparathyroidism related to chronic renal failure. (I) Enlarged parathyroid gland with densely shadowing peripheral calciications in the setting of secondary hyperparathyroidism.

have these features. In many cases, carcinomas are indistinguishable sonographically from large, benign adenomas.45 Some authors report that a depth-to-width ratio of 1 or greater is a sonographic feature more associated with carcinoma than with adenoma, with sensitivity and speciicity of 94% and 95%, respectively.47 Gross evidence of invasion of adjacent structures, such as vessels or muscles, is a reliable preoperative sonographic criterion for the diagnosis of malignancy, but this is an uncommon inding.

ADENOMA LOCALIZATION Sonographic Examination and Typical Locations he sonographic examination of the neck for parathyroid adenoma localization is performed with the patient supine. he patient’s neck is hyperextended by a pad centered under the scapulae, and the examiner usually sits at the patient’s head. High-frequency

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FIG. 20.4 Typical Hypervascularity of Parathyroid Adenoma. (A) Transverse gray-scale and (B) transverse and (C) longitudinal power Doppler ultrasound images show hypervascularity of a parathyroid adenoma with polar feeding vessel and prominent peripheral vascular arcs.

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The Parathyroid Glands

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FIG. 20.5 Spectrum of Size of Parathyroid Adenomas. Longitudinal sonograms. (A) Minimally enlarged, 0.5 × 0.2–cm parathyroid adenoma (calipers). See also Video 20.2. (B) Typical midsized, 1.5 × 0.6–cm, 400-mg adenoma (arrow). (C) Large, 3.5 × 2–cm, >4000-mg adenoma (calipers).

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FIG. 20.6 Multiple Gland Disease. (A) Longitudinal sonogram of the right neck shows superior and inferior parathyroid gland enlargement (arrows) in the setting of secondary hyperparathyroidism, which can be dificult to distinguish from multiple adenomas. T, Thyroid. (B) Transverse sonogram in another patient shows enlargement of bilateral superior parathyroid glands in the setting of secondary hyperparathyroidism. C, Common carotid artery; Tr, trachea. See also Videos 20.3 and 20.4.

T

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FIG. 20.7 Parathyroid Carcinoma. (A) Longitudinal sonogram shows heterogeneous 4-cm parathyroid carcinoma (arrow) located near tip of lower pole of the left thyroid lobe (T). (B) Transverse sonogram with color Doppler low imaging shows prominent internal vascularity of the carcinoma. C, Common carotid artery. (C) Longitudinal sonogram in another patient shows lobulated, solid and cystic, 4-cm parathyroid carcinoma (arrows) adjacent to the lower pole of the thyroid. (D) Longitudinal sonogram in another patient shows a 3-cm heterogeneous solid low-grade parathyroid carcinoma (calipers) with irregular lobulated margins (arrows) posterior to the thyroid.

transducers (6-15 MHz and 8-18 MHz) are used to provide optimal spatial resolution and visualization in most patients; the highest frequency possible should be used that still allows for tissue penetration to visualize the deeper structures, such as the longus colli muscles. In obese patients with thick necks or with large multinodular thyroid glands, use of a 5- to 8-MHz transducer may be necessary to obtain adequate depth of penetration.

he pattern of the sonographic survey of the neck for adenoma localization can be considered in terms of the pattern of dissection and visualization that the surgeon uses in a thorough neck exploration. he typical superior parathyroid adenoma is usually adjacent to the posterior aspect of the midportion of the thyroid (Fig. 20.8, Videos 20.5 and 20.6). he location of the typical inferior parathyroid adenoma is more variable but usually lies

CHAPTER 20

The Parathyroid Glands

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FIG. 20.8 Superior Parathyroid Adenoma. (A) Longitudinal and (B) transverse sonograms show an adenoma (arrows) adjacent to the posterior aspect of the midportion of the left lobe of the thyroid (T). C, Common carotid artery; E, esophagus; Tr, trachea. See also Videos 20.5 and 20.6.

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FIG. 20.9 Inferior Parathyroid Adenoma. (A) Longitudinal and (B) transverse sonograms show an adenoma (arrows) adjacent to lower pole of right lobe of the thyroid (T). C, Common carotid artery; Tr, trachea. See also Videos 20.7 and 20.8.

close to the lower pole of the thyroid (Fig. 20.9, Videos 20.7 and 20.8). Most of these inferior adenomas are adjacent to the posterior aspect of the lower pole of the thyroid, and the rest are in the sot tissues 1 to 2 cm inferior to the thyroid. herefore the examination is initiated on one side of the neck, centered in the region of the thyroid gland, with the focal zone placed deep to the thyroid. High-resolution gray-scale images are obtained in the transverse (axial) and longitudinal (sagittal) planes. Any potential parathyroid adenomas detected in the transverse scan plane must be conirmed by longitudinal imaging to prevent mistaking other structures for an adenoma. Some authors recommend the use of compression of the supericial sot tissues to aid in adenoma detection.12,43,48 his has been described as “graded” compression with the transducer to efect minimal deformity of the overlying subcutaneous tissues and strap muscles and increase the conspicuity of deeper, smaller adenomas (2-10% >10%-≤50% >50%-2-3 mm and increasing in size with Valsalva maneuver or standing) of the pampiniform plexus located posterior to the testis.

CHAPTER OUTLINE SONOGRAPHIC TECHNIQUE NORMAL ANATOMY INTRATESTICULAR SCROTAL MASSES Malignant Tumors Germ Cell Tumors Non–Germ Cell Tumors Testicular Metastases Lymphoma and Leukemia Extramedullary Myeloma Metastatic Disease Benign Intratesticular Lesions Cysts Tubular Ectasia of Rete Testis Cystic Dysplasia Epidermoid Cysts

D

Abscess Segmental Infarction Adrenal Rests Splenogonadal Fusion Calciications EXTRATESTICULAR PATHOLOGIC LESIONS Tunica Vaginalis Hydrocele, Hematocele, and Pyocele Paratesticular Masses Hernia Calculi Varicocele Fibrous Pseudotumor Polyorchidism

iagnostic ultrasound is the most common imaging technique used to supplement the physical examination of the scrotum and is an accurate means of evaluating many scrotal processes. Technical advancements in high-resolution real-time sonography and the ability of color and power Doppler sonography to evaluate testicular perfusion have improved and expanded the clinical applications of scrotal sonography to include (among other indications) assessment of scrotal masses, evaluation of acute scrotal pain, evaluation of scrotal trauma, assessment of varicoceles in the infertility workup, assessment for tumors and metastatic disease, and evaluation of an undescended testis.

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Epididymal Lesions Cystic Lesions Tumors Sperm Granuloma Postvasectomy Changes in the Epididymis Chronic Epididymitis Sarcoidosis ACUTE SCROTAL PAIN Torsion Epididymitis and Epididymo-orchitis Fournier Gangrene TRAUMA CRYPTORCHIDISM

SONOGRAPHIC TECHNIQUE Scrotal ultrasound examination is performed with the patient in the supine position. he scrotum is elevated on top of a towel draped over the thighs, and the penis is placed on the patient’s abdomen and covered with a towel. Optimal results are typically obtained with a high-frequency (14-18 MHz) linear array transducer. If greater penetration is needed because of scrotal swelling, a lower-frequency transducer may be used. A directcontact scan is performed using acoustic coupling gel. Images of both testes are obtained in transverse and sagittal planes. he

CHAPTER 22

Scrotal Sonography: Current Uses Evaluation of location and characteristics of scrotal masses Evaluation of acute scrotal pain Evaluation of scrotal trauma, including surgical or iatrogenic injury Evaluation for varicoceles in infertile men Evaluation of testicular ischemia with color and power Doppler sonography Follow-up of patients with previous testicular neoplasms, lymphoma, or leukemia Detection of occult primary tumor in patients with known metastatic disease Localization of the undescended testis

NORMAL ANATOMY he normal scrotal wall consists of the epidermis, supericial dartos muscle, dartos fascia, external spermatic fascia, cremasteric muscle and fascia, and internal spermatic fascia. he scrotum is a ibromuscular sac that is divided by the midline raphe, forming a right and let hemiscrotum. Each hemiscrotum contains a testis, epididymis, spermatic cord, and vascular and lymphatic networks (Fig. 22.1). he two layers of the tunica vaginalis separate the testis from much of the scrotal wall and form an isolated mesothelial lined sac.1,2 During embryologic development, the tunica vaginalis arises from the processus vaginalis, an outpouching of fetal peritoneum that accompanies the testis in its descent into the scrotum. he upper portion of the processus vaginalis, extending from the internal inguinal ring to the upper pole of the testis, is normally obliterated. he lower portion, the tunica vaginalis, remains as a closed pouch within each hemiscrotum, partially folded around the testis. Only the posterior aspect of the testis, the site of attachment of the testis and epididymis, is not in continuity with the tunica vaginalis. he inner or visceral layer of the tunica vaginalis covers the testis, epididymis, and lower portion of the spermatic cord. he outer or parietal layer of the tunica vaginalis lines the walls of the scrotal pouch and is attached to the fascial coverings of the testis. A small amount of luid is normally present between these two layers.3

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Spermatic cord

Testicular artery Pampiniform plexus Head of epididymis Efferent ductules

Septa Seminiferous tubules

size and appearance of each testis and epididymis should be noted and compared to the contralateral structures. Color and pulsed Doppler parameters should be optimized to evaluate for low low velocities and to demonstrate blood low in the testes and surrounding structures. Transverse images including portions of both testes should be acquired in gray-scale and color Doppler modes to demonstrate symmetry. Scrotal structures should be examined thoroughly to evaluate for extratesticular masses or processes. Additional techniques, such as upright positioning of the patient or performing the Valsalva maneuver, may be used to evaluate venous vascularity for varicocele or for inguinal hernia assessment.

The Scrotum

Tunica albuginea

Cremasteric artery Vas deferens Deferential artery Rete testes

Body of epididymis

Tunica vaginalis Tail of epididymis FIG. 22.1 Normal Intrascrotal Anatomy. (With permission from Sudakoff GS, Quiroz F, Karcaaltincaba M, Foley WD. Scrotal ultrasonography with emphasis on the extratesticular space: anatomy, embryology, and pathology. Ultrasound Q. 2002;18[4]:255-273.78)

he ibrous tunica albuginea covers and protects the testis. Posteromedially, the tunica albuginea projects inward into the testis to form the mediastinum. Numerous ibrous septations project inward from the mediastinum, dividing the testis into 250 to 400 lobules. Each lobule consists of one to three seminiferous tubules supporting the Sertoli cells and spermatocytes. he Leydig cells are adjacent to the tubules, within the loose interstitial tissue, and are responsible for testosterone secretion. he adult testes are ovoid glands measuring 3 to 5 cm in length, 2 to 4 cm in width, and 3 cm in anteroposterior dimension. Testicular size and weight decrease with age.3,4 Sonographically, the normal testis has relatively homogeneous, medium-level, granular echotexture (Fig. 22.2A). Prepubertal testes are typically less echogenic than postpubertal testes secondary to incomplete maturation of the germ cell elements and tubules.5 he tunica (tunica vaginalis and tunica albuginea) can oten be seen as an echogenic outline of the testes. Where the tunica invaginates to form the mediastinum testis, the mediastinum testis is sometimes seen as a linear echogenic band extending craniocaudally within the testis (Fig. 22.2C). Its appearance varies according to the amount of ibrous and fatty tissue present. he ibrous septum, or septula testis, may be seen as a linear echogenic or hypoechoic structure (Fig. 22.2B). he seminiferous tubules converge to form larger tubuli recti, which open into the dilated spaces of the rete testis. he normal rete testis can be identiied in 20% of patients as a hypoechoic region near the mediastinum.6 he rete testis drains into the epididymal head via 15 to 20 eferent ductules. he epididymis is a curved structure measuring 6 to 7 cm in length and lying posterolateral to the testis. It is composed

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FIG. 22.2 Normal Intrascrotal Anatomy. Longitudinal scans show (A) normal homogeneous echotexture of the testis; (B) striated appearance of the septula testis; (C) mediastinum testis (arrow) as a linear echogenic band of ibrofatty tissue; (D) head (white arrow) and body (black arrow) of epididymis; (E) hydrocele (H) and appendix testis (arrow); and (F) appendages of epididymis (arrows). (G) Color Doppler scan shows normal testicular arteries. (H) Transverse scan shows hypoechoic band of transmediastinal artery (arrow). (I) Color Doppler scan shows transmediastinal artery.

of a head, a body, and a tail. he pyramid-shaped epididymal head, or globus major, is located at the superoposterior aspect of the testis, measuring 5 to 12 mm in diameter (Fig. 22.2D). It is formed by the eferent ductules from the rete testis, which join together to form a single convoluted duct, the ductus epididymis. his duct forms the body and the majority of the tail of the epididymis, measures approximately 6 m in length and follows a convoluted course from the head to the tail of the epididymis. he body (corpus) of the epididymis lies adjacent to the posterolateral margin of the testis. he tail (globus minor) is loosely attached to the lower pole of the testis by areolar tissue. he ductus epididymis forms an acute angle at the inferior aspect of the globus minor and courses cephalad as the vas deferens to the spermatic cord. Sonographically, the epididymal head is normally isoechogenic or slightly more echogenic than the testis,

and its echotexture may be coarser. he body tends to be isoechoic or slightly less echogenic than the globus major and testis. he normal body measures less than 4 mm in diameter, averaging 1 to 2 mm. he appendix testis, a remnant of the upper end of the paramesonephric (Müllerian) duct, is a small ovoid structure usually located on the superior pole of the testis or in the groove between the testis and the head of the epididymis. he appendix testis is identiied sonographically in 80% of testes and is more readily visible when a hydrocele is present7 (Fig. 22.2E). he appendix testis may appear stalklike and pedunculated, cystic, or even calciied.8 he appendices of the epididymis are blindending tubules (vasa aberrantia) derived from the mesonephric (Wolian) duct; they form small stalks, which may be duplicated, and project from the epididymis9 (Fig. 22.2F). In rare cases,

CHAPTER 22

A

The Scrotum

821

B

FIG. 22.3 Spectral Doppler of Normal Intratesticular and Extratesticular Arterial Flow. (A) Intratesticular artery has a low-impedance waveform with large amount of end diastolic low. (B) Extratesticular scrotal arterial supply (cremasteric and deferential arteries) has high-impedance waveform with reversed low in diastole.

other appendages, such as the paradidymis (organ of Giraldés) and the superior and inferior vas aberrans of Haller, may be seen.10 he appendages of the epididymis are most oten identiied sonographically as separate structures when a hydrocele is present. Knowledge of the arterial supply of the testis is important for interpretation of color low Doppler sonography of the testis. Testicular blood low is supplied primarily by the testicular, deferential, and cremasteric (external spermatic) arteries. he testicular arteries arise from the anterior aspect of the aorta immediately below the origin of the renal arteries. hey course through the inguinal canal with the spermatic cord to the posterosuperior aspect of the testis. On reaching the testis, the testicular artery divides into branches that pierce the tunica albuginea where the capsular arteries form and arborize over the surface of the testis in a layer known as the tunica vasculosa, deep to the tunica albuginea. Centripetal branches arise from these capsular arteries; these branches course along the septa to converge on the mediastinum. From the mediastinum, these branches form recurrent rami that course into the testicular parenchyma, where they branch into arterioles and capillaries11 (Fig. 22.2G). In about 50% of normal testes a transmediastinal artery supplies the testis, entering through the mediastinum and coursing toward the periphery of the gland to supply the capsular arteries, and is accompanied by a large vein, frequently seen as a hypoechoic band in the midtestis11,12 (Fig. 22.2H and I). he transmediastinal artery may be associated with acoustic shadowing obscuring the distal aspect of the testis and giving

rise to the “two-tone” testis appearance.13 he deferential artery originates from the superior vesical artery and courses to the tail of the epididymis, where it divides and forms a capillary network. he cremasteric artery arises from the inferior epigastric artery. It courses with the remainder of the structures of the spermatic cord through the inguinal ring, continuing to the surface of the tunica vaginalis, where it anastomoses with capillaries of the testicular and deferential arteries. he velocity waveforms of the normal capsular and intratesticular arteries show high levels of antegrade diastolic low throughout the cardiac cycle, relecting the low vascular resistance of the testis (Fig. 22.3A). Supratesticular arterial waveforms vary in appearance. Two main types of waveforms exist: a low-resistance waveform similar to that seen in the capsular and intratesticular arteries, relecting the testicular artery; and a high-resistance waveform with sharp, narrow systolic peaks and little or no diastolic low14 (Fig. 22.3B). his high-resistance waveform is believed to relect the high vascular resistance of the extratesticular tissues. he deferential and cremasteric arteries within the spermatic cord primarily supply the epididymis and extratesticular tissues, but they also supply the testis through anastomoses with the testicular artery. he spermatic cord consists of the vas deferens; the testicular, cremasteric, and deferential arteries; a pampiniform plexus of veins; the lymphatics; and the nerves of the testis. It courses superiorly toward the supericial and deep (also called “internal”) inguinal rings. Sonographically, the normal spermatic cord lies just beneath the skin and may be diicult to distinguish from

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the adjacent sot tissues of the inguinal canal.15 Distally, it may be visualized within the scrotum when a hydrocele is present or with the use of color low Doppler sonography.

Pathologic Classiication of Testicular Tumors32 GERM CELL TUMORS Seminoma Classic Spermatocytic Nonseminomatous germ cell tumors Mixed malignant germ cell Embryonal cell carcinoma Yolk sac tumor (endodermal sinus tumor) Teratoma Choriocarcinoma Placental site trophoblastic tumor Trophoblastic tumor, unspeciied Regressed tumor

INTRATESTICULAR SCROTAL MASSES When a scrotal mass is palpated, the concern is for the presence of a testicular neoplasm. With sonographic examination, intrascrotal masses can be detected with a sensitivity of nearly 100%.16 Delineation between intratesticular and extratesticular processes is 98% to 100% accurate.16-19 In general, intratesticular masses should be considered malignant.19,20 If the mass is extratesticular and cystic, then this process is almost certainly benign, with the general accepted prevalence of malignancy of extratesticular lesions being 3% to 6%.19,21-24 Testicular neoplasms account for 1% to 2% of all malignant neoplasms in men and represent the most common nonhematologic malignancy in men in the 15- to 49-year-old age group.25-27 Most (65%-94%) patients with testicular neoplasms present with painless unilateral testicular masses or difuse testicular enlargement, and 4% to 14% present with symptoms of metastatic disease.3,28,29 Approximately 10% to 15% of patients will present with pain and initially may be misdiagnosed as having epididymo-orchitis.30 Testicular tumors are subdivided into two major categories: germ cell and stromal tumors, with germ cell tumors accounting for 90% to 95% of all testicular tumors. Germ cell tumors arise from primitive germ cells and are further divided into seminoma and nonseminomatous germ cell tumors (NSGCTs). hese tumors are uniformly malignant. Non–germ cell (sex cord– stromal) primary tumors of the testis derive from the sex cords (Sertoli cells) and the stroma (Leydig cells) and are malignant in approximately 10% of cases.3,29 Nonprimary tumors include lymphoma, leukemia, and metastases and can present as intratesticular masses. Color Doppler imaging has limited ability to distinguish between malignant and benign solid intratesticular masses.31

Malignant Tumors Germ Cell Tumors Intratubular germ cell neoplasia is believed to be the precursor of most germ cell tumors and is the equivalent of carcinoma in situ. It is thought that these abnormal cells develop along a unipotential line and form seminoma, or develop along a totipotential line and form nonseminomatous tumors.33,34 Seminomas are radiosensitive tumors, whereas NSGCTs respond better to surgery and chemotherapy.27 Approximately 95% of primary testicular neoplasms larger than 1.6 cm in diameter show increased vascularity on color low Doppler examination. However, color Doppler indings do not appear to be important in the evaluation of adult testicular tumors.35 Color low may help to identify tumors that are relatively isoechoic with testicular parenchyma,36 but focal or difuse inlammatory lesions cannot be distinguished from neoplasms on the basis of color low Doppler or spectral Doppler indings. Nonpalpable testicular tumors have also been detected with

STROMAL TUMORS Leydig cell (interstitial) Sertoli cell Granulosa cell Mixed undifferentiated sex cord MIXED GERM CELL–STROMAL TUMORS Gonadoblastoma Germ cell–stromal–sex cord, unclassiied METASTATIC NEOPLASMS Lymphoma Leukemia Myeloma Carcinoma OTHERa Adrenal rests Epidermoid cyst Malacoplakia Carcinoid tumor Mesenchymal tumor Granulomatous disease a

Rare tumors and nonneoplastic tumorous conditions. Modiied from Moch H, Cubilla AL, Humphrey PA, et al. The 2016 WHO classiication of tumours of the urinary system and male genital organs-Part A: renal, penile, and testicular tumors. Eur Urol. 2016:70(10):93-105.32

sonography in patients presenting for scrotal discomfort or infertility.37-40 Incidentally discovered nonpalpable lesions are oten benign, but 20% to 30% are malignant.38,39,41 Tumor markers have a role in diagnosis, staging, prognosis, and follow-up of a number of germ cell tumors, with three markers having clinical use: α-fetoprotein, human chorionic gonadotropin, and, less so, lactate dehydrogenase. α-Fetoprotein is produced by the fetal liver, gastrointestinal tract, and yolk sac and is elevated in yolk sac tumors or mixed germ cell tumors containing yolk sac elements. Human chorionic gonadotropin is a glycoprotein produced by syncytiotrophoblasts of the developing placenta. It is elevated in tumors containing syncytiotrophoblasts, including choriocarcinoma and seminoma. Lactate dehydrogenase, although not speciic, correlates with bulk of disease and is used in staging.20

CHAPTER 22

FIG. 22.4 Mixed Tumor. Transverse scan of coexistent solid masses— a mixed germ cell tumor (M) and a seminoma (S).

Seminoma. Seminoma is the most common pure, or single cell–type, germ cell tumor in adults, accounting for 35% to 50% of all germ cell neoplasms.20,30 It is also a common component of mixed germ cell tumors, occurring in 30% of these tumors. Seminomas tend to occur in slightly older patients than do other testicular neoplasms, with a peak incidence in the fourth and ith decades, and they rarely occur before puberty.3,42,43 hey are typically conined within the tunica albuginea at presentation, with approximately 25% of patients having metastases at diagnosis. As a result of the radiosensitivity and chemosensitivity of the primary tumor and its metastases, seminomas have the most favorable prognosis of the malignant testicular tumors. A second primary synchronous or metachronous germ cell tumor occurs in 1% to 2.5% of patients with seminomas (Fig. 22.4). Seminoma is the most common tumor type in cryptorchid testes. Between 8% and 30% of patients with seminoma have a history of undescended testes.29,43 he risk of a seminoma developing is substantially increased in an undescended testis, even ater orchiopexy. Patients with a normally located but atrophic testis have an increased risk of seminoma (Video 22.1). here is also an increased risk of malignancy developing in the contralateral, normally located testis. herefore sonography is oten used to screen for an occult tumor in both testes ater orchiopexy. Seminomas range from a small, well-circumscribed lesion to large masses replacing the testis. Macroscopically, cellular morphology resembles that of primitive germ cells, which are relatively uniform.25 he sonographic features of pure seminoma parallel this homogeneous macroscopic appearance. Pure seminomas usually have predominantly uniform, low-level echoes without calciication, and they appear hypoechoic compared with normally echogenic testicular parenchyma (Fig. 22.5).44 Larger tumors may have a more heterogeneous appearance. In rare cases, seminomas become necrotic and appear partly cystic on sonography (Fig. 22.5I).

The Scrotum

823

Nonseminomatous Germ Cell Tumors. NSGCTs include embryonal carcinomas, teratomas, yolk sac (endodermal sinus) tumors, choriocarcinomas, and mixed germ cell tumors. hese tumors occur more oten in younger patients than do seminomas, with a peak incidence during the latter part of the second decade and the third decade. hey are uncommon before puberty and ater age 50. Approximately 70% of NSGCTs produce hormonal markers.45 Up to 60% of germ cell tumors are mixed germ cell tumors, composed of at least two diferent cell types.20,46 Pure NSGCTs are rare and occur more oten in the pediatric population.20 he sonographic appearance of NSGCTs relects the histologic features and relative proportions of each component, although as a group these tumors are more heterogeneous than seminoma, demonstrating irregular margins, echogenic foci, and solid and cystic components (Fig. 22.6). hese malignancies are more aggressive than seminomas, frequently invading the tunica albuginea and resulting in distortion of the testicular contour (see Fig. 22.6). Approximately 60% of NSGCTs have metastatic involvement at presentation.46 Mixed germ cell tumors are the most common germ cell tumors, constituting up to 60% of all germ cell tumors. hey contain nonseminomatous germ cell elements in various combinations. Seminomatous elements may also be present but do not inluence prognosis or treatment.47 Embryonal carcinoma is the most common component, although any combination of cell types may occur. Imaging features are variable, relecting the diversity of this group of tumors. Nonseminomatous tumors are not as radiosensitive as seminomas. Embryonal carcinoma is composed of primitive anaplastic cells that resemble early embryonic cells. It is present in 87% of mixed germ cell tumors, but in its pure form it is rare, accounting for only 2% to 3% of testicular germ cell neoplasms (Fig. 22.6C).48 As with other NSGCTs, embryonal cell tumors occur in younger patients than seminomas do, with a peak incidence during the latter part of the second and third decades. he sonographic features of pure embryonal cell carcinoma are nonspeciic, especially in children, in whom the only inding may be testicular enlargement without a deined mass.36,49 Totipotent germ cells that diferentiate toward extraembryonic fetal membranes give rise to yolk sac tumors, or endodermal sinus tumors. Yolk sac tumors are the most common germ cell tumor in infants younger than 2 years, accounting for 80% of childhood testicular neoplasms.49 Yolk sac tumor is rare in its pure form in adults, although it is present in 44% of adult cases of mixed germ cell tumor (Fig. 22.6D).20 Yolk sac tumor is associated with elevated levels of α-fetoprotein in greater than 90% of infants. Teratomas constitute 5% to 10% of primary testicular neoplasms. hey are deined according to the World Health Organization (WHO) classiication on the basis of the presence of derivatives of the diferent germinal layers (endoderm, mesoderm, and ectoderm). Histologically, teratomas can be divided into mature and immature. he peak incidence is in infancy and early childhood, with another peak in the third decade of life. In infants and young children, teratomas are the second most common testicular tumor ater yolk sac tumor and are considered benign, even when they are histologically immature.43,50,51 Postpubertal testicular teratomas are malignant and

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FIG. 22.5 Seminoma: Spectrum of Appearances. Longitudinal scans. (A) and (B) Subtle hypoechoic seminoma (arrows) with increased low. (C) Typical homogeneous hypoechoic seminoma. (D) Two small foci of seminoma. (E) Slightly heterogeneous seminoma. (F) Seminoma associated with microlithiasis and coarser calciications. (G) Seminoma occupying most of testis. Typical homogeneous hypoechoic sonographic appearance. (H) Gross specimen of seminoma in G. (I) Necrotic seminoma replacing testicle. See also Video 22.1.

have a higher metastatic rate, approximately 20%, than their ovarian counterpart.52 Teratomas in their pure form are rare in adults, although teratomatous elements occur in approximately half of all adult cases of mixed germ cell tumor (Fig. 22.6B). Both mature and immature teratomas are generally associated with normal tumor markers, although elevated levels of α-fetoprotein or human chorionic gonadotropin may be found.47 Sonographically, the teratoma is usually a well-deined, markedly heterogeneous mass containing cystic and solid areas of various sizes and appears similar to other NSGCTs. Dense echogenic foci causing acoustic shadowing are common, resulting from focal calciication, cartilage, immature bone, ibrosis, and noncalciic scarring (Fig. 22.6E).44 Choriocarcinoma accounts for less than 1% of malignant primary testicular tumors in its pure form but occurs in 8% of mixed germ cell tumors.20,43,48,50 he peak incidence is in the second and third decades. hese tumors are highly malignant and metastasize early by hematogenous and lymphatic routes. he primary tumor and metastases are oten hemorrhagic, and patients may have symptoms resulting from hemorrhagic

metastases, including hemoptysis, hematemesis, and central nervous system–related symptoms. Focal necrosis of the primary tumor secondary to hemorrhage is an almost invariable feature, and calciication may be present, giving a sonographic appearance similar to the other NSGCTs (Fig. 22.6F). he levels of human chorionic gonadotropin are elevated and cause gynecomastia in 10% of cases.20,53 Choriocarcinoma has the worst prognosis of any of the germ cell tumors.50 Regressed Germ Cell Tumor. Sonography is an important diagnostic tool for patients who present with widespread metastatic testicular carcinoma (Fig. 22.7) even though the primary tumor has involuted (Fig. 22.8); ultrasound is an important component in the search for a primary testicular neoplasm. Mediastinal and central nervous system extragonadal tumors can oten present as primary lesions, although retroperitoneal germ cell tumors are more likely to have a testicular origin.54,55 he primary testicular tumor may regress, despite widespread advancing metastatic disease, resulting in an echogenic ibrous and possibly calciic scar. Regression may be caused by the high metabolic rate of the tumor and vascular compromise from the

CHAPTER 22

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FIG. 22.6 Nonseminomatous Germ Cell Tumor: Spectrum of Appearances. (A) and (B) Mixed germ cell tumor. (A) Longitudinal scan shows a large tumor with cystic changes occupying most of the testis and invading the tunica (arrow). (B) Transverse scan shows a heterogeneous, mixed germ cell tumor that has 85% teratoma elements. (C) Embryonal carcinoma. Longitudinal scan shows relatively homogeneous tumor (arrow). (D) Yolk sac, or Endodermal sinus tumor. Longitudinal scan shows a mildly heterogenous tumor extending to the mediastinum (arrow). (E) Teratoma. Longitudinal scans shows a large heterogeneous mass with cystic foci and scattered calciications. (F) Choriocarcinoma. Longitudinal scan shows a relatively homogeneous tumor (arrows).

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FIG. 22.7 Occult Testicular Seminoma With Retroperitoneal Metastases. (A) Contrast-enhanced CT scan shows extensive retroperitoneal adenopathy from seminoma. (B) Longitudinal sonographic scan shows occult homogeneous hypoechoic seminoma. The physical examination of the testis was negative.

tumor outgrowing its blood supply. Tumors are typically clinically occult with the afected testis normal or small on palpation. Histologic analysis may reveal no residual tumor, although intratubular malignant germ cells may be present.25,28,54 hese lesions, also known as “Azzopardi tumors,” have a variable sonographic appearance; they can be hypoechoic or hyperechoic or seen as focal calciications. Although sonographic appearance is not speciic for a “burned-out” or regressed tumor, indings

are suggestive in the context of histologically proven testicular metastases.56

Non–Germ Cell Tumors Sex Cord–Stromal Tumors. Sex cord–stromal tumors account for 3% to 6% of all testicular neoplasms. he prevalence is greater in the pediatric population where non–germ cell tumors account for 10% to 30% of all testicular neoplasms. he term

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FIG. 22.8 Regressed, or “Burned-Out,” Germ Cell Tumor. (A) Longitudinal scan shows a partly calciied nonviable germ cell tumor in a patient with retroperitoneal metastases. Notice the hypoechoic mass around the focus of calciication. (B) Contrast-enhanced CT scan in the same patient shows heterogeneous left retroperitoneal adenopathy (arrow) from regressed primary testicular teratoma.

sex cord–stromal tumor refers to a neoplasm containing Leydig, Sertoli, thecal, granulosa, or lutein cells and ibroblasts in various degrees of diferentiation. hese tumors may contain single or multiple cell types because of the totipotentiality of the gonadal stroma.29 he most common type of sex cord–stromal tumor is a Leydig cell tumor, accounting for 1% to 3% of all testicular neoplasms; these can occur in any age group, although predominantly in patients aged 20 to 50 years.42,43,53 Patients most oten present with painless testicular enlargement or a palpable mass. Approximately 30% of patients present with an endocrinopathy secondary to secretions of androgens or estrogens by the tumor, which may manifest as precocious virilization, impotence, or loss of libido. he tumor is bilateral in 3% of cases. From 10% to 15% of the tumors are malignant, having invaded the tunica at diagnosis. hese gonadal tumors are usually small, solid, homogeneous hypoechoic masses on sonography and may show mainly peripheral low on color Doppler imaging (Fig. 22.9A and B).57 Foci of hemorrhage and necrosis are present in 25% of tumors,42,53 and thus cystic spaces due to hemorrhage and/or necrosis are occasionally seen in larger lesions. Sertoli cell tumors are rare and account for less than 1% of all testicular tumors; they occur with equal frequency in all age groups.58 hey can be of one of three histologic types: Sertoli cell tumor not otherwise speciied, sclerosing Sertoli cell tumor, or large cell calcifying Sertoli cell tumor. he most common presentation is with a painless intratesticular mass. hese tumors are less likely than Leydig cell tumors to be hormonally active, although gynecomastia may occur. Sertoli cell tumors may occur in undescended testes, in patients with testicular feminization, Klinefelter syndrome, and Peutz-Jeghers syndrome.59 Sertoli cell tumors are typically well-circumscribed, unilateral, rounded to lobulated masses. Occasionally, hemorrhage or necrosis may occur, giving a more heterogeneous appearance on sonography. he large-cell calcifying Sertoli cell tumor is a subtype with distinctive clinical, histologic, and sonographic features.59 hese tumors are oten bilateral and multifocal and may be almost completely calciied. Carney complex, a very rare autosomal

dominant multiple endocrine neoplasia syndrome, is oten associated with Sertoli cell tumors (Fig. 22.9C). Additional, less common tumors in this category include granulosa cell tumors, ibroma-thecomas, and mixed sex cord–stromal tumors (Fig. 22.9D). Gonadal stromal tumors in conjunction with germ cell tumors are called gonadoblastomas. he majority of gonadoblastomas occur in the setting of gonadal dysgenesis and intersex syndromes.43,60

Testicular Metastases Lymphoma and Leukemia Lymphoma accounts for 5% of all testicular tumors and is the most common testicular tumor in men older than 60 years, where it can account for up to 50% of intratesticular masses. However, testicular involvement occurs in only 1% to 3% of patients with lymphoma.29,61 he peak age at diagnosis of lymphoma is 60 to 70 years; 80% of the patients are older than 50 years at diagnosis. Malignant lymphoma is the most common bilateral testicular tumor, occurring bilaterally either in a synchronous or, more oten, in a metachronous manner in up to 38% of cases.60 One-half of bilateral testicular neoplasms are lymphoma.29,42 Most lymphomas of the testis are B-cell lymphomas, with difuse large cell lymphoma being the most common. Hodgkin lymphoma of the testis is extremely rare. Testicular Metastases LYMPHOMA Mostly non-Hodgkin lymphoma LEUKEMIA Second most common Acute leukemia: 40%-65% “Sanctuary” site NONLYMPHOMA METASTASES Lung and prostate most common Kidney, stomach, colon, pancreas, melanoma

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FIG. 22.9 Stromal Tumors: Spectrum of Appearances. (A) and (B) Leydig cell tumor. (A) Transverse scan shows several small, hypoechoic solid masses in the midtestis consistent with Leydig cell hyperplasia. (B) Longitudinal scan shows a hypoechoic solid mass in the midtestis. The patient had bilateral Leydig cell tumors. (C) Longitudinal scan of multifocal large-cell calcifying Sertoli cell tumor. (D) Stromal tumor. Transverse scan demonstrates a large, heterogeneous tumor (which was a stromal tumor, not otherwise speciied) replacing the testis. (C courtesy of Theodora Potretzke, MD, Mayo Clinic.)

Testicular lymphoma most frequently occurs in association with disseminated disease, as the initial manifestation of occult nodal disease, or as a site of recurrent disease.29 True primary lymphoma of the testis has not been conclusively documented.47 Although most patients with lymphoma of the testis present with a painless intratesticular mass or difuse testicular enlargement, approximately 25% of the patients have constitutional symptoms, such as fever, weakness, anorexia, or weight loss. Lymphoma of the testis is oten large at diagnosis. he tunica vaginalis is usually intact, but unlike germ cell tumors, extension into the epididymis and spermatic cord is common, occurring in up to 50% of cases.62 he scrotal skin is rarely involved. Grossly, the tumor is not encapsulated but compresses the parenchyma to the periphery. he sonographic appearance of lymphoma is nonspeciic, although generally appears as homogeneous, hypoechoic lesions which may difusely iniltrate the testis29; however, focal hypoechoic lesions can occur (Fig. 22.10). Hemorrhage and necrosis are rare. Color low Doppler imaging shows increased vascularity in testicular lymphoma, regardless of lesion size, and the appearance may resemble difuse inlammation63 (Fig. 22.10C). Unlike inlammation, lymphoma is usually painless, and the testes are not tender to palpation.

Leukemia is the second most common metastatic testicular neoplasm. Primary testicular leukemia is rare, but leukemic iniltration of the testis during bone marrow remission is common in children.29,64 he testis appears to act as a “sanctuary” site for leukemic cells during chemotherapy because of the blood-testis barrier, which inhibits concentration of chemotherapeutic agents.64 he highest frequency of testicular involvement is found at autopsy in patients with acute leukemia (40%-65%). Approximately 20% to 35% of patients with chronic leukemia have testicular involvement.65 Most cases of testicular involvement occur within 1 year of the discontinuation of long-term remission maintenance chemotherapy. he sonographic appearance of leukemia is nonspeciic and similar to lymphoma. Patients most frequently present with difuse iniltration, which produces difusely enlarged, hypoechoic testes (Fig. 22.10E).63 he diferential diagnosis includes inlammation.

Extramedullary Myeloma Involvement of the testis is usually a manifestation of difuse myeloma, although rarely the testis may be the site of primary focal myeloma (plasmacytoma).66 he testis may have single or multiple nodules that appear hypoechoic and homogeneous

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FIG. 22.10 Lymphoma, Leukemia, and Metastases. (A)-(D) Lymphoma. (A) Longitudinal scan shows two subtle hypoechoic foci of lymphoma. In another patient, sagittal gray-scale (B) and power Doppler (C) images show diffuse, homogeneous hypoechoic hypervascular mass. (D) Heterogeneous involvement of the testes in patient with lymphoma. (E) Leukemia. Longitudinal scan shows diffuse hypoechoic involvement. (F) Melanoma metastasis. Longitudinal scan shows a hypoechoic lobulated mass in the upper pole of the testis and epididymis.

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located within the parenchyma. Cystic testicular lesions are not always benign; testicular tumors (especially NSGCTs) can undergo cystic degeneration from hemorrhage or necrosis. he distinction between a benign cyst and a cystic neoplasm is of utmost clinical importance (Fig. 22.12). Simple intratesticular cysts can be managed conservatively without the need for surgical intervention.73 Of the 34 cystic testicular masses discovered with sonography by Hamm et al.,72 16 were neoplastic, and all of these had sonographic features of complicated cysts. NCGCTs, especially those with teratoma elements, are the most common tumors to contain both cystic and solid components. FIG. 22.11 Multiple Testicular Hamartomas in Cowden Disease. Dual transverse image shows multiple bilateral small echogenic hamartomas. The patient had Cowden disease, an inherited autosomal dominant disorder, which causes multiple hamartomas in the gastrointestinal tract.

on sonographic examination with marked hypervascularity.67,68 Bilateral involvement occurs in approximately 20% of cases.47

Metastatic Disease Nonlymphomatous metastases to the testes are uncommon, representing 0.02% to 5% of all testicular neoplasms.69 he most frequent primary sites are the lung and prostate gland.42 Other frequent primary sites for metastatic neoplasms include melanoma, kidney, colon, stomach, and pancreas.70 Most metastases are clinically silent, being discovered incidentally at autopsy. Testicular metastases are most common in patients during the sixth and seventh decades.3 hey are usually multiple and are bilateral in 15% of cases.42 Because primary germ cell tumors may also be multicentric and bilateral, these features are not helpful in distinguishing primary from metastatic testicular neoplasms. Widespread systemic metastases are usually present in patients with testicular metastases. Possible routes of metastases to the testis include retrograde venous, hematogenous, retrograde lymphatic, and direct tumor invasion. Metastases from sites remote from the testis, such as the lung and skin, most likely spread hematogenously. Retrograde venous extension through the testicular vein occurs in renal cell carcinoma and may also occur in urinary bladder and prostate tumors.71 Neoplasms with metastases to the periaortic lymph nodes may involve the testis through retrograde lymphatic extension. Sonographic features of nonlymphomatous testicular metastases vary. he appearance is oten hypoechoic but may be echogenic or complex3 (Fig. 22.10F). Other rare tumors of the testis include hamartoma (Fig. 22.11), dermoid tumor, hemangioma, intratesticular adenomatoid tumor, carcinoid tumor, carcinoma of the mediastinum testis, neuroectodermal tumor, leiomyoma, Brenner tumor, ibroma, ibrosarcoma, osteosarcoma, chondrosarcoma, and undiferentiated sarcoma, among others.

Benign Intratesticular Lesions Cysts Intratesticular cystic lesions are discovered incidentally on sonography in 8% to 10% of men.72 Benign testicular cysts may be associated with the tunica albuginea, tunica vaginalis, or

Testicular Cystic Lesions BENIGN Tunica albuginea cysts Tunica vaginalis cysts Intratesticular cysts Tubular ectasia of rete testis Cystic dysplasia Epidermoid cysts Abscess MALIGNANT Nonseminomatous germ cell tumor Necrosis or hemorrhage in tumor Tubular obstruction by tumor

Cysts of the tunica albuginea are located within the tunica, which surrounds the testis. hey vary in size from 2 to 30 mm and are well deined. hey are usually solitary and unilocular but may be multiple or multilocular72,74 (Fig. 22.12A). he mean age at presentation is 40 years, but cysts also occur in the ith and sixth decades.75 he cysts may be asymptomatic, but patients frequently present with cysts that are clinically palpable, irm scrotal nodules. Histologically, they are simple cysts lined with cuboid or low columnar cells and illed with serous luid.76 Careful scanning in multiple planes allows delineation of the cyst as arising from the tunica albuginea and clariies its benign nature. Complex tunica albuginea cysts may simulate a testicular neoplasm.77 Cysts of the tunica vaginalis are rare and arise from the visceral or parietal layer of the tunica vaginalis. hey may be single or multiple. Sonographically, they usually appear anechoic but may have septations or may contain echoes caused by hemorrhage.78 Intratesticular cysts are simple cysts illed with clear serous luid; they vary in size from 2 to 18 mm.79 Sonographically, they are well-deined, anechoic cysts with thin, smooth walls and posterior acoustic enhancement. Hamm et al.72 reported that in all 13 of their cases, the cysts were located near the mediastinum testis, supporting the theory that they originate from the rete testis, possibly secondary to posttraumatic or postinlammatory stricture formation (Fig. 22.12B).

Tubular Ectasia of Rete Testis Tubular ectasia of the rete testis is a benign, normal variant that may be mistaken for a testicular neoplasm.80-83 Dilatation of the

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FIG. 22.12 Intratesticular Cystic Lesions. (A) Tunica albuginea cyst. Longitudinal scan shows a cyst arising from the tunica albuginea. These cysts are usually palpable. (B) Intratesticular cyst. Transverse scan shows bilateral benign intratesticular cysts. (C) Cystic dilatation in rete testis. Transverse scan shows dilated tubules of the rete testis in both testes. (D)-(F) Epidermoid cyst (benign). See also Video 12.2. (D) Typical whorled appearance; (E) heterogeneous hypoechoic lesion (arrows); (F) typical peripheral calciications. (G) Transverse scan shows an intratesticular cystic lesion with minimal mural nodularity (arrow). (H) Transverse scan at 6-month interval follow-up shows interval development of an isoechoic, solid mass (arrow) partially illing the cystic lesion, surgically proven to represent teratoma. (G and H courtesy of Shane Macauley, MD.)

rete testis is thought to result from obstruction in the eferent tubules or epididymis, with epididymal obstruction caused by inlammation, trauma, or surgery. Sonographic appearance is of multiple luid-illed tubular structures in or adjacent to the mediastinum testis with no associated sot tissue abnormality and no low on color low Doppler imaging (Fig. 22.12C). Rete testis dilatation is oten bilateral, asymmetric, and is frequently associated with a spermatocele. he characteristic sonographic appearance and location should allow recognition as a benign condition, thus preventing an orchiectomy. Characteristic indings of the dilated rete testis on magnetic resonance imaging (MRI) include intratesticular signal intensity similar to that of luid in the region of the mediastinum testis.80 his appearance is in contrast to the MRI appearance of testicular tumors, which typically have low signal intensity on T2-weighted imaging.

Cystic Dysplasia Cystic dysplasia is a rare congenital malformation, usually occurring in infants and young children, although one case was reported in a 30-year-old man.84,85 his lesion is thought to result from an embryologic defect that prevents connection of the tubules of the rete testis and the eferent ductules. Pathologically, the lesion consists of multiple, interconnecting cysts of various sizes and shapes, separated by ibrous septa. his lesion originates in the rete testis and extends into the adjacent parenchyma, resulting in pressure atrophy of the adjacent testicular parenchyma. he cysts are lined by a single layer of lat or cuboidal epithelium. Sonographically, the appearance is similar to acquired cystic dilatation of the rete testis. Renal agenesis or dysplasia frequently coexists with testicular cystic dysplasia.85

CHAPTER 22 Epidermoid Cysts An epidermoid cyst is an uncommon, benign, generally well-circumscribed tumor of germ cell origin, representing approximately 1% of all testicular tumors. hese tumors occur at any age but are most common during the second to fourth decades.42 Usually, patients present with a painless testicular nodule; one-third of the tumors are discovered incidentally on physical examination. Difuse, painless testicular enlargement occurs in 10% of patients. Pathologically, epidermoid cysts are composed of keratinizing, stratiied, squamous epithelium with a well-deined, ibrotic wall. Although the histogenesis of epidermoid cysts is controversial, the current prevailing theory is that these entities represent teratomas that have undergone monodermal diferentiation. However, a complete absence of mesodermal or ectodermal components and absence of intraepithelial neoplasia, a histologic precursor of germ cell tumors, brings this theory into question. Additionally, unlike germ cell tumors, epidermoid cysts have an invariably benign course without recurrence or metastatic disease following resection.86 Squamous metaplasia of seminiferous epithelium or rete testis is an alternative diagnosis.87 hese benign lesions can be differentiated from premalignant teratomas only through histologic examination. Sonographically, epidermoid cysts are generally well-deined, round to ovoid, avascular masses and may be multiple or bilateral.86 A characteristic whorled or laminated appearance, like the layers of an onion skin, corresponds to the alternating layers of compacted keratin and desquamated squamous cells seen histologically88-90 (Fig. 22.12D, Video 22.2). his appearance, however, may not be pathognomonic because it is rarely seen with teratoma.91 Another typical appearance of an epidermoid cyst is a well-deined hypoechoic mass with an echogenic capsule

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that may be calciied (Fig. 22.12F). here may be central calciication, giving a “bull’s eye” or target appearance.86 Epidermoid cysts may also have the nonspeciic appearance of a hypoechoic mass with or without calciications and may resemble germ cell tumors (Fig. 22.12E). Avascularity is a clue to the diagnosis.89 Although the sonographic appearance is characteristic, it is not pathognomonic, and histologic conirmation should be obtained by a conservative testis-sparing approach with local excision (enucleation).92 MRI has been used to support the sonographic diagnosis of epidermoid cysts as they have a target appearance with low signal capsule. he layers of keratinizing material are rich in water and lipid and can appear as areas of high signal intensity on both T1- and T2-weighted imaging.93,94

Abscess Testicular abscesses are usually a complication of epididymoorchitis, although they may also result from an undiagnosed testicular torsion, testicular infarct, trauma, a gangrenous or infected tumor, or a primary pyogenic orchitis. Infectious causes of abscess formation are mumps, smallpox, scarlet fever, inluenza, typhoid, sinusitis, osteomyelitis, and appendicitis.95 A testicular abscess may cross the mesothelial lining of the tunica vaginalis, resulting in formation of a pyocele or a istula to the scrotal skin. Most oten, sonography demonstrates an irregularly marginated, hypoechoic or mixed echogenic intratesticular mass (Fig. 22.13). Testicular abscesses have no diagnostic sonographic features but can oten be distinguished from tumors on the basis of clinical symptoms and short-term interval change. In patients with acquired immunodeiciency syndrome (AIDS), distinguishing an abscess from a neoplastic process may be diicult on sonographic examination. Clinical indings may

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FIG. 22.13 Testicular Abscesses. (A) Transverse gray-scale image shows typical hypoechoic intratesticular abscesses, which may be indistinguishable from a tumor. However, heterogeneity of the parenchyma, skin thickening, and developing pyocele suggest that these masses represent abscesses. (B) Transverse color Doppler image shows echogenic and hypoechoic areas in the intratesticular abscesses with increased vascularity around the abscesses.

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be helpful; however, orchiectomy is frequently necessary to obtain a histologic diagnosis.96,97

Segmental Infarction Segmental testicular infarction may occur ater torsion, trauma, surgery, bacterial endocarditis, vasculitis, leukemia, or hypercoagulable states.98 Spontaneous infarction of the testis is rare. he sonographic appearance depends on the age of the infarction. Initially, a typical segmental infarct is seen as a focal, wedgeshaped or round hypoechoic mass, with approximately 80% occurring in the upper pole, likely secondary to vascular supply between the upper and lower poles.99 he focal hypoechoic mass may not be distinguishable from a neoplasm on the basis of its gray-scale sonographic appearance.100,101 hese lesions should have reduced or absent blood low, depending on the age of the infarction.99 If a well-circumscribed, nonpalpable, relatively peripheral, hypoechoic mass shows a complete lack of vascularity on power Doppler imaging or ater the administration of sonographic contrast agent, it may be possible to distinguish such

benign infarctions from neoplasm102,103 (Fig. 22.14). With time, the hypoechoic mass or the entire testis oten decreases in size and develops areas of increased echogenicity because of ibrosis or dystrophic calciication.104 he early sonographic appearance may be diicult to distinguish from a testicular neoplasm, but infarcts decrease substantially in size, whereas tumors characteristically enlarge with time.3,101,105

Adrenal Rests Adrenal rests are a rare cause of intertesticular masses and can be seen in the setting of congenital adrenal hyperplasia (CAH), and rarely in the setting of Cushing syndrome. CAH is an autosomal recessive disease involving an adrenocortical enzyme defect. his disease typically becomes clinically obvious early in life or in early adulthood. Patients oten present with a testicular mass or enlargement, precocious puberty, and with or without salt-depletion syndrome. Adrenal rests arise from aberrant adrenocortical cells that migrate with gonadal tissues in the fetus. hey can form tumorlike masses in response to elevated levels

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FIG. 22.14 Testicular Infarcts: Spectrum of Appearances. (A) and (B) Acute infarct. (A) Longitudinal power Doppler scan shows an avascular area at the upper pole from partial torsion. (B) Longitudinal color Doppler scan shows an avascular area in the midtestis caused by vasculitis. (C) and (D) Chronic infarct. (C) Longitudinal scan shows a peripheral wedge-shaped hypoechoic area caused by prior mumps orchitis. (D) Longitudinal power Doppler scan shows lack of vascularity in the lower pole.

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FIG. 22.15 Adrenal Rests in Patient With Congenital Adrenal Hyperplasia. (A) Longitudinal scan shows multifocal hypoechoic masses (arrows) within the testis that cannot be distinguished from tumor. (B) CT in same patient shows bilateral adrenal hyperplasia (arrows).

of circulating adrenocorticotropic hormone in CAH and Cushing syndrome. hese lesions are typically multifocal, bilateral, and eccentrically located. Sonographically, they are variable in appearance, typically presenting as hypoechoic masses, although they may be heterogeneous, hyperechoic masses with posterior acoustic shadowing (Fig. 22.15). Adrenal rests can demonstrate spokelike vascularity with multiple peripheral vessels radiating toward a central point within the mass. Usually, if the patient has the appropriate hormonal abnormalities associated with CAH and if sonography shows the appropriate indings, no further workup is necessary.106,107 If conirmation of the diagnosis is required, a biopsy under ultrasound guidance may be obtained intraoperatively when the testis is exposed. Additionally, testicular vein sampling will show elevated cortisol levels compared with peripheral blood levels.108 Treatment with glucocorticoid replacement therapy results in stabilization or regression of the masses.109

Splenogonadal Fusion Splenogonadal fusion is a rare congenital anomaly in which there is fusion of the spleen and gonad. It typically occurs on the let side and is most oten associated with cryptorchidism.110 here are two types of splenogonadal fusion: continuous and discontinuous. In the more common continuous form, the gonad is linked to the spleen by a ibrous cord of splenic tissue. In the discontinuous form, ectopic splenic tissue is attached to the testis. Rarely, ectopic splenic tissue may occur on the epididymis or spermatic cord. Splenogonadal fusion may mimic testicular malignancy. he diagnosis may be established by documenting uptake on a technetium-99m sulfur colloid scan. Calciications Scrotal calciications may be seen within the parenchyma of the testis or epididymis, attached to the tunica, or freely located in the luid between the layers of the tunica vaginalis. Large, smooth, curvilinear intratesticular calciications without an associated sot tissue mass are characteristic of a large-cell calcifying Sertoli cell tumor111 (see Fig. 22.9C). Scattered calciications may be found in tuberculosis, ilariasis, and scarring from regressed germ cell tumor or trauma.

Scrotal Calciications TESTICULAR Solitary, postinlammatory granulomatous, vascular Microlithiasis Regressed, or “burned-out,” germ cell tumor Large-cell calcifying Sertoli cell tumor Teratoma Mixed germ cell tumor Sarcoid Tuberculosis Chronic infarct Posttraumatic EXTRATESTICULAR Tunica vaginalis, “scrotal pearls” Torsed appendages Chronic epididymitis Schistosomiasis

Testicular microlithiasis is a condition in which calciications are present within the seminiferous tubules of the testis either unilaterally or bilaterally. It is postulated that microlithiasis is caused by defective Sertoli cell phagocytosis of degenerating tubular cells, which then calcify within the seminiferous tubules.112,113 Microlithiasis has been classiied as difuse and limited.114 In the difuse form, innumerable small, hyperechoic foci are difusely scattered throughout the testicular parenchyma. hese tiny (1-3 mm) foci rarely shadow and occasionally demonstrate a comet-tail appearance (Fig. 22.16). In the limited form, less than ive hyperechoic foci are seen per image of the testis (Fig. 22.16B). Microlithiasis is seen in 1% to 2% of patients referred for testicular sonography and has a reported prevalence in the general population of 0.6% to 0.9%.115 Microlithiasis has been associated with cryptorchidism, Klinefelter syndrome, Down syndrome, pulmonary alveolar microlithiasis, AIDS, neuroibromatosis, previous radiotherapy, and subfertility.112,115-117 Microlithiasis is typically an incidental inding on scrotal ultrasound, and if

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FIG. 22.16 Microlithiasis and Associated Testicular Tumors: Spectrum of Appearances. (A) Light microscopy examination shows multiple intratubular calciications (dark areas) characteristic of microlithiasis. (B) Longitudinal scan shows a few tiny calciications of limited microlithiasis. (C) and (D) Diffuse microlithiasis. (E) Transverse scan of testis shows microlithiasis and partially cystic mass caused by mixed germ cell tumor. (F) Limited microlithiasis with seminoma. Longitudinal scan shows a few tiny calciications and a homogeneous hypoechoic mass. (G) Longitudinal scan shows microlithiasis and two hypoechoic homogeneous masses (arrows) due to seminoma. (H) Longitudinal scan shows large hypoechoic mass with multiple small and coarser calciications. (I) Dual transverse image shows large hypoechoic left testicular mass and microcalciications in the right testis.

associated with a mass, management is dictated by the intratesticular mass itself. It has been correlated with testicular carcinoma, although the extent of the risk for subsequent development of neoplasm and the recommended surveillance in the setting of microlithiasis remain controversial.114,115,118 Annual physical examination and periodic self-examination have been suggested for those who have no additional risk factors.114,115,119,120 Recent literature suggests that there is no causal link and that sonographic follow-up of microlithiasis should be determined by any additional risk factors and not the microlithiasis itself.121

EXTRATESTICULAR PATHOLOGIC LESIONS Tunica Vaginalis Hydrocele, Hematocele, and Pyocele he normal scrotum contains a few milliliters of serous luid between the layers of the tunica vaginalis, and this is usually

visible on sonographic examination. Larger volumes of serous luid, and blood, pus, or urine may also accumulate in the space between the parietal and visceral layers of the tunica vaginalis lining the scrotum. hese luid collections should be conined to the anterolateral portions of the scrotum because of the attachment of the testis to the epididymis and scrotal wall posteriorly (the bare area)9 (Fig. 22.17). Hydrocele is an abnormal accumulation of serous luid between the layers of the tunica vaginalis. Hydrocele is the most common cause of painless scrotal swelling14 and may be congenital or acquired. he congenital type results from incomplete closure of the processus vaginalis, with persistent open communication between the scrotal sac and the peritoneum, usually resolving by 18 months of age (Fig. 22.17D). Acquired hydroceles may be idiopathic or caused by epididymitis, epididymo-orchitis, torsion, or, in rare cases, tumors. Hydroceles associated with testicular tumors are usually small.3,122,123 Sonography is useful in detecting a potential cause of the hydrocele by allowing evaluation of the testis when a

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FIG. 22.17 Scrotal Fluid Collections: Spectrum of Appearances. (A) Hydrocele. Transverse scan shows a large hydrocele anterolaterally with testis partially enveloped by tunica vaginalis posteriorly. (B) Encysted hydrocele. Longitudinal scan along the spermatic cord shows a luid collection present in the inguinal canal. (C) Encysted hydrocele. Coronal CT image of patient in B demonstrates a well circumscribed luid collection (arrow) corresponding to sonographic examination. (D) Patent processus vaginalis. Longitudinal scan of inguinal region shows an elongated luid collection (arrows) above the level of the testis and epididymis (E) in patient with chronic hydrocele. (E) Hematocele. Transverse scan shows loculated luid with internal echoes and mass affect on the testis (T). (F) Pyocele. Longitudinal scan shows an irregular, centrally hypodense, extratesticular (T, testis) collection (arrow) adjacent to the epididymis (E) in the setting of epididymo-orchitis.

large hydrocele hampers palpation. Hydroceles are characteristically anechoic collections with good sound transmission surrounding the anterolateral aspects of the testis. Low-level to medium-level echoes from ibrin bodies or cholesterol crystals may occasionally be visualized moving freely within a

hydrocele.124 Rarely, a large hydrocele may impede testicular venous drainage and cause absence of antegrade arterial diastolic low.122 Uncommonly, a hydrocele may be loculated around the spermatic cord above the testis and epididymis, representing a noncommunicating, encysted hydrocele; or the

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collection communicates with the peritoneum but not the scrotum, a funicular hydrocele125 (Fig. 22.17B and C). Hematoceles and pyoceles are less common than simple hydroceles. Hematoceles (accumulation of blood within the tunica vaginalis) result from trauma, surgery, neoplasms, or torsion.126 Pyoceles result from untreated epididymo-orchitis or rupture of an intratesticular abscess into the space between the layers of the tunica vaginalis. Both hematoceles and pyoceles appear as complex luid collections with internal septations and loculations (Fig. 22.17). hickening of the scrotal skin and calciications may be seen in chronic cases.

Paratesticular Masses Most extratesticular neoplasms in adults are benign, but extratesticular neoplasms in children are frequently malignant.127

Extratesticular Tumors/Masses BENIGN Hernia Adenomatoid tumor Fibroma/ibrous pseudotumor Lipoma Hemangioma Leiomyoma Neuroibroma Cholesterol granuloma Polyorchidism Papillary cystadenoma Adrenal rest MALIGNANT Fibrosarcoma Liposarcoma Rhabdosarcoma Histiocytoma Lymphoma Metastases

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Hernia An inguinal hernia is a common paratesticular mass.128 Although scrotal hernias are usually diagnosed on the basis of clinical history and physical examination, sonography is useful in the evaluation of atypical cases. Hernias are classiied as either direct or indirect. An indirect hernia exits the abdominal cavity through the internal inguinal ring, can traverse the inguinal canal, and extend into the scrotum. Indirect hernias are associated with a patent processus vaginalis. A direct hernia represents a protrusion through the abdominal wall at Hesselbach triangle, an area of weakness bordered by the lateral border of the rectus sheath medially, the inferior epigastric artery laterally, and the inguinal ligament inferiorly. Sonographic appearance of an inguinal hernia depends on its contents. Bowel will oten be luid illed with multiple internal bright echoes. Bowel gas may cause shadowing, a inding also seen with abscesses and thus potentially confusing. he presence of bowel loops within the hernia may be conirmed by the visualization of valvulae conniventes or haustrations and detection of peristalsis on real-time examination (Fig. 22.18A). he presence of highly echogenic material within the scrotum may result from a hernia containing omentum or other fatty masses such as lipomas, although lipomas are typically well deined and herniated omentum can typically be traced back to the inguinal canal (Fig. 22.18B). Sonographic examination of the inguinal canal into the scrotum is necessary to make the diagnosis.129 Additional discussion of hernias can be found in Chapter 13. Calculi Extratesticular scrotal calculi are calciications within the tunica vaginalis (Fig. 22.19). hese ibrinoid loose bodies have been called scrotoliths, or “scrotal pearls” because of their macroscopic appearance, which is usually rounded, pearly white, and rubbery. Histologically, they consist of ibrinoid material deposited around a central nucleus of hydroxyapatite.130 hey may result from inlammatory deposits that form and then ultimately separate

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FIG. 22.18 Indirect Inguinal Hernias: Spectrum of Appearances. (A) Herniated small bowel. Oblique scan shows herniated small bowel (arrow) superior to and abutting the testis (T). (B) Herniated mesenteric fat. Longitudinal scan shows herniated fat (H) above testis (T) and epididymis (E).

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FIG. 22.19 Benign Intrascrotal Calciication. (A) Calciied tunica plaque (arrow) on the tunica vaginalis. (B)-(D) Scrotal pearls. (B) Mobile scrotal calciication in a small hydrocele. (C) Longitudinal scan shows a mostly calciied scrotal pearl (arrow) in a hydrocele. T, Testis. (D) Bilateral scrotal pearls.

from the tunica vaginalis, or from torsion of the appendix testis or appendix epididymis. Sonographically, they appear as free loating, echogenic calculi with posterior acoustic shadowing; can be multiple; and range in size from a few millimeters to larger than a centimeter. Hydroceles facilitate the sonographic diagnosis of scrotal calculi.

Varicocele A varicocele is an abnormal dilatation of the veins of the pampiniform plexus located posterior to the testis, adjacent to the epididymis, and accompanying the vas deferens within the spermatic cord14 (Fig. 22.20). A varicocele is the most frequently encountered mass of the spermatic cord. he veins of the pampiniform plexus normally range from 0.5 to 1.5 mm in diameter, with a main draining vein up to 2 mm in diameter.

he size for normal varies, with some diagnosticians using greater than 2 mm as a guideline for the diagnosis of a varicocele and others using 3 mm.131 here are two types of varicoceles: primary (idiopathic) and secondary. he idiopathic varicocele is caused by incompetent valves in the internal spermatic vein, which results in impaired drainage of blood from the spermatic vein and pampiniform plexus with the patient in an upright position. Varicoceles afect approximately 15% of men but occur in up to 40% of men attending infertility clinics.132,133 Varicocele is the most common correctable cause of male infertility.134 Idiopathic varicoceles occur much more commonly on the let side and are most common in men aged 15 to 25 years. he let-sided predominance probably occurs because the let testicular vein is longer, with venous drainage into the let renal vein entering the renal vein

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FIG. 22.20 Varicocele. (A) Longitudinal and (B) color Doppler images show serpentine, hypoechoic, dilated veins posterior to the testis. The blood low in a varicocele is slow and may be detected only with low-low Doppler settings or the Valsalva maneuver. See also Video 22.3.

at a right angle, as opposed to the right spermatic vein, which drains directly into the vena cava. Idiopathic varices normally distend when the patient is upright or performs the Valsalva maneuver and decompress when the patient is supine. Primary varicoceles are bilateral in up to 50% of cases.135 Secondary varicoceles result from increased pressure on the spermatic vein or its tributaries by marked hydronephrosis, an enlarged liver, abdominal neoplasms, or venous compression by a retroperitoneal mass.43 Secondary varicoceles may also occur in nutcracker syndrome (nutcracker phenomenon), in which the superior mesenteric artery compresses the let renal vein.136 A search for neoplastic obstruction of gonadal venous return must be undertaken in cases of a right-sided, nondecompressible, or newly discovered varicocele in a patient older than 40 years14 (Fig. 22.21). he appearance of secondary varicoceles is not afected by patient position. In infertile men, sonography aids in the diagnosis of clinically palpable and subclinical varicoceles. Sonography is also of value in assessing testicular size before and ater treatment, because varicocele may be associated with a decreased testicular volume.133 here is poor correlation between the size of the varicocele and the degree of testicular tissue damage leading to infertility, and surgical repair of subclinical varicoceles for infertility has been controversial.137 Sonographically, a varicocele consists of multiple, serpentine, anechoic structures more than 2 mm in diameter, creating a tortuous, multicystic collection located adjacent or proximal to the upper pole of the testis and head of the epididymis. A highfrequency transducer in conjunction with low-low Doppler settings should be used to optimize slow-low detection within varices. Slowly moving red blood cells may be visualized with

high-frequency transducers, even when low is too slow to be detected by Doppler imaging. Venous low can be augmented with the patient in the upright position or during Valsalva maneuver (Video 22.3). Varicoceles follow the course of the spermatic cord into the inguinal canal and are easily compressed by the transducer.3 Rarely, varicoceles may be intratesticular, either in a subcapsular location or around the mediastinum testis138,139 (Fig. 22.22).

Fibrous Pseudotumor Fibrous pseudotumor is a rare, nonneoplastic mass of reactive ibrous tissue that most commonly involves the tunica vaginalis. hese masses are known by a number of names, including ibroma, paratesticular ibrosis, or inlammatory pseudotumor, and can become quite large and mimic neoplasms. Most patients present with a painless scrotal mass, possibly with a prior history of infection or trauma. Histologically, masses are composed of hyalinized collagen and granulation tissue and may be partially calciied. On sonography, ibrous pseudotumors may appear as one or more solid masses attached to or closely associated with the capsule of the testis. here may be an associated hydrocele. Echogenicity is variable and they may be seen as a hypoechoic, hyperechoic, or heterogeneous paratesticular mass with posterior acoustic shadowing depending on extent of calicications140-142 (Fig. 22.23A and B). Polyorchidism Polyorchidism, or supernumerary testes, is a rare entity thought to result from abnormal division of the genital ridge embryologically. he supernumery testes are intrascrotal in location in approximately 75% of cases and present as a painless scrotal

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FIG. 22.21 Varicocele Caused by Retroperitoneal Paraganglioneuroma. (A) Longitudinal scan shows extremely dilated veins of large, right varicocele. (B) Transverse abdominal sonogram shows paraganglioneuroma (arrow) adjacent to the inferior vena cava (I). A, Aorta; GB, gallbladder. (C) Axial CT scan shows the vascular mass (arrows) adjacent to inferior vena cava.

Epididymal Lesions

FIG. 22.22 Intratesticular Varicocele. Longitudinal scan shows the dilated intratesticular veins.

mass (Fig. 22.24). Twenty percent of supernumery testes are inguinal with the remaining retroperitoneal in location.60 hese supernumery testes have similar imaging characteristics to normal testes, but they are more mobile and therefore at increased risk of torsion. here has also been an increased risk of carcinoma reported.131,135,137,143

Cystic Lesions he most common epididymal mass is a cyst, which includes epididymal cysts and spermatoceles. Both were seen in 20% to 40% of all asymptomatic patients studied by Leung et al.,144 and were multiple in 30% of cases. Both epididymal cysts and spermatoceles are thought to result from dilatation of the epididymal ductules, but the contents of these masses difer.14 Epididymal cysts contain clear serous luid, whereas spermatoceles are illed with spermatozoa and sediment containing lymphocytes, fat globules, and cellular debris, giving the luid a thick, milky appearance.3 Both lesions may result from prior episodes of epididymitis or trauma. Spermatoceles and epididymal cysts appear identical on sonography: anechoic, circumscribed masses with no or few internal echoes. Loculations and septations are oten seen (Fig. 22.25). In rare cases, a spermatocele may be hyperechoic.9 Diferentiation between a spermatocele and an epididymal cyst is rarely important clinically. Spermatoceles almost always occur in the head of the epididymis and represent cystic dilatation of eferent ductules, whereas epididymal cysts arise throughout the length of the epididymis.

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FIG. 22.23 Extratesticular Scrotal Solid Masses: Spectrum of Appearances. (A) Fibrous pseudotumor. Transverse scan shows a mass of mixed echogenicity lateral to and separate from the testis. (B) Fibrous pseudotumor. Longitudinal scan shows a lamellated extratesticular mass (arrow) with a central echogenic focus adjacent to the tunica of the testis (T). (C) Benign adenomatoid tumor of epididymis. Longitudinal scan shows a hypoechoic mass (arrow) in the epididymal tail separate from the testis (T). (D) Spermatic cord lipoma. Longitudinal scan shows an echogenic mass superior to the epididymis and testis, along the spermatic cord. (E) Liposarcoma. Transverse scan shows a large heterogeneous mass (arrow) deep to the testis (T) in the scrotal wall or spermatic cord. (F) Liposarcoma. Contrast-enhanced axial CT image shows a heterogeneous mass containing fat and solid components (arrow) associated with the spermatic cord in patient E, consistent with a liposarcoma. (G) Leiomyoma of cord. Longitudinal scan shows a solid mass superior to the testis. (H) Rhabdomyosarcoma. Longitudinal extended–ield of view scan in a 12-year-old shows a large, paratesticular mass inferior to the testis. (I) Metastasis from lung carcinoma. Longitudinal scan shows a heterogenous mass with calciications in the tail of the epididymis.

Tumors he most common epididymal neoplasm is the benign adenomatoid tumor, which accounts for approximately 30% of all paratesticular neoplasms, second only to lipoma.28 Although most frequently located in the tail (see Fig. 22.23C), adenomatoid tumors may occur anywhere in the epididymis and have also been reported in the spermatic cord, as well as the tunica albuginea, where they may grow intratesticularly. Adenomatoid tumor may occur at any age but most oten afects patients aged 20 to 50 years.3,145 Adenomatoid tumors are generally unilateral, solitary, well deined, and round or oval, rarely measuring more than 5 cm in diameter. Occasionally, they may appear plaquelike and poorly deined. Sonography usually shows a solid,

well-circumscribed mass with echogenicity that is at least as great as the testis,3 although they may also be hypoechoic. Other benign extratesticular tumors are rare and include lipomas (see Fig. 22.23D), leiomyomas (see Fig. 22.23G), ibromas, hemangiomas, neuroibromas, and cholesterol granulomas. Adrenal rests may also be encountered in the spermatic cord, testis, epididymis, rete testis, and tunica albuginea, typically in the setting of CAH. Papillary cystadenoma of the epididymis is a rare tumor with a strong association with von Hippel–Lindau disease. Up to 40% of cystadenomas are bilateral, a inding that is virtually pathognomic for von Hippel–Lindau disease. hese tumors are benign epithelial tumors of the epididymis, occurring in the

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dilated vas deferens may be seen in addition to the enlarged epididymis. An unusual appearance described as “dancing megasperm” is occasionally seen in patients with vasectomy (Video 22.5). High relective echoes within the dilated epididymis appear to move independently, shown histologically to be aggregations of spermatozoa and macrophages.152

FIG. 22.24 Polyorchidism. Transverse extended ield of view image of the right hemiscrotum shows a right testis (R) and two additional intrascrotal masses with similar imaging characteristics to the right testis (*) consistent with supernumery testes in an asymptomatic patient with a palpable mass.

eferent ductules of the epididymal head. hey generally present as a hard, palpable mass, and at ultrasound appear as an echogenic, solid mass with distinct, small cystic spaces. he majority of solid epididymal masses are benign. However, primary extratesticular scrotal malignant neoplasms do occur, including adenocarcinoma, ibrosarcoma, liposarcoma (see Fig. 22.23E and F), histiocytoma, and lymphoma in adults and rhabdomyosarcoma in children (see Fig. 22.23H). Metastatic tumors to the epididymis are also rare. he most common primary sites include the testis, stomach, kidney, prostate, colon, and, less oten, the pancreas146,147 (see Fig. 22.23I). Size of the lesion and the presence of color low may be helpful in the diagnosis of extratesticular scrotal masses.23,148 Larger masses (>1.5 cm) with prominent color low that present without cl inical symptoms of inlammation are more likely to be malignant.23,148

Sperm Granuloma Sperm granulomas are thought to arise from extravasation of spermatozoa into the sot tissues surrounding the epididymis, producing a necrotizing granulomatous response.3 hese lesions may be painful or asymptomatic, and they are most oten found in patients ater vasectomy. It is assumed that vasectomy produces increased pressure in the epididymal ductules, causing rupture with subsequent formation of sperm granulomas. Sperm granulomas may also be associated with prior epididymal infection or trauma. he typical sonographic appearance is that of a solid, hypoechoic or heterogeneous mass, usually located in or adjacent to the epididymis, although it may simulate an intratesticular lesion (Fig. 22.26A). Chronic sperm granulomas may contain calciication.149 Postvasectomy Changes in the Epididymis Sonographic changes in the epididymis are very common in patients ater vasectomy.150,151 In addition to the formation of sperm granulomas, these indings include epididymal enlargement with ductular ectasia involving the epididymis (Fig. 22.26B) and rete testis, as well as the development of cysts (Video 22.4). A

Chronic Epididymitis Chronic epididymitis is more commonly seen with conditions associated with granulomatous reactions, including tuberculosis, brucellosis, syphilis, and parasitic and fungal infections.60 Tuberculosis epididymal infections are the most common of these and are believed to result from renal disease seeding the lower genitourinary tract, with 25% of patients having bilateral involvement.153 Patients with chronic granulomatous epididymitis caused by spread of tuberculosis from the genitourinary tract complain of a hard, nontender scrotal mass.14 Sonography most oten shows a thickened tunica albuginea and a thickened, irregular epididymis with variable appearance (Fig. 22.27). Calciication may be identiied within the tunica albuginea or epididymis.3 Associated indings include hydroceles, scrotal wall thickening, and istulas.153 Untreated granulomatous epididymitis can spread to the testes, causing an epididymo-orchitis, although this is less common than isolated epididymal disease. Focal testicular involvement may demonstrate a variable sonographic appearance and may simulate the appearance of a testicular neoplasm on sonography. Patients may also develop chronic epididymitis ater episodes of acute bacterial epididymitis that do not subside. Sarcoidosis Sarcoidosis is a noninfectious, chronic, granulomatous disease that may involve the genital tract.154-156 In an autopsy series, approximately 5% of cases had genital tract involvement, with the epididymis most frequently involved.60 he clinical presentation is acute or recurrent epididymitis or painless enlargement of the testis or epididymis. Sonographically, sarcoid lesions are irregular, hypoechoic solid masses in the testis or epididymis (Fig. 22.28). Occasionally, hyperechoic, calciic foci with acoustic shadowing may be seen. Distinguishing sarcoidosis from an inlammatory process or a neoplasm is diicult on sonography alone. Resection or orchiectomy may be necessary for deinitive diagnosis. As noted previously, tuberculosis can also cause a chronic granulomatous reaction of the genital tract, typically a granulomatous epididymitis.

ACUTE SCROTAL PAIN Acute scrotal pain may have numerous causes. More common causes include torsion of the spermatic cord and testis, epididymitis or orchitis, torsion of a testicular appendage, acute hydrocele, strangulated hernia, idiopathic scrotal edema, Henoch-Schönlein purpura, abscess, traumatic hemorrhage, hemorrhage into a testicular neoplasm, and scrotal fat necrosis. Torsion of the spermatic cord and acute epididymitis or epididymo-orchitis are the most common causes of acute scrotal pain. hese entities cannot be distinguished by

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FIG. 22.25 Extratesticular Scrotal Cysts: Spectrum of Appearances. (A) Spermatocele. Longitudinal scan shows an anechoic cyst in head of the epididymis. (B) Spermatocele. Longitudinal scan shows a large cyst containing internal echoes in head of the epididymis. (C) Septate spermatocele. Longitudinal scan shows a septate cyst in head of the epididymis. (D) Epididymal cyst. Longitudinal scan shows a cyst in body of the epididymis. (E) Cyst of vas deferens remnant. Longitudinal scan shows a cyst with internal echoes inferior to the testis (surgically proven). (F) Epidermoid inclusion cyst of epididymis. Longitudinal color Doppler scan shows bilobed cystic mass in head of the epididymis surrounded by vessels.

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FIG. 22.26 Postvasectomy Changes. (A) Sperm granuloma. Transverse scan shows a heterogeneous mass (arrow) along the vas deferens and separate from the epididymis (E) in a postvasectomy patient. (B) Postvasectomy changes in epididymis. Longitudinal image of the scrotum shows ectasia of the ductules of the epididymis (arrows) in a patient who had a vasectomy. See also Videos 22.4 and 22.5.

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FIG. 22.27 Tuberculous Epididymo-orchitis. (A) Longitudinal scan shows a heterogeneous mass with calciication involving the head and body of the epididymis and the adjacent testis (T). (B) Longitudinal color Doppler image shows increased vascularity in the epididymis and adjacent testis.

rate from torsion but also an increase in unnecessary surgical procedures. Real-time sonography, Doppler sonography, testicular radionuclide scintigraphy, and MRI have been used to increase the accuracy of distinguishing between infection and torsion.158 Currently, sonography using color low or power Doppler is the imaging study of choice to diagnose the cause of acute scrotal pain.

FIG. 22.28 Testicular Sarcoid. Longitudinal scan of the testis shows multiple, small, hypoechoic, solid masses resulting from sarcoid.

routine physical examination or laboratory tests in up to 50% of patients.157 In the past, immediate surgical exploration was been advised in boys and young men with acute scrotal pain, unless a deinitive diagnosis of epididymitis or orchitis was made. his aggressive approach resulted in an increased testicular salvage

Causes of Acute Scrotal Pain Torsion of the testis Epididymo-orchitis Testicular or epididymal appendage torsion Strangulated hernia Trauma Idiopathic scrotal edema Henoch-Schönlein purpura

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Torsion Torsion is more common in adolescent boys and represents approximately 20% of the acute scrotal pathologic phenomena in postpubertal males.3 Prompt diagnosis is necessary because torsion requires immediate surgery to preserve the testis. he testicular salvage rate is over 80% if surgery is performed within 5 or 6 hours of the onset of pain, 70% if surgery is performed within 6 to 12 hours, and only 20% if surgery is delayed for more than 12 hours.159 Two types of testicular torsion have been described: intravaginal and extravaginal. Extravaginal torsion occurs prenatally and in newborns up to 30 days ater delivery. Torsion occurs outside of the tunica vaginalis when the testis, gubernaculum, and tunica vaginalis are not ixed to the scrotal wall, allowing rotation of these structures as a unit and causing torsion of the cord at the level of the external ring. If this occurs prenatally, the afected neonate presents with a irm, painless mass in the scrotum, and swelling and discoloration of the afected side. he testis is typically infarcted and necrotic at birth. Postnatal testicular torsion is detected as a change in the testicular examination.160,161 Intravaginal torsion is the more common type, arising within the tunica vaginalis and occurring most frequently at puberty. It results from anomalous suspension of the testis by a long stalk of spermatic cord mesentery, resulting in complete investment of the distal cord, testis, and epididymis by the tunica vaginalis. his allows the testis to swing and rotate within the tunica vaginalis like a clapper inside a bell, the so-called bell-clapper deformity (Fig. 22.29). Anomalous testicular suspension is bilateral in 50% to 80% of patients; hence the contralateral testis is usually ixed at the time of surgery as well. Sonography is considered the irst step in evaluation of the acute scrotum, and its role is well established.162-164 Sonographic indings vary with duration and degree of rotation. Gray-scale sonographic changes are nonspeciic in the acute phase of torsion.157,161,165 A torsed testis with normal, homogeneous echogenicity on gray-scale imaging has a high chance of successful salvage at surgery.166 Testicular enlargement and decreased echogenicity are the most common indings 4 to 6 hours ater the onset of torsion. With continued torsion, at 24 hours the testis can develop heterogeneous echotexture secondary to vascular congestion, hemorrhage, and infarction167-169 (Fig. 22.30). A hypoechoic or heterogeneous echogenicity may indicate nonviability, although this is not speciic.166 Torsion may change the position of the long axis of the testis. Extratesticular sonographic indings typically occur in torsion and are important to recognize. he spermatic cord immediately cranial to the testis and epididymis is twisted, causing a characteristic torsion knot or “whirlpool pattern” of concentric layers seen on sonography or MRI161,170,171 (Fig. 22.30G and H). he epididymis may be enlarged and heterogeneous because of hemorrhage or ischemia, and may be diicult to separate from the torsion knot of the spermatic cord. his spherical epididymiscord complex can be mistaken for epididymitis.161 A reactive hydrocele and scrotal skin thickening are oten seen with torsion. Large, echogenic, or complex extratesticular masses caused by hemorrhage in the tunica vaginalis or epididymis may be seen

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FIG. 22.29 “Bell-Clapper” Anomaly, Intravaginal Torsion, and Extravaginal Torsion. (A) Normal anatomy. The tunica vaginalis (arrows) does not completely surround the testis and epididymis, which are attached to the posterior scrotal wall (short arrow). (B) Bell-clapper anomaly. The tunica vaginalis (arrows) completely surrounds the testis, epididymis, and part of the spermatic cord, predisposing to torsion. (C) Intravaginal torsion. Bell-clapper anomaly with complete torsion of the spermatic cord, compromising the blood supply to the testis. (D) Extravaginal torsion in a neonate. Tunica vaginalis (arrows) is in normal position, but abnormal motility allows rotation of the testis, epididymis, and spermatic cord.

in patients with undiagnosed torsion.172 he gray-scale indings of acute and subacute torsion are not speciic and may be seen in testicular infarction caused by epididymitis, epididymo-orchitis, and traumatic testicular rupture or infarction. Doppler sonography is the most useful and most rapid technique to establish the diagnosis of testicular ischemia and to help distinguish torsion from epididymo-orchitis.157,162,167 he absence of intratesticular blood low at color and power Doppler ultrasound is considered diagnostic of ischemia (color and power techniques appear to have equivalent sensitivity in the diagnosis of torsion).173-178 Meticulous scanning of the testicular parenchyma with the use of low-low detection Doppler settings (low pulse repetition frequency, low wall ilter, high Doppler gain, small color sampling box, lowest possible threshold setting) is important because intratesticular vessels are small and have low low velocities, especially in prepubertal boys. Color low Doppler sonography is more sensitive for showing decreased testicular low in incomplete torsion than is nuclear scintigraphy, which is rarely

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FIG. 22.30 Torsion of Spermatic Cord and Testis: Spectrum of Appearances. (A)-(D) Acute torsion. Longitudinal power Doppler scans show (A) no low in the testis and (B) abnormal, transverse, and vertical orientation of the testis with no low. (C) After manual detorsion of case in B, longitudinal color Doppler scan shows the normal orientation of the testis with blood low present. The testis has a striated appearance caused by the previous ischemia. (D) Dual transverse gray-scale scan shows enlarged hypoechoic right testis resulting from torsion and skin thickening in the right hemiscrotum. (E) Partial torsion. Longitudinal scan with spectral Doppler shows a high-resistance testicular arterial waveform with little diastolic low because of venous occlusion; a small, reactive hydrocele was found. (F) After spontaneous detorsion of case in E, longitudinal scan with spectral Doppler shows return of diastolic low. (G) Torsion knot. Longitudinal scan with acute spermatic cord torsion shows the “torsion knot” complex of epididymis and spermatic cord. (H) Acute torsion. Intraoperative photograph shows the twisted spermatic cord that gives the torsion knot appearance on sonograph. (I) Subacute torsion (3 days of pain). Transverse power Doppler scan shows absent low within the testis with surrounding hyperemia. (H with permission from Winter TC. Ultrasonography of the scrotum. Appl Radiol 2002;31[3]:9-18.169)

used anymore to diagnose torsion.179 In testicular torsion, color Doppler sonography has a sensitivity of 80% to 98%, speciicity of 97% to 100%, and accuracy of 97%.161,162,180 he use of intravascular contrast agents in sonography can improve the sensitivity and speciicity of detecting blood low in the scrotum.175,181 In pediatric patients, it may be diicult to document low in a normal testis.182 In practice, many surgeons elect to explore the testis

surgically if clinical symptoms and signs are suggestive and results of the sonographic examination are equivocal. Torsion is not an all or none phenomenon. Potential pitfalls in using sonography in the diagnosis of torsion are partial torsion, torsion/detorsion, and ischemia from orchitis. Torsion of at least 540 degrees is necessary for complete arterial occlusion.162,183 With partial torsion of 360 degrees or less, arterial low may still

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occur, but venous outlow is oten obstructed, causing diminished diastolic arterial low on spectral Doppler examination184,185 (Fig. 22.30E). If spontaneous detorsion occurs, low within the afected testis may be normal, or it may be increased and mimic orchitis.186 Spontaneous detorsion can occur with sequelae including a segmental testicular infarction.102,103 Segmental testicular infarction may also occur with Henoch-Schönlein purpura or with orchitis (see Fig. 22.14). Orchitis may also cause global ischemia of the testis and mimic torsion.186 In subacute or chronic torsion, Doppler sonography demonstrates no low in the testis and increased low in the paratesticular tissues, including the epididymis-cord complex and dartos fascia (Fig. 22.30I). Torsion of the appendix testis or appendix epididymis can present with acute scrotal pain, potentially mimicking testicular torsion clinically, although there are no other clinical symptoms and the cremasteric relex can still be elicited. Patients are rarely referred for imaging because the pain is usually not severe, and the twisted appendage may be evident on physical examination as a small irm nodule palpable at the superior aspect of the testis, with a bluish discoloration, or the “blue dot” sign.187 Up to 95% of twisted appendages involve the appendix testis and occur most oten in boys aged 7 to 14 years.65 he sonographic appearance of the twisted testicular appendage has been described as an avascular hyperechoic mass with a central hypoechoic focus adjacent to the head of a normally perfused testis and surrounded by an area of increased color Doppler perfusion.162,188 hese cases are managed conservatively with pain typically resolving in 2 to 3 days with interval atrophy of the torsed appendage. he role of sonography is to exclude testicular torsion or epididymoorchitis. Idiopathic scrotal edema typically afects prepubertal boys, with acute onset of relatively painless scrotal erythema and subcutaneous edema. Idiopathic scrotal edema typically resolves spontaneously in 1 to 3 days without sequelae.

Epididymitis and Epididymo-orchitis Epididymitis is the most common cause of acute scrotal pain in postpubertal men. It may be acute or chronic, depending on the inciting organism and the duration of the process. Acute epididymitis usually results from a lower urinary tract infection and is less oten hematogenous or traumatic in origin. he common causative organisms are Escherichia coli, Pseudomonas, and Klebsiella. Sexually transmitted organisms causing urethritis, such as Neisseria gonorrhoeae and Chlamydia trachomatis, are common causes of epididymitis in younger men. Less frequently, epididymitis may be caused by tuberculosis, mumps, or syphilitic orchitis.153,189 he age of peak incidence is 40 to 50 years. Typically, patients present with the insidious onset of pain which increases over 1 or 2 days. Fever, dysuria, and urethral discharge may also be present. In acute epididymitis, sonography characteristically shows enlargement of the epididymis, involving the tail initially and frequently spreading to the entire epididymis190 (Fig. 22.31A and B). he echogenicity of the epididymis is usually decreased and its echotexture is oten coarse and heterogeneous, likely secondary to edema, hemorrhage, or both. Color low Doppler sonography usually shows increased blood low in the epididymis or testis,

or both, compared with the asymptomatic side.191 Reactive hydrocele formation is common, and associated scrotal wall thickening may be seen. Direct extension of epididymal inlammation to the testis, called epididymo-orchitis, occurs in up to 20% of patients with acute epididymitis. Isolated orchitis may also occur. In such cases, increased blood low is localized to the testis (Fig. 22.31D and E, Video 22.6). Testicular involvement may be focal or difuse. Characteristically, focal orchitis produces a hypoechoic area adjacent to an enlarged portion of the epididymis. Color Doppler shows increased low in the hypoechoic area of the testis; increased low in the tunica vasculosa may also be visible as lines of color signal radiating from the mediastinum testis.192 hese lines of color correspond to septal accentuation visible as hypoechoic bands on gray-scale sonography (Fig. 22.31H and I). Spectral Doppler shows increased diastolic low in uncomplicated orchitis (Fig. 22.32A). If let untreated, the entire testis may become involved, appearing hypoechoic and enlarged. As pressure in the testis increases from edema, venous infarction with hemorrhage may occur, appearing hyperechoic initially and hypoechoic later.192 Ischemia and subsequent infarction may also occur when the vascularity of the testis is compromised by venous occlusion or venous thrombosis.193 When vascular disruption is severe, resulting in complete testicular infarction, the changes are indistinguishable from those seen in testicular torsion. Color Doppler sonography may show focal areas of reactive hyperemia and increased blood low associated with relatively avascular areas of infarction in both the testis and the epididymis in patients with severe epididymo-orchitis. Diastolic low reversal in the arterial waveforms of the testis is an ominous inding, associated with testicular infarction in severe epididymo-orchitis194 (Fig. 22.32B). In addition to infarction, other complications of acute epididymo-orchitis include intratesticular abscess formation and development of a pyocele (see Figs. 22.13 and 22.17F). Chronic changes may be seen in the epididymis or testis from clinically resolved epididymo-orchitis. Swelling of the epididymis may persist and appear as a heterogeneous mass on sonography. he testis may have a persistent, striated appearance of septal accentuation from ibrosis (Figs. 22.33 and 22.34). his striated appearance of the testis is nonspeciic and may also be seen ater ischemia from torsion or during a hernia repair.192,195 A similar heterogeneous appearance in the testis may be seen in older patients because of seminiferous tubule atrophy and sclerosis.196 Focal areas of infarction in the testis may persist as wedge-shaped or cone-shaped hypoechoic areas or may appear as hyperechoic scars.192 If complete infarction of the testis has occurred because of epididymo-orchitis, the testis may become small, with a hypoechoic or heterogeneous echotexture.

Fournier Gangrene Fournier gangrene is a necrotizing fasciitis of the perineum, external genitalia, and perianal area occurring most frequently in men aged 50 to 70 years. he origin is usually a disease process from the overlying skin, urinary tract, or colorectal area, frequently due to a synergistic polymicrobial infection.197 Predisposing factors include systemic immunosuppression, diabetes mellitus,

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C E FIG. 22.31 Epididymo-orchitis, Epididymitis, and Orchitis: Spectrum of Appearances. (A) and (B) Acute epididymitis. Longitudinal gray-scale and color Doppler images show enlargement and a heterogeneous echotexture of tail of the epididymis, with greatly increased low in tail of the epididymis and minimally increased low in the adjacent testis. (C) Acute epididymo-orchitis. Longitudinal color Doppler scan shows increased low in the epididymis and testis. (D) and (E) Acute orchitis. Longitudinal dual-image gray-scale and color Doppler images show that right testis is hypoechoic and has greatly increased low.

chronic alcoholism, and steroid therapy.152 Multiple organisms are usually involved, including Klebsiella, Streptococcus, Proteus, and Staphylococcus. Surgical debridement of devitalized tissue is usually required, and morbidity and mortality are high without prompt treatment. Ultrasound is helpful in diagnosis by demonstrating scrotal wall thickening containing gas with accompanying shadowing.

TRAUMA When evaluating testicular integrity in the setting of acute trauma, the primary role of sonography is to assess for the continuity of the tunica albuginea: this determines clinical management. Disruption of the tunica albuginea indicates testicular rupture. Prompt diagnosis of a ruptured testis is crucial because of the

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F

G

H

I

FIG. 22.31, cont’d. (F) Longitudinal gray-scale scan with 3 weeks of epididymo-orchitis unresolved with antibiotic therapy shows hypoechoic areas in the testis and an enlarged heterogeneous tail of the epididymis. (G) Color Doppler image shows increased low in the testis and epididymis with an area of decreased low due to ischemia (arrow). (H) and (I) Acute orchitis. Longitudinal gray-scale and color Doppler images show hypoechoic bands caused by septal accentuation from edema and increased vascularity of the testis. See also Video 22.6.

direct relationship between early surgical intervention and testicular salvageability. Approximately 90% of ruptured testes can be saved if surgery is performed within the irst 72 hours, whereas only 45% may be salvaged ater 72 hours.198 Sonographic features of testicular rupture include focal areas of altered testicular echogenicity, corresponding to areas of hemorrhage or infarction, and hematocele formation in 33% of patients. A discrete fracture plane may not be identiied. Tunical disruption associated with extrusion of the seminiferous tubules is speciic for rupture (Fig. 22.35E, Video 22.7). However, the sensitivity of the diagnosis of rupture based on tunical disruption alone is only 50%. Heterogeneity of the testis with associated testicular contour irregularity may be helpful in making the diagnosis of rupture.110,199,200 Color Doppler imaging can be helpful because rupture of the tunica albuginea is almost always associated

with disruption of the tunica vasculosa and loss of blood supply to part or all of the testis.110 Although not speciic for a ruptured testicle, these features may suggest the diagnosis in the appropriate clinical setting, prompting immediate surgical exploration. Clinical diagnosis is oten impossible because of marked scrotal pain and swelling; thus sonography can be invaluable in the assessment of tunica albuginea integrity and the extent of testicular hematoma.110,198-200 A visibly intact tunica albuginea should exclude rupture, but a complex intrascrotal hematoma may be diicult to distinguish from testicular rupture and may obscure the tunica110,201 (Fig. 22.35A). Patients with large intrascrotal hematomas or hematoceles will oten undergo surgical exploration because it is diicult to exclude rupture sonographically in the presence of surrounding complex luid.110 If a patient with a presumed intratesticular hematoma is not surgically explored,

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FIG. 22.32 Spectral Doppler Changes in Orchitis. (A) Uncomplicated orchitis. Longitudinal scan with spectral Doppler tracing shows increased diastolic low in the testis. (B) Orchitis with venous compromise. Longitudinal scan with spectral Doppler tracing in more severe orchitis shows reversal of low in diastole caused by edema impeding venous low.

FIG. 22.33 Heterogeneous “Striped” Testis. Transverse dual image shows heterogeneity in the right testis with marked septal accentuation from previous orchitis. This appearance may also be seen after ischemia.

FIG. 22.34 Fibrosis of Testis After Orchitis. Pathologic specimen of testis shows linear bands of ibrosis (white areas) caused by previous severe orchitis. A similar “end-stage” testis could have this appearance due to ischemia.

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H H A

D

B

C

F

E

G

H

FIG. 22.35 Testicular Trauma: Spectrum of Appearances. (A) Hematoma. Longitudinal image shows hematoma (arrows) on the anterior surface of the testis. Tunica intact at surgery. (B) Fracture of testis. Transverse scan shows a heterogeneous testicle with a linear band (arrows) indicating a fracture. H, Testicular hematoma. (C) Tunical tear. Longitudinal color Doppler image shows contour irregularity of the testis with disruption of the tunica (arrow). Extruded testis parenchyma shows no color low. (D) Same case as C. Photograph during surgery shows tunical tear in the exposed right testis. (E) Rupture of testis. Longitudinal image shows rupture of the testis with extrusion of seminiferous tubules (arrow). (F) In same case as E, photograph during surgery shows a tear in the tunica inferiorly with extrusion of seminiferous tubules. (G) and (H) Fracture of testis. Longitudinal and transverse color Doppler images of the left testis show an irregular linear, hypoechoic, avascular band representing a testicular fracture following acute blunt trauma. The tunica albuginea was intact. See also Video 22.7.

it is incumbent upon the clinician to follow the intratesticular abnormality to resolution because a testicular tumor can mimic an intratesticular hematoma and also predispose to rupture following relatively minor trauma. Testicular fracture refers to discontinuity of normal testicular parenchyma, which may be present in the absence of disruption of the tunica albuginea. An associated intratesticular hematoma or hematocele may be present. Sonographically, the fracture appears as a linear, hypoechoic, avascular band extending across the testicular parenchyma (Fig. 22.35).

Sonography can also be used to discern the severity of scrotal trauma resulting from penetrating scrotal injury. Gunshot injury is the most common cause; other causes include stabbing, self mutilation, human and animal bites, and projectile injuries. Bilateral injuries are more common in the setting of penetrating trauma.202 Penetrating trauma can disrupt the tunica albuginea, as well as penetrate the parenchyma, causing a fracturelike injury. Ultrasound can assess the degree of injury and evaluate for the presence of foreign bodies and for the presence of air, which may denote the path of the penetrating injury.203 Doppler

CHAPTER 22 sonography can assess for viability of the testis in the setting of penetrating trauma. A careful gray-scale and color low Doppler evaluation of the epididymis should be performed in all examinations of blunt trauma. Traumatic epididymitis may be an isolated inding that should not be confused with an infectious process.204

CRYPTORCHIDISM he testes remain near the deep inguinal ring until the seventh month of gestation when they normally begin their descent through the inguinal canal into the twin scrotal sacs.1,2 he gubernaculum testis is a ibromuscular structure that extends from the inferior pole of the testis to the scrotum and guides the testis in its descent, a process normally completed before birth. Undescended testis is one of the most common genitourinary anomalies in male infants. At birth, 3.5% of male infants weighing more than 2500 g have an undescended testis; 10% to 25% of these cases are bilateral. his igure decreases to 0.8% by age 1 year because the testes descend spontaneously in most infants. he incidence of undescended testes increases to 30% in premature infants, approaching 100% in neonates who weigh less than 1000 g at birth. Complete descent is necessary for full testicular maturation.205,206 Malpositioned testes may be located anywhere along the pathway of descent from the retroperitoneum to the scrotum. Most (80%) undescended testes are palpable, lying distal to the external inguinal ring. Anorchia occurs in 4% of the remaining patients with impalpable testes.206 Localization of the undescended testis is important for the prevention of two potential complications of cryptorchidism: infertility and cancer. he undescended testis is more likely to undergo malignant change than is the normally descended testis.3 he most common malignancy is seminoma. he risk of malignancy is increased in both the undescended testis ater orchiopexy and the normally descended testis. herefore careful serial examinations of both testes are essential. Sonographically, the undescended testis is oten smaller and slightly less echogenic than the contralateral, normally descended testis (Fig. 22.36). he pars infravaginalis gubernaculi, which is the distal bulbous segment of the gubernaculum testis, can be

FIG. 22.36 Testis in Inguinal Canal. Longitudinal scan shows an elongated, ovoid, undescended testis.

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mistaken for the testis. Ater completion of testicular descent, the pars infravaginalis gubernaculi and the gubernaculum normally atrophy. If the testis remains undescended, both structures persist. he pars infravaginalis gubernaculi is located distal to the undescended testis, usually in the scrotum, but it may be found in the inguinal canal. Sonographically, the pars infravaginalis gubernaculi is a hypoechoic, cordlike structure of echogenicity similar to the testis, with the gubernaculum leading to it.207 Sonography is oten used in the initial evaluation of cryptorchidism, although the value of this has been questioned because it is insensitive in detecting high intraabdominal testes.208 MRI has also been used in cryptorchidism because it is more sensitive than ultrasound in detecting undescended testes in the retroperitoneum.209,210 Nonvisualization of an undescended testis on sonography or MRI does not exclude its presence, and therefore laparoscopy or surgical exploration should be performed if clinically indicated. REFERENCES 1. Larsen WJ. Human embryology. New York: Churchill Livingstone; 1993. p. 235-280. 2. Moore KL, Persaud TVN. he developing human: clinically oriented embryology. 5th ed. Philadelphia: Saunders; 1993. 3. Krone KD, Carroll BA. Scrotal ultrasound. Radiol Clin North Am. 1985;23(1): 121-139. 4. Trainer TD. Histology of the normal testis. Am J Surg Pathol. 1987;11(10): 797-809. 5. Siegel MJ. he acute scrotum. Radiol Clin North Am. 1997;35(4): 959-976. 6. homas RD, Dewbury KC. Ultrasound appearances of the rete testis. Clin Radiol. 1993;47(2):121-124. 7. Johnson KA, Dewbury KC. Ultrasound imaging of the appendix testis and appendix epididymis. Clin Radiol. 1996;51(5):335-337. 8. Sellars ME, Sidhu PS. Ultrasound appearances of the testicular appendages: pictorial review. Eur Radiol. 2003;13(1):127-135. 9. Black JA, Patel A. Sonography of the normal extratesticular space. AJR Am J Roentgenol. 1996;167(2):503-506. 10. Allen TD. Disorders of the male external genitalia. In: Kelalis PP, King LR, editors. Clinical pediatric urology. Philadelphia: Saunders; 1976. p. 636-668. 11. Middleton WD, Bell MW. Analysis of intratesticular arterial anatomy with emphasis on transmediastinal arteries. Radiology. 1993;189(1):157-160. 12. Fakhry J, Khoury A, Barakat K. he hypoechoic band: a normal inding on testicular sonography. AJR Am J Roentgenol. 1989;153(2):321-323. 13. Bushby LH, Sellars ME, Sidhu PS. he “two-tone” testis: spectrum of ultrasound appearances. Clin Radiol. 2007;62(11):1119-1123. 14. Middleton WD, horne DA, Melson GL. Color Doppler ultrasound of the normal testis. AJR Am J Roentgenol. 1989;152(2):293-297. 15. Gooding GA. Sonography of the spermatic cord. AJR Am J Roentgenol. 1988;151(4):721-724. 16. Benson CB, Doubilet PM, Richie JP. Sonography of the male genital tract. AJR Am J Roentgenol. 1989;153(4):705-713. 17. Rikin MD, Kurtz AB, Pasto ME, Goldberg BB. Diagnostic capabilities of high-resolution scrotal ultrasonography: prospective evaluation. J Ultrasound Med. 1985;4(1):13-19. 18. Rikin MD, Kurtz AB, Pasto ME, et al. he sonographic diagnosis of focal and difuse iniltrating intrascrotal lesions. Urol Radiol. 1984;6(1): 20-26. 19. Carroll BA, Gross DM. High-frequency scrotal sonography. AJR Am J Roentgenol. 1983;140(3):511-515. 20. Woodward PJ, Sohaey R, O’Donoghue MJ, Green DE. From the archives of the AFIP: tumors and tumorlike lesions of the testis: radiologic-pathologic correlation. Radiographics. 2002;22(1):189-216.

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50. Mostoi FK, Price EB. Tumors of the male genital system. Atlas of tumor pathology. Washington, DC: Armed Forces Institute of Pathology; 1973. 51. Rushton HG, Belman AB, Sesterhenn I, et al. Testicular sparing surgery for prepubertal teratoma of the testis: a clinical and pathological study. J Urol. 1990;144(3):726-730. 52. Carver BS, Al-Ahmadie H, Sheinfeld J. Adult and pediatric testicular teratoma. Urol Clin North Am. 2007;34(2):245-251. 53. Emory TH, Charboneau JW, Randall RV, et al. Occult testicular interstitial-cell tumor in a patient with gynecomastia: ultrasonic detection. Radiology. 1984;151(2):474. 54. Tasu JP, Faye N, Eschwege P, et al. Imaging of burned-out testis tumor: ive new cases and review of the literature. J Ultrasound Med. 2003;22(5): 515-521. 55. Mindrup SR, Konety BR. Testicular recurrence from “primary” retroperitoneal germ cell tumor. Urology. 2004;64(5):1031. 56. Shawker TH, Javadpour N, O’Leary T, et al. Ultrasonographic detection of “burned-out” primary testicular germ cell tumors in clinically normal testes. J Ultrasound Med. 1983;2(10):477-479. 57. Maizlin ZV, Belenky A, Kunichezky M, et al. Leydig cell tumors of the testis: gray scale and color Doppler sonographic appearance. J Ultrasound Med. 2004;23(7):959-964. 58. Gabrilove JL, Freiberg EK, Leiter E, Nicolis GL. Feminizing and nonfeminizing Sertoli cell tumors. J Urol. 1980;124(6):757-767. 59. Young S, Gooneratne S, Straus FH 2nd, et al. Feminizing Sertoli cell tumors in boys with Peutz-Jeghers syndrome. Am J Surg Pathol. 1995;19(1): 50-58. 60. Ulbright TM, Amin MB, Young RH. Tumors of the testis, adnexa, spermatic cord, and scrotum. In: Rosai J, Sobin LH, editors. Atlas of tumor pathology, fasc 25, ser 3. Washington, DC: Armed Forces Institute of Pathology; 1999. p. 1-366. 61. Duncan PR, Checa F, Gowing NF, et al. Extranodal non-Hodgkin’s lymphoma presenting in the testicle: a clinical and pathologic study of 24 cases. Cancer. 1980;45(7):1578-1584. 62. Mostoi FK, Sobin LH. Histological typing of testis tumours. International histological classiication of tumors of the testes. Geneva: World Health Organization; 1977. 63. Mazzu D, Jefrey Jr RB, Ralls PW. Lymphoma and leukemia involving the testicles: indings on gray-scale and color Doppler sonography. AJR Am J Roentgenol. 1995;164(3):645-647. 64. Rayor RA, Scheible W, Brock WA, Leopold GR. High resolution ultrasonography in the diagnosis of testicular relapse in patients with acute lymphoblastic leukemia. J Urol. 1982;128(3):602-603. 65. Dogra VS, Gottlieb RH, Oka M, Rubens DJ. Sonography of the scrotum. Radiology. 2003;227(1):18-36. 66. Iizumi T, Shinohara S, Amemiya H, et al. Plasmacytoma of the testis. Urol Int. 1995;55(4):218-221. 67. Bude RO. Testicular plasmacytoma: appearance on gray-scale and power Doppler sonography. J Clin Ultrasound. 1999;27(6):345-346. 68. Avitable AM, Gansler TS, Tomaszewski JE, et al. Testicular plasmacytoma. Urology. 1989;34(1):51-54. 69. Grignon DJ, Shum DT, Hayman WP. Metastatic tumours of the testes. Can J Surg. 1986;29(5):359-361. 70. Werth V, Yu G, Marshall FF. Nonlymphomatous metastatic tumor to the testis. J Urol. 1982;127(1):142-144. 71. Hanash KA, Carney JA, Kelalis PP. Metastatic tumors to testicles: routes of metastasis. J Urol. 1969;102(4):465-468. 72. Hamm B, Fobbe F, Loy V. Testicular cysts: diferentiation with US and clinical indings. Radiology. 1988;168(1):19-23. 73. Shergill IS, hwaini A, Kapasi F, et al. Management of simple intratesticular cysts: a single-institution 11-year experience. Urology. 2006;67(6): 1266-1268. 74. Martinez-Berganza MT, Sarria L, Cozcolluela R, et al. Cysts of the tunica albuginea: sonographic appearance. AJR Am J Roentgenol. 1998;170(1): 183-185. 75. Dogra VS, Gottlieb RH, Rubens DJ, Liao L. Benign intratesticular cystic lesions: US features. Radiographics. 2001;21:S273-S281. 76. Warner KE, Noyes DT, Ross JS. Cysts of the tunica albuginea testis: a report of 3 cases with a review of the literature. J Urol. 1984;132(1):131-132.

CHAPTER 22 77. Poster RB, Spirt BA, Tamsen A, Surya BV. Complex tunica albuginea cyst simulating an intratesticular lesion. Urol Radiol. 1991;13(2):129132. 78. Sudakof GS, Quiroz F, Karcaaltincaba M, Foley WD. Scrotal ultrasonography with emphasis on the extratesticular space: anatomy, embryology, and pathology. Ultrasound Q. 2002;18(4):255-273. 79. Takihara H, Valvo JR, Tokuhara M, Cockett AT. Intratesticular cysts. Urology. 1982;20(1):80-82. 80. Tartar VM, Trambert MA, Balsara ZN, Mattrey RF. Tubular ectasia of the testicle: sonographic and MR imaging appearance. AJR Am J Roentgenol. 1993;160(3):539-542. 81. Brown DL, Benson CB, Doherty FJ, et al. Cystic testicular mass caused by dilated rete testis: sonographic indings in 31 cases. AJR Am J Roentgenol. 1992;158(6):1257-1259. 82. Weingarten BJ, Kellman GM, Middleton WD, Gross ML. Tubular ectasia within the mediastinum testis. J Ultrasound Med. 1992;11(7): 349-353. 83. Older RA, Watson LR. Tubular ectasia of the rete testis: a benign condition with a sonographic appearance that may be misinterpreted as malignant. J Urol. 1994;152(2 Pt 1):477-478. 84. Cho CS, Kosek J. Cystic dysplasia of the testis: sonographic and pathologic indings. Radiology. 1985;156(3):777-778. 85. Keetch DW, McAlister WH, Manley CB, Dehner LP. Cystic dysplasia of the testis. Sonographic features with pathologic correlation. Pediatr Radiol. 1991;21(7):501-503. 86. Atchley JT, Dewbury KC. Ultrasound appearances of testicular epidermoid cysts. Clin Radiol. 2000;55(7):493-502. 87. Bruni SG, Glanc P. Bilateral epidermoid cysts of the testes: a characteristic appearance on ultrasonography. Ultrasound Q. 2015;31(3):205-207. 88. Sanderson AJ, Birch BR, Dewbury KC. Case report: multiple epidermoid cysts of the testes—the ultrasound appearances. Clin Radiol. 1995;50(6):414-415. 89. Malvica RP. Epidermoid cyst of the testicle: an unusual sonographic inding. AJR Am J Roentgenol. 1993;160(5):1047-1048. 90. Stein MM, Stein MW, Cohen BC, et al. Unusual sonographic appearance of an epidermoid cyst of the testis. J Ultrasound Med. 1999;18(10): 723-726. 91. Maizlin ZV, Belenky A, Baniel J, et al. Epidermoid cyst and teratoma of the testis: sonographic and histologic similarities. J Ultrasound Med. 2005;24(10):1403-1409. 92. Eisenmenger M, Lang S, Donner G, et al. Epidermoid cysts of the testis: organ-preserving surgery following diagnosis by ultrasonography. Br J Urol. 1993;72(6):955-957. 93. Cho JH, Chang JC, Park BH, et al. Sonographic and MR imaging indings of testicular epidermoid cysts. AJR Am J Roentgenol. 2002;178(3): 743-748. 94. Langer JE, Ramchandani P, Siegelman ES, Banner MP. Epidermoid cysts of the testicle: sonographic and MR imaging features. AJR Am J Roentgenol. 1999;173(5):1295-1299. 95. Hermansen MC, Chusid MJ, Sty JR. Bacterial epididymo-orchitis in children and adolescents. Clin Pediatr (Phila). 1980;19(12):812-815. 96. Korn RL, Langer JE, Nisenbaum HL, et al. Non-Hodgkin’s lymphoma mimicking a scrotal abscess in a patient with AIDS. J Ultrasound Med. 1994;13(9):715-718. 97. Smith FJ, Bilbey JH, Filipenko JD, Goldenberg SL. Testicular pseudotumor in the acquired immunodeiciency syndrome. Urology. 1995;45(3): 535-537. 98. Wu VH, Dangman BC, Kaufman Jr RP. Sonographic appearance of acute testicular venous infarction in a patient with a hypercoagulable state. J Ultrasound Med. 1995;14(1):57-59. 99. Bilagi P, Sriprasad S, Clarke JL, et al. Clinical and ultrasound features of segmental testicular infarction: six-year experience from a single centre. Eur Radiol. 2007;17(11):2810-2818. 100. Flanagan JJ, Fowler RC. Testicular infarction mimicking tumour on scrotal ultrasound—a potential pitfall. Clin Radiol. 1995;50(1):49-50. 101. Einstein DM, Paushter DM, Singer AA, et al. Fibrotic lesions of the testicle: sonographic patterns mimicking malignancy. Urol Radiol. 1992;14(3): 205-210.

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102. Ledwidge ME, Lee DK, Winter 3rd TC, et al. Sonographic diagnosis of superior hemispheric testicular infarction. AJR Am J Roentgenol. 2002;179(3):775-776. 103. Sriprasad S, Kooiman GG, Muir GH, Sidhu PS. Acute segmental testicular infarction: diferentiation from tumour using high frequency colour Doppler ultrasound. Br J Radiol. 2001;74(886):965-967. 104. Mevorach RA, Lerner RM, Dvoretsky PM, Rabinowitz R. Testicular abscess: diagnosis by ultrasonography. J Urol. 1986;136(6):1213-1216. 105. hompson JP, Bhatt S, Rubens D. Identify before orchiectomy: segmental testicular infarct. Ultrasound Q. 2015;31(3):198-201. 106. Avila NA, Premkumar A, Shawker TH, et al. Testicular adrenal rest tissue in congenital adrenal hyperplasia: indings at gray-scale and color Doppler US. Radiology. 1996;198(1):99-104. 107. Vanzulli A, DelMaschio A, Paesano P, et al. Testicular masses in association with adrenogenital syndrome: US indings. Radiology. 1992;183(2): 425-429. 108. Shawker TH, Doppman JL, Choyke PL, et al. Intratesticular masses associated with abnormally functioning adrenal glands. J Clin Ultrasound. 1992;20(1):51-58. 109. Seidenwurm D, Smathers RL, Kan P, Hofman A. Intratesticular adrenal rests diagnosed by ultrasound. Radiology. 1985;155(2):479-481. 110. Bhatt S, Dogra VS. Role of US in testicular and scrotal trauma. Radiographics. 2008;28(6):1617-1629. 111. Gierke CL, King BF, Bostwick DG, et al. Large-cell calcifying Sertoli cell tumor of the testis: appearance at sonography. AJR Am J Roentgenol. 1994;163(2):373-375. 112. Vegni-Talluri M, Bigliardi E, Vanni MG, Tota G. Testicular microliths: their origin and structure. J Urol. 1980;124(1):105-107. 113. Bieger RC, Passarge E, McAdams AJ. Testicular intratubular bodies. J Clin Endocrinol Metab. 1965;25(10):1340-1346. 114. Middleton WD, Teefey SA, Santillan CS. Testicular microlithiasis: prospective analysis of prevalence and associated tumor. Radiology. 2002;224(2): 425-428. 115. Kim B, Winter 3rd TC, Ryu JA. Testicular microlithiasis: clinical signiicance and review of the literature. Eur Radiol. 2003;13(12):2567-2576. 116. Nistal M, Paniagua R, Diez-Pardo JA. Testicular microlithiasis in 2 children with bilateral cryptorchidism. J Urol. 1979;121(4):535-537. 117. Janzen DL, Mathieson JR, Marsh JI, et al. Testicular microlithiasis: sonographic and clinical features. AJR Am J Roentgenol. 1992;158(5): 1057-1060. 118. Backus ML, Mack LA, Middleton WD, et al. Testicular microlithiasis: imaging appearances and pathologic correlation. Radiology. 1994;192(3):781-785. 119. Dagash H, Mackinnon EA. Testicular microlithiasis: what does it mean clinically? BJU Int. 2007;99(1):157-160. 120. Lam DL, Gerscovich EO, Kuo MC, McGahan JP. Testicular microlithiasis: our experience of 10 years. J Ultrasound Med. 2007;26(7):867-873. 121. Winter TC, Kim B, Lowrance W, Middleton W. Testicular microlithiasis: what should you recommend? AJR Am J Roentgenol. 2016;206(6): 1164-1169. 122. Nye PJ, Prati Jr RC. Idiopathic hydrocele and absent testicular diastolic low. J Clin Ultrasound. 1997;25(1):43-46. 123. Worthy L, Miller EI, Chinn DH. Evaluation of extratesticular indings in scrotal neoplasms. J Ultrasound Med. 1986;5(5):261-263. 124. Gooding GA, Leonhardt WC, Marshall G, et al. Cholesterol crystals in hydroceles: sonographic detection and possible signiicance. AJR Am J Roentgenol. 1997;169(2):527-529. 125. Rathaus V, Konen O, Shapiro M, et al. Ultrasound features of spermatic cord hydrocele in children. Br J Radiol. 2001;74(885):818-820. 126. Cunningham JJ. Sonographic indings in clinically unsuspected acute and chronic scrotal hematoceles. AJR Am J Roentgenol. 1983;140(4):749-752. 127. Sung T, Riedlinger WF, Diamond DA, Chow JS. Solid extratesticular masses in children: radiographic and pathologic correlation. AJR Am J Roentgenol. 2006;186(2):483-490. 128. Fitzgibbons Jr RJ, Forse RA. Clinical practice. Groin hernias in adults. N Engl J Med. 2015;372(8):756-763. 129. Bhosale PR, Patnana M, Viswanathan C, Szklaruk J. he inguinal canal: anatomy and imaging features of common and uncommon masses. Radiographics. 2008;28(3):819-835.

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130. Linkowski GD, Avellone A, Gooding GA. Scrotal calculi: sonographic detection. Radiology. 1985;156(2):484. 131. Kim ED, Lipshultz LI. Role of ultrasound in the assessment of male infertility. J Clin Ultrasound. 1996;24(8):437-453. 132. Beddy P, Geoghegan T, Browne RF, Torreggiani WC. Testicular varicoceles. Clin Radiol. 2005;60(12):1248-1255. 133. Zucchi A, Mearini L, Mearini E, et al. Varicocele and fertility: relationship between testicular volume and seminal parameters before and ater treatment. J Androl. 2006;27(4):548-551. 134. Gonda Jr RL, Karo JJ, Forte RA, O’Donnell KT. Diagnosis of subclinical varicocele in infertility. AJR Am J Roentgenol. 1987;148(1):71-75. 135. Doherty FJ. Ultrasound of the nonacute scrotum. Semin Ultrasound CT MR. 1991;12(2):131-156. 136. Graif M, Hauser R, Hirshebein A, et al. Varicocele and the testicular-renal venous route: hemodynamic Doppler sonographic investigation. J Ultrasound Med. 2000;19(9):627-631. 137. Howards SS. Treatment of male infertility. N Engl J Med. 1995; 332(5):312-317. 138. Tétreau R, Julian P, Lyonnet D, Rouvière O. Intratesticular varicocele: an easy diagnosis but unclear physiopathologic characteristics. J Ultrasound Med. 2007;26(12):1767-1773. 139. Atasoy C, Fitoz S. Gray-scale and color Doppler sonographic indings in intratesticular varicocele. J Clin Ultrasound. 2001;29(7):369-373. 140. Krainik A, Sarrazin JL, Camparo P, et al. Fibrous pseudotumor of the epididymis: imaging and pathologic correlation. Eur Radiol. 2000;10(10): 1636-1638. 141. al-Otaibi L, Whitman GJ, Chew FS. Fibrous pseudotumor of the epididymis. AJR Am J Roentgenol. 1997;168(6):1586. 142. Oliva E, Young RH. Paratesticular tumor-like lesions. Semin Diagn Pathol. 2000;17(4):340-358. 143. hum G. Polyorchidism: case report and review of literature. J Urol. 1991;145(2):370-372. 144. Leung ML, Gooding GA, Williams RD. High-resolution sonography of scrotal contents in asymptomatic subjects. AJR Am J Roentgenol. 1984;143(1):161-164. 145. Pavone-Macaluso M, Smith PH, Bagshaw MA, editors. Testicular cancer and other tumors of the genitourinary tract. New York: Plenum Press; 1985. 146. Smallman LA, Odedra JK. Primary carcinoma of sigmoid colon metastasizing to epididymis. Urology. 1984;23(6):598-599. 147. Wachtel TL, Mehan DJ. Metastatic tumors of the epididymis. J Urol. 1970;103(5):624-627. 148. Yang DM, Kim SH, Kim HN, et al. Diferential diagnosis of focal epididymal lesions with gray scale sonographic, color Doppler sonographic, and clinical features. J Ultrasound Med. 2003;22(2):135-142. 149. Oh C, Nisenbaum HL, Langer J, et al. Sonographic demonstration, including color Doppler imaging, of recurrent sperm granuloma. J Ultrasound Med. 2000;19(5):333-335. 150. Reddy NM, Gerscovich EO, Jain KA, et al. Vasectomy-related changes on sonographic examination of the scrotum. J Clin Ultrasound. 2004;32(8):394-398. 151. Ishigami K, Abu-Yousef MM, El-Zein Y. Tubular ectasia of the epididymis: a sign of postvasectomy status. J Clin Ultrasound. 2005;33(9):447-451. 152. Stewart VR, Sidhu PS. he testis: the unusual, the rare and the bizarre. Clin Radiol. 2007;62(4):289-302. 153. Chung JJ, Kim MJ, Lee T, et al. Sonographic indings in tuberculous epididymitis and epididymo-orchitis. J Clin Ultrasound. 1997;25(7): 390-394. 154. Carmody JP, Sharma OP. Intrascrotal sarcoidosis: case reports and review. Sarcoidosis Vasc Difuse Lung Dis. 1996;13(2):129-134. 155. Winter 3rd TC, Keener TS, Mack LA. Sonographic appearance of testicular sarcoid. J Ultrasound Med. 1995;14(2):153-156. 156. Eraso CE, Vrachliotis TG, Cunningham JJ. Sonographic indings in testicular sarcoidosis simulating malignant nodule. J Clin Ultrasound. 1999;27(2): 81-83. 157. Mueller DL, Amundson GM, Rubin SZ, Wesenberg RL. Acute scrotal abnormalities in children: diagnosis by combined sonography and scintigraphy. AJR Am J Roentgenol. 1988;150(3):643-646.

158. Watanabe Y, Dohke M, Ohkubo K, et al. Scrotal disorders: evaluation of testicular enhancement patterns at dynamic contrast-enhanced subtraction MR imaging. Radiology. 2000;217(1):219-227. 159. Hricak H, Lue T, Filly RA, et al. Experimental study of the sonographic diagnosis of testicular torsion. J Ultrasound Med. 1983;2(8):349-356. 160. Pillai SB, Besner GE. Pediatric testicular problems. Pediatr Clin North Am. 1998;45(4):813-830. 161. Prando D. Torsion of the spermatic cord: sonographic diagnosis. Ultrasound Q. 2002;18(1):41-57. 162. Lerner RM, Mevorach RA, Hulbert WC, Rabinowitz R. Color Doppler US in the evaluation of acute scrotal disease. Radiology. 1990;176(2): 355-358. 163. Horstman WG, Middleton WD, Melson GL, Siegel BA. Color Doppler US of the scrotum. Radiographics. 1991;11(6):941-957. 164. Middleton WD, Siegel BA, Melson GL, et al. Acute scrotal disorders: prospective comparison of color Doppler US and testicular scintigraphy. Radiology. 1990;177(1):177-181. 165. Sidhu PS. Clinical and imaging features of testicular torsion: role of ultrasound. Clin Radiol. 1999;54(6):343-352. 166. Middleton WD, Middleton MA, Dierks M, et al. Sonographic prediction of viability in testicular torsion: preliminary observations. J Ultrasound Med. 1997;16(1):23-27. 167. Middleton WD, Melson GL. Testicular ischemia: color Doppler sonographic indings in ive patients. AJR Am J Roentgenol. 1989;152(6): 1237-1239. 168. Chinn DH, Miller EI. Generalized testicular hyperechogenicity in acute testicular torsion. J Ultrasound Med. 1985;4(9):495-496. 169. Winter TC. Ultrasonography of the scrotum. App Radiol. 2002;31:3. 170. Vijayaraghavan SB. Sonographic diferential diagnosis of acute scrotum: real-time whirlpool sign, a key sign of torsion. J Ultrasound Med. 2006;25(5): 563-574. 171. Trambert MA, Mattrey RF, Levine D, Berthoty DP. Subacute scrotal pain: evaluation of torsion versus epididymitis with MR imaging. Radiology. 1990;175(1):53-56. 172. Vick CW, Bird K, Rosenield AT, et al. Extratesticular hemorrhage associated with torsion of the spermatic cord: sonographic demonstration. Radiology. 1986;158(2):401-404. 173. Barth RA, Shortlife LD. Normal pediatric testis: comparison of power Doppler and color Doppler US in the detection of blood low. Radiology. 1997;204(2):389-393. 174. Bader TR, Kammerhuber F, Herneth AM. Testicular blood low in boys as assessed at color Doppler and power Doppler sonography. Radiology. 1997;202(2):559-564. 175. Coley BD, Frush DP, Babcock DS, et al. Acute testicular torsion: comparison of unenhanced and contrast-enhanced power Doppler US, color Doppler US, and radionuclide imaging. Radiology. 1996;199(2):441-446. 176. Luker GD, Siegel MJ. Scrotal US in pediatric patients: comparison of power and standard color Doppler US. Radiology. 1996;198(2): 381-385. 177. Albrecht T, Lotzof K, Hussain HK, et al. Power Doppler US of the normal prepubertal testis: does it live up to its promises? Radiology. 1997;203(1): 227-231. 178. Lee Jr FT, Winter DB, Madsen FA, et al. Conventional color Doppler velocity sonography versus color Doppler energy sonography for the diagnosis of acute experimental torsion of the spermatic cord. AJR Am J Roentgenol. 1996;167(3):785-790. 179. Fitzgerald SW, Erickson S, DeWire DM, et al. Color Doppler sonography in the evaluation of the adult acute scrotum. J Ultrasound Med. 1992;11(10): 543-548. 180. Burks DD, Markey BJ, Burkhard TK, et al. Suspected testicular torsion and ischemia: evaluation with color Doppler sonography. Radiology. 1990;175(3):815-821. 181. Hedayati V, Sellars ME, Sharma DM, Sidhu PS. Contrast-enhanced ultrasound in testicular trauma: role in directing exploration, debridement and organ salvage. Br J Radiol. 2012;85(1011):e65-e68. 182. Atkinson Jr GO, Patrick LE, Ball Jr TI, et al. he normal and abnormal scrotum in children: evaluation with color Doppler sonography. AJR Am J Roentgenol. 1992;158(3):613-617.

CHAPTER 22 183. Bude RO, Kennelly MJ, Adler RS, Rubin JM. Nonpulsatile arterial waveforms: observations during graded testicular torsion in rats. Acad Radiol. 1995;2(10):879-882. 184. Dogra VS, Rubens DJ, Gottlieb RH, Bhatt S. Torsion and beyond: new twists in spectral Doppler evaluation of the scrotum. J Ultrasound Med. 2004;23(8):1077-1085. 185. Sanelli PC, Burke BJ, Lee L. Color and spectral Doppler sonography of partial torsion of the spermatic cord. AJR Am J Roentgenol. 1999;172(1): 49-51. 186. Alcantara AL, Sethi Y. Imaging of testicular torsion and epididymitis/orchitis: diagnosis and pitfalls. Emerg Radiol. 1998;5:394-402. 187. Dresner ML. Torsed appendage. Diagnosis and management: blue dot sign. Urology. 1973;1(1):63-66. 188. Hesser U, Rosenborg M, Gierup J, et al. Gray-scale sonography in torsion of the testicular appendages. Pediatr Radiol. 1993;23(7):529-532. 189. Basekim CC, Kizilkaya E, Pekkafali Z, et al. Mumps epididymo-orchitis: sonography and color Doppler sonographic indings. Abdom Imaging. 2000;25(3):322-325. 190. Gondos B, Wong TW. Non-neoplastic diseases of the testis and epididymis. In: Murphy WM, editor. Urological pathology. 2nd ed. Philadelphia: Saunders; 1997. p. 277-341. 191. Horstman WG, Middleton WD, Melson GL. Scrotal inlammatory disease: color Doppler US indings. Radiology. 1991;179(1):55-59. 192. Cook JL, Dewbury K. he changes seen on high-resolution ultrasound in orchitis. Clin Radiol. 2000;55(1):13-18. 193. Hourihane DO. Infected infarcts of the testis: a study of 18 cases preceded by pyogenic epididymoorchitis. J Clin Pathol. 1970;23(8):668-675. 194. Sanders LM, Haber S, Dembner A, Aquino A. Signiicance of reversal of diastolic low in the acute scrotum. J Ultrasound Med. 1994;13(2): 137-139. 195. Casalino DD, Kim R. Clinical importance of a unilateral striated pattern seen on sonography of the testicle. AJR Am J Roentgenol. 2002;178(4): 927-930. 196. Harris RD, Chouteau C, Partrick M, Schned A. Prevalence and signiicance of heterogeneous testes revealed on sonography: ex vivo sonographicpathologic correlation. AJR Am J Roentgenol. 2000;175(2):347-352.

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197. Eke N. Fournier’s gangrene: a review of 1726 cases. Br J Surg. 2000;87(6): 718-728. 198. Jefrey RB, Laing FC, Hricak H, McAninch JW. Sonography of testicular trauma. AJR Am J Roentgenol. 1983;141(5):993-995. 199. Kim SH, Park S, Choi SH, et al. Signiicant predictors for determination of testicular rupture on sonography: a prospective study. J Ultrasound Med. 2007;26(12):1649-1655. 200. Buckley JC, McAninch JW. Use of ultrasonography for the diagnosis of testicular injuries in blunt scrotal trauma. J Urol. 2006;175(1):175-178. 201. Cohen HL, Shapiro ML, Haller JO, Glassberg K. Sonography of intrascrotal hematomas simulating testicular rupture in adolescents. Pediatr Radiol. 1992;22(4):296-297. 202. Cass AS, Ferrara L, Wolpert J, Lee J. Bilateral testicular injury from external trauma. J Urol. 1988;140(6):1435-1436. 203. Learch TJ, Hansch LP, Ralls PW. Sonography in patients with gunshot wounds of the scrotum: imaging indings and their value. AJR Am J Roentgenol. 1995;165(4):879-883. 204. Gordon LM, Stein SM, Ralls PW. Traumatic epididymitis: evaluation with color Doppler sonography. AJR Am J Roentgenol. 1996;166(6): 1323-1325. 205. Elder JS. Cryptorchidism: isolated and associated with other genitourinary defects. Pediatr Clin North Am. 1987;34(4):1033-1053. 206. Harrison JH, Gittes RF, Stamey TA, et al. Campbell’s urology. 4th ed. Philadelphia: Saunders; 1979. 207. Rosenield AT, Blair DN, McCarthy S, et al. Society of Uroradiology Award paper. he pars infravaginalis gubernaculi: importance in the identiication of the undescended testis. AJR Am J Roentgenol. 1989;153(4):775-778. 208. Friedland GW, Chang P. he role of imaging in the management of the impalpable undescended testis. AJR Am J Roentgenol. 1988;151(6): 1107-1111. 209. Fritzsche PJ, Hricak H, Kogan BA, et al. Undescended testis: value of MR imaging. Radiology. 1987;164(1):169-173. 210. Kier R, McCarthy S, Rosenield AT, et al. Nonpalpable testes in young boys: evaluation with MR imaging. Radiology. 1988;169(2):429-433.

CHAPTER

23

Overview of Musculoskeletal Ultrasound Techniques and Applications Colm McMahon and Corrie Yablon

SUMMARY OF KEY POINTS • A wide variety of inlammatory, degenerative, traumatic, and neoplastic conditions can be imaged accurately and cost-effectively with ultrasound. • Understanding optimal imaging techniques and recognizing and avoiding common artifacts is essential to musculoskeletal ultrasound.

• Ultrasound can provide higher-resolution imaging of nerves and tendons compared with standard clinical magnetic resonance imaging examinations. • Dynamic imaging may be performed with ultrasound, which can assist in the diagnosis of tendon and ligamentous injury.

CHAPTER OUTLINE GENERAL CONSIDERATIONS Doppler Imaging Elastography Extended Field of View Imaging MUSCLES

TENDONS LIGAMENTS NERVES JOINT ASSESSMENT SOFT TISSUE MASSES

GENERAL CONSIDERATIONS Ultrasound is becoming a central part of the diagnostic pathway for patients with musculoskeletal complaints. In many cases, ultrasound is performed as an alternative or complement to magnetic resonance imaging (MRI). Ultrasound has several advantages over MRI that have been described in the literature, succinctly by Nazarian in a 2008 perspective article.1 Ultrasound is well tolerated by patients and can be performed in those with contraindications to MRI, such as implanted cardiac devices or other MRI-incompatible implants, large size, or claustrophobia. Ultrasound examinations oten take less time to perform than the corresponding MRI examinations. Ultrasound provides higher-resolution imaging of tendons and ligaments than routine musculoskeletal MRI. Ultrasound also provides the ability to image dynamically, which can be important in the diagnosis of disorders of impingement and subluxation of nerves or tendons. It is excellent at determining the fundamental tissue characterization of solid versus cystic in the setting of a mass lesion—this type of characterization may otherwise require the administration of intravenous contrast when MRI is used to distinguish a T2-hyperintense solid mass from a simple cyst.

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In many cases, patients can be given results at the time of their examination. As a general rule, a systematic approach to musculoskeletal ultrasound examination of the joints using deined protocols is preferred to a focal examination when time permits. Focused imaging of symptomatic areas of concern adds additional diagnostic information to the routine protocol.2 When evaluating a foreign body or palpable sot tissue mass, focal assessment can be performed, with attention to the relationship to nearby anatomic structures, critical to treatment planning. As with MRI interpretation, it is imperative that the radiologist have a clear understanding of musculoskeletal anatomy before performing or interpreting a sonographic examination, especially when previous studies are not available for comparison. High-frequency linear ultrasound probes (12-15 MHz) are recommended for musculoskeletal imaging. Higher-frequency probes (15-17 MHz) can be helpful for evaluating supericial anatomy, for example, ligaments and tendons in the ingers. Hockey stick–style high-frequency probes can be very useful for evaluation of ine structures, providing focused small ield of view images and permitting good skin contact in the peripheral extremities. Lower-frequency (3-9 MHz) linear probes may be

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P

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FIG. 23.1 Effect of Examination Technique on Power Doppler Findings. (A) Longitudinal sonogram obtained without pressure exerted on the tendon shows hypervascularity. (B) Longitudinal sonogram obtained with the usual pressure on the transducer shows the near complete disappearance of hypervascularity. P, Patella.

needed for greater tissue penetration in deeper structure evaluation or when attempting to determine the relationships of a deep pathologic process to the underlying bone and muscle. Although lower-frequency probes provide deeper penetration of sot tissues, there is a corresponding trade-of of lower resolution. In some cases, a low-frequency curvilinear probe may be necessary (2-5 MHz), for example, in the evaluation of the thigh and hip region or the examination of deep thigh or gluteal masses. By using more than one probe, the user may obtain complementary information about a single disease process. As is the case for all ultrasound imaging, careful attention to image optimization, such as positioning the focal zone at the appropriate depth, is important. Adequate ultrasound wave transduction is facilitated by good skin contact with the transducer and the use of ultrasound gel. A standof pad can help for imaging very supericial structures.

Doppler Imaging he role of Doppler imaging in musculoskeletal ultrasound includes characterization of neoplastic, inlammatory, and degenerative conditions.3 Doppler ultrasound is helpful in conirming vascularization of solid masses in distinction from avascular cystic lesions. It is also helpful in characterization of inlammatory conditions, including synovitis, tenosynovitis, myositis, and sot tissue infection. Finally, tendon neovascularization is a sign occasionally seen with the development of degenerative tendinosis. As in other areas of the body, setting the appropriate Doppler gain is important, and imaging with a small sample volume will minimize motion artifacts. Because many structures of interest in musculoskeletal imaging are supericial, care should be taken to avoid excessive probe pressure during imaging, because this can limit low detection in areas of vascularization (Fig. 23.1).

Elastography An exciting recent development is imaging and quantiication of tissue elasticity. his is deined by the tissue deformability and can be measured as a Young modulus for a given tissue expressed in kilopascals (kPa).4 he range of Young modulus

for musculoskeletal tissue ranges from 1 to 10 kPa. Depending on available hardware, ultrasound elastography may be performed using strain elastography or shear-wave elastography. In the musculoskeletal system, early application of elastography has shown substantial promise in the evaluation of tendinosis. In tendinosis, collagen disorganization and mucoid and lipoid degeneration result in tendon sotening, which can be visualized and quantiied with sonoelastography.5 Other emerging applications include diagnosis of muscle disorders such as myositis6 and characterization of sot tissue masses.7

Extended Field of View Imaging Although high-resolution linear array probes are optimal for imaging relatively supericial musculoskeletal structures with ine anatomic detail, the overall ield of view during imaging is limited. his may cause diiculty when viewing the images ater acquisition, because the scale and anatomic position and orientation, which are intuitive when scanning real time, may be diicult to convey in the retained static images. his can be overcome by use of cine-clips and also with use of extended ield of view (panorama) imaging. With this technique, an image is acquired while the probe is moved in the direction of the probe footprint long axis. he image acquired is a composite panoramic image of the anatomy scanned during the motion path of the probe. he scanners equipped with this technology recognize the degree of probe motion by the degree of frame shit during the movement of the probe. By utilizing knowledge of this motion vector, a blended image of successively acquired image frames during the probe sweep can be formed.8 his technique can be extremely helpful in putting a speciic inding in overall anatomic context, measuring a lesion that is larger than the probe ield of view, and can also provide some diagnostic beneit—for example, in comparing the echogenicity and bulk of muscles of the rotator cuf.9

MUSCLES Normal muscle is composed of multiple fascicles each embedded in perimysium, a thin layer of connective tissue and fat.10 he

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A

B

FIG. 23.2 Normal Muscle. (A) In short-axis view a normal vastus lateralis (VL) muscle demonstrates a speckled or “starry sky” appearance (arrows). (B) In long-axis view the normal muscle demonstrates a pennate appearance (arrows). F, Femur; VI, vastus intermedius.

ultrasound pattern of muscle is typically feathery, or pennate, with iber orientation usually directed along the long axis of the muscle. In the short-axis view, the muscle ibers demonstrate a speckled appearance (Fig. 23.2). Fibers typically converge to the myotendinous junction and the muscle tapers in diameter at this point (Videos 23.1 and 23.2). A thin layer of fascia surrounds the muscle unit, separating it from adjacent muscles and subcutaneous fat. Muscle is usually overall hypoechoic, with more echogenic internal linear interfaces generated by the perimysium. Muscle injuries of diferent grades can be identiied with ultrasound.11 A grade I injury is a minor strain and is depicted on ultrasound as just minimal iber elongation and hypoechogenicity, but without detectible discontinuity. Ultrasound is less sensitive than MRI to these minor grades of injury, which are usually treated conservatively.12 A grade II injury is a partial tear. Fiber discontinuity is seen, with a focal anechoic or hypoechoic gap, usually illed by more echogenic hematoma. Gentle probe pressure can demonstrate muscle ibers loating freely within luid and hematoma, referred to as the “bell-clapper” sign. At the most severe end of the spectrum of muscle injury is a grade III injury, or complete tear (Fig. 23.3). In the case of a grade III injury, the muscle is completely interrupted with retraction of the muscle ends and an interposed gap, which should be measured. A large hematoma is expected in association with a complete tear. A distinct form of muscle injury that deserves special mention is the avulsion of a muscle from its aponeurosis, a pattern of injury particularly common in the calf in the clinical spectrum of “tennis leg” (Fig. 23.4). In this injury the medial gastrocnemius muscle tears away from the aponeurosis with the underlying soleus muscle. Fluid and hematoma may dissect along the aponeurotic plane and there may be some retraction of the medial gastrocnemius. his usually occurs during forceful plantar lexion

FIG. 23.3 Muscle Tear. Long-axis image of the medial groin region demonstrates hypoechoic luid (arrows) at the pubic symphysis (P) origin of the adductor muscles, consistent with a grade III muscle tear.

during sports, for example, in a forceful lunge in tennis. his injury may be accompanied by a plantaris tendon tear. Symptomatic myofascial defects lend themselves well to ultrasound evaluation. In this injury a defect in the muscular fascia allows herniation of muscle ibers, leading to a palpable and oten painful mass (Fig. 23.5). In some cases, the patient may have associated neuropathy resulting from compression of adjacent nerves.13 he mass may be more apparent to the patient during certain movements and activities that lead to muscle contraction, and these can be reproduced during scanning to assist in diagnosis. On ultrasound imaging, focused evaluation of the region of concern reveals focal bulging of muscle ibers through the otherwise smooth fascia. If this is equivocal or the patient reports symptoms only in certain positions such as

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FIG. 23.4 Medial Head Gastrocnemius Tear From the Aponeurosis. (A) Long-axis image shows blunting and retraction of the medial head gastrocnemius ibers (arrows) from the aponeurosis (*) with an associated hematoma (arrowheads). (B) Short-axis image shows effacement of the normal gastrocnemius muscle (G) architecture and a hematoma of mixed echogenicity at the site of the tear from the aponeurosis (arrowheads). S, Soleus muscle.

FIG. 23.5 Forearm Muscle Herniation. At the site of the palpable abnormality, there is focal herniation of a portion of the pronator teres muscle (PT) (arrows) through the muscle fascia (arrowheads). This patient noticed a forearm bulge while weightlifting. U, Ulna.

standing, the area should be scanned with the patient reproducing the relevant position where possible. Muscle atrophy can occur in response to denervation or chronic injury, for example, in the setting of a chronic complete rotator cuf tear. Muscle atrophy is characterized on ultrasound as a decrease in muscle bulk and a relative increase in echogenicity, relecting replacement of muscle ibers with fatty tissue (Fig. 23.6). Comparison with adjacent muscles or the contralateral side can assist in subtle cases. As a result of increased echogenicity, the visibility of the central tendon at the myotendinous junction is diminished, and there is a loss of normal pennate pattern.14

TENDONS Imaging the musculoskeletal system with ultrasound has built on early success in evaluation of tendons, with initial reports of Achilles tendon assessment.15 Many tendons are ideally suited

to ultrasound evaluation, as they are supericial and require the high-resolution imaging that ultrasound afords. Normal tendons are composed of longitudinally oriented bundles of collagen ibers, which give a highly organized echogenic linear ibrillar or striated pattern on ultrasound when viewed in long axis (Fig. 23.7). In short-axis view, normal tendons are usually smooth and ovoid in outline, with a homogenous stippled appearance, representing the tendon ibers viewed en face. Some tendons, such as the lexor and extensor tendons of the hand and wrist, are invested in a synovial lined sheath, whereas others, such as the Achilles tendon, are enveloped in a layer of loose areolar tissue called a paratenon. It is critically important to understand the concept of aniso­ tropy when performing the sonographic evaluation of tendons (Fig. 23.8). Collagen bundles, because of their smooth parallel organization within tendons, act as specular relectors, such that sound waves are relected in a single direction. When these specular relectors are imaged with ultrasound, if the angle of insonation is not perpendicular to the tendon ibers, sound waves will be relected away from the transducer, leading to the generation of an image with artifactual hypoechogenicity within the tendon.16 his can be resolved by correcting the angle of insonation to 90 degrees when an area of hypoechogenicity is observed. he inding of focal persistent abnormal hypoechogenicity in a second plane with optimized imaging adds further corroboration to the observation of an apparent pathologic hypoechoic region. Tendon injuries are usually caused by overuse and range from tendinosis to complete tear. he term tendinosis refers to intratendinous degeneration without tearing. Histologically, tendinosis consists of tendon expansion and loss of clear demarcation of collagen bundles, with increased mucoid ground substance among collagen bundles.17 here is noninlammatory ibroblastic and myoibroblastic cellular proliferation. On ultrasound, tendinosis appears as an area of hypoechogenicity, without discontinuity, frequently associated with varying degrees of tendon thickening (Fig. 23.9). Dystrophic calciication, and even ossiication, can be seen within afected tendons. An additional characteristic feature is the development of neovascularization,

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FIG. 23.6 Muscle Atrophy. Patient with a remote history of quadriceps injury presented with noticeable volume loss in his right anterior thigh. (A) Ultrasound of the abnormal right side shows marked volume loss in the rectus femoris muscle (arrows) with echogenic fatty iniltration of the remaining muscle. (B) The normal left side demonstrates normal muscle bulk and echotexture (arrows).

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FIG. 23.7 Normal Quadriceps Tendon. (A) In long-axis view, the normal tendon demonstrates a ibrillar appearance (arrows). (B) In short-axis view, the tendon is ovoid and echogenic with a speckled appearance (arrows). P, Patella.

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FIG. 23.8 Anisotropy. (A) In this long-axis scan of the Achilles insertion on the calcaneus, the proximal portion of the imaged tendon demonstrates a normal ibrillar appearance (arrow), whereas the distal tendon insertion is hypoechoic (arrowhead). (B) When the transducer is angled 90 degrees to the distal tendon insertion, the tendon then becomes ibrillar and is normal in appearance (arrowhead). C, Calcaneus.

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which can be visualized on Doppler ultrasound in tendinosis but not in normal tendons.18 Tendinosis is common in the Achilles tendon, where it most commonly afects the midportion of the tendon, or “watershed,” where there is overlapping blood supply. Tendon degeneration can also occur at the bone-tendon interface or enthesis, seen in the Achilles as insertional tendinosis at the calcaneus. Tendinosis at the tendon-bone interface is the most common pattern of degeneration seen in the common lexor and extensor origins at the medial and lateral humeral epicondyles at the elbow, forming part of the clinical spectrum of epicondylitis. Similar to tendinosis elsewhere, insertional tendinosis or enthesopathy is characterized by tendon expansion and hypoechogenicity.19,20 Enthesitis, or inlammation at the enthesis, can occur in patients with rheumatoid arthritis, psoriatic arthritis, or spondyloarthropathy. he imaging features of enthesitis can overlap with tendinosis, with tendon expansion and hypoechogenicity, but neovascularization may be a more prominent feature and bony erosion may also be present.21,22 Patients with tendinosis are more prone to tendon tears. Tendon tears may be partial or complete. Partial tears may be transversely oriented (parallel to the short axis of the tendon) or longitudinally oriented (parallel to the long axis of the tendon, also referred to as a “longitudinal split tear”). Tears are manifested by anechoic or hypoechoic clets, with focal tendon iber

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FIG. 23.9 Tendinosis. (A) The long-axis image of the mid Achilles tendon demonstrates fusiform, hypoechoic swelling of the tendon (arrowheads), although the ibrillar architecture can still be discerned. (B) In short-axis view, the Achilles appears thickened and is ovoid in morphology (arrowheads). (C) In a different patient, the Achilles tendon at the insertion on the calcaneus is thickened and hypoechoic with loss of the normal ibrillar pattern (arrows). There is marked hyperemia on color Doppler imaging. Note the dorsal calcaneal enthesophytes (arrowheads). C, Calcaneus.

discontinuity23 (Fig. 23.10). When a complete rupture occurs, the tendon ibers are entirely discontinuous and some degree of tendon retraction may occur because of now-unopposed muscle contraction (Fig. 23.11). he extent of retraction is of importance for surgical planning and thus should be measured. In an acute tear, there may be complex luid and hematoma within and about the tear site. When evaluating lexor and extensor tendons at the hand and wrist, passive and active motion can facilitate accurate identiication of the tendon of interest and can provide mechanical correlation for the integrity of a tendon (Video 23.3).

Sonographic Signs of Tendon Tears Discontinuity of ibers (partial or complete) with hypoechoic or anechoic gap Focal thinning of the tendon Hematoma (usually small) Bone fragment (in cases of avulsion) Nonvisualization of retracted tendon (in complete tear)

In tendons with surrounding tendon sheaths, inlammation of the tendon sheath (tenosynovitis) may occur as an overuse phenomenon or as a result of an inlammatory condition, such as rheumatoid arthritis. Tenosynovitis is manifest on ultrasound

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FIG. 23.10 Partial Tear of the Distal Achilles Tendon. (A) There is focal anechoic clefting of the anterior ibers of the Achilles distal insertion (arrows) although the posterior ibers remain intact. (B) Color Doppler imaging in the same patient demonstrates marked hyperemia in the injured tendon.

FIG. 23.11 Achilles Tendon Rupture. A panoramic view of the Achilles tendon demonstrates a rupture within the midportion of the tendon. The proximal aspect of the tendon is chronically thickened and hypoechoic (arrows). Refraction artifact (arrowheads) is caused by the interfaces between the ruptured tendon edges and hemorrhage. C, Calcaneus.

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FIG. 23.12 Tenosynovitis. In this patient with rheumatoid arthritis and ankle pain, the peroneus brevis tendon (*) in long-axis (A) and short-axis (B) views is thickened and heterogeneous. The tendon sheath contains a large amount of echogenic synovium (arrows), hypoechoic luid, and hyperemia on color Doppler imaging.

as an increase of luid volume around a tendon within its sheath (Fig. 23.12). he tendon sheath itself can thicken and demonstrate hypervascularity on Doppler evaluation.24 In patients with imaging indings of tenosynovitis and a history of penetrating injury or foreign body, septic tenosynovitis should be considered.25

LIGAMENTS Ultrasound is an excellent technique for the evaluation of liga­ mentous injuries, with some advantages over MRI in this regard. Ultrasound permits high-resolution imaging of small ligaments

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in planes that can be individualized to the structure of interest in any given patient, overcoming some intrinsic diiculties that can be encountered with scan plane prescription for MRI. In addition to static imaging, dynamic assessment may provide additional diagnostic information. Normal ligaments consist of interweaved bundles of collagen, extending between bones, usually restricting joint movements to prevent pathologic motion.26 Ligament injury leads to pain and instability. Normal ligaments are linear bandlike structures and appear hyperechoic and ibrillar27 (Fig. 23.13). Low-grade injuries consist of mild sprains, which typically have a good prognosis with conservative care. Mild sprains are characterized on ultrasound by swelling, hypoechogenicity, and some loss of ibrillar pattern (Fig. 23.14). Tears can be partial or complete. In the case of complete tears, there may be retraction of the torn ligament components from each other, a inding that can be exaggerated by dynamic imaging with stress maneuvers (Figs. 23.15 and 23.16). he use of stress maneuvers is somewhat controversial, however, because of concerns that a partial tear may be exacerbated or even converted to a complete tear by additional stress.28,29

863

FIG. 23.13 Normal Anterior Taloibular Ligament. Note that the ligament (arrows) demonstrates a ibrillar appearance and that the ibers are more densely packed than those seen in a normal tendon. F, Fibula, T, talus.

FIG. 23.14 Ligament Sprain. The anterior taloibular ligament (arrows) is diffusely thickened and hypoechoic, with intact ibers, consistent with sprain. Note the cortical irregularity at the lateral ibula (*) consistent with prior avulsion. F, Fibula, T, talus.

FIG. 23.15 Chronic Ligament Rupture. In this patient with a history of multiple ankle sprains, the anterior taloibular ligament is absent and the joint is widened on dynamic stress maneuver. Hypoechoic luid (*) appears in the lateral recess. F, Fibula, T, talus.

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FIG. 23.16 Elbow Joint Widening on Dynamic Valgus Stress. (A) The medial joint is 2 mm (calipers) wide at rest in this patient with an ulnar collateral ligament (UCL) tear. Note the UCL is markedly thickened at the proximal humeral attachment and a hypoechoic cleft is present within the ligament consistent with a tear (arrows). (B) With valgus stress, the medial joint space widens to 4 mm, conirming the presence of a UCL tear. The overlying common extensor tendon (*) is intact. ME, Medial epicondyle of the humerus; U, ulna.

FIG. 23.17 Stener Lesion. The ulnar collateral ligament (arrows) of the thumb is torn and the stump is retracted proximal to the metacarpophalangeal joint and to the adductor aponeurosis (arrowheads), which is thickened and hypoechoic. MC, Metacarpal; P, proximal phalanx.

Ultrasound has been efectively utilized to diagnose injury of ligaments at the hand and wrist, notably the ulnar collateral ligament of the thumb metacarpophalangeal joint28-30 in addition to the scapholunate ligament.31 Other ligaments, such as the anterior oblique ligament of the thumb, have been identiied with ultrasound, but the role of ultrasound in diagnosis has yet to be deined.32,33 Ultrasound may also be used to evaluate the collateral ligaments of the elbow,34-39 ankle ligaments,40 and collateral ligaments of the knee.41 When evaluating ligamentous injury, it is important to assess nearby structures such as tendons, which may also have been injured (e.g., common lexor tendon origin injury in the setting of ulnar collateral ligament injury at the elbow) or which may be relevant to the ligamentous injury, as in the case of a Stener lesion. A Stener lesion occurs when a thumb metacarpal phalangeal ulnar collateral ligament tear entraps the adductor aponeurosis such that the ligament lies supericial to the aponeurosis (Fig. 23.17). his injury is important to recognize, as the treatment

is surgical. he appearance of a Stener lesion on ultrasound is of retracted hypoechoic ligament ibers displaced over the linear aponeurosis, giving rise to the “yo­yo on a string” appearance.28

NERVES Normal peripheral nerves are well visualized with high-resolution ultrasound. Nerves have a characteristic honeycomb morphology on ultrasound when imaged in short axis42 (Fig. 23.18). Nerves are tubular structures, and on longitudinal axis, they demonstrate an internal striated pattern, somewhat similar to tendons but with a coarser pattern referred to as a “fascicular pattern.”43,44 his pattern consists of alternating internal hypoechoic and hyperechoic linear components. he hypoechoic components represent fascicles or groups of fascicles, whereas the hyperechoic parts correspond with the epineurium.44 he epineurium consists of connective tissue that surrounds nerve fascicles, composed

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of collagenous and adipose components, with small blood vessels and lymphatics. On short-axis view, peripheral nerves appear ovoid or round and have punctate internal hypoechoic fat representing nerve fascicles within the echogenic epineurium. Dynamic maneuvers including lexion and extension of the imaged region should show no substantial motion of a peripheral nerve, as distinct from tendons. Assessment of peripheral nerves using ultrasound is performed primarily in the short-axis plane. he nerve is evaluated at a known anatomic location and followed proximally and distally as needed. Anisotropy is less problematic for peripheral nerves than for tendons.23 Longitudinal scanning is helpful for providing an overview and illustrating relative caliber changes of peripheral nerves detected on transverse imaging. Caution should be exercised in primary interpretation of longitudinal sonographic images of peripheral nerves because of the potential to scan in a plane, which is not parallel to the nerve with potential artifactual changes in caliber and echogenicity. Nerve dysfunction can result from compression by masses arising from or adjacent to the nerve, entrapment within ibroosseous tunnels (such as the carpal tunnel in the case of median nerve compression at the wrist), or subluxation from ibro-osseous tunnels. Masses include neurogenic tumors, neuroibromas and schwannomas, considered more fully later. Sot tissue ganglia, usually appearing anechoic on ultrasound, may also cause nerve compression.45-47 In the setting of nerve compression by any cause, the indings detectible on ultrasound relate to echotextural and caliber changes. Local compression causes venous congestion, which can lead to intraneural edema. Chronic compression can ultimately lead to intraneural ibrosis. hese alterations in

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FIG. 23.18 Normal Median Nerve. (A) In long axis, the nerve demonstrates a fascicular appearance (arrows), although coarser than a tendon. The hypoechoic fascicles are distinguishable from the intervening echogenic epineurium. (B) In short axis, in the forearm, the median nerve shows a honeycomb appearance (arrows). (C) In short axis, at the level of the carpal tunnel, the echogenic tendons (arrows) are seen adjacent to the median nerve (arrowheads).

intraneural composition lead to loss of normal hyperechogenicity of the interfascicular epineural tissue, causing an overall hypoechoic appearance of the nerve in addition to poor deinition or disappearance of the normal fascicular pattern.43 One of the most common clinical forms of entrapment neuropathy is carpal tunnel syndrome. In this condition, compression and lattening of the nerve occurs within the carpal tunnel, at the palmar aspect of the wrist, and the nerve is typically swollen and expanded just proximal to the carpal tunnel. he sonographic diagnosis of carpal tunnel syndrome is made by measuring the cross-sectional area of the median nerve at the level of the pronator quadratus and comparing this to the crosssectional area of the median nerve in the carpal tunnel at the level of the pisiform. A diference of more than 2 mm2 between the two measurements is highly associated with carpal tunnel syndrome48 (Fig. 23.19). Variable cut-of values for the diagnosis of carpal tunnel syndrome based on single cross-sectional measurements of the median nerve in the carpal tunnel have been reported in the literature, in the 9- to 11-mm2 range.49-51 Bowing and thickening of the overlying lexor retinaculum can also be observed.51 Symptoms may also arise from dynamic nerve subluxation from ibro-osseous tunnels. One example of this is at the cubital tunnel, at the medial posterior aspect of the elbow. he ulnar nerve normally passes through this ibro-osseous tunnel at the posterior aspect of the humerus and is stabilized by an overlying retinaculum. his retinaculum normally passes between the olecranon and the medial epicondyle of the humerus. Developmental or posttraumatic deiciency of this retinaculum can allow the ulnar nerve to dynamically subluxate out of the cubital tunnel

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FIG. 23.19 Carpal Tunnel Entrapment of the Median Nerve. (A) Short-axis cross-sectional area of the median nerve obtained at the level of the pronator quadratus (PQ) at the distal forearm. (B) Cross-sectional area obtained in the carpal tunnel at the level of the pisiform (P). The 4-mm2 difference in area between the two images is consistent with carpal tunnel syndrome.

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FIG. 23.20 Ulnar Nerve Dislocation at the Elbow. (A) At rest, with the elbow extended and the probe positioned between the medial epicondyle (M) and the ulnar olecranon (O), the ulnar nerve (circled) is positioned posterior to the epicondyle. Note the ulnar nerve is enlarged at this location. (B) On lexion the ulnar nerve (circled) dislocates anterior to the medial epicondyle along with the medial head (MT) of the triceps muscle (known as “snapping triceps” syndrome). Most patients with ulnar dislocation do not exhibit medial head triceps dislocation. See also Video 23.4.

during elbow lexion, and this subluxation can be captured on dynamic imaging (Video 23.4). Scan technique is important in this diagnosis. he probe should be positioned in a transverse plane with respect to the medial posterior elbow. he nerve should normally be visible within the cubital tunnel with the elbow in an extended position. he osseous landmark of the medial epicondyle should be maintained in the visualized ield as the patient slowly lexes the elbow. Excessive probe pressure should be avoided because this can limit dynamic motion of the nerve. he nerve should normally remain lateral to the medial epicondyle. Subluxation, where the nerve moves medially and anteriorly along the epicondyle, or dislocation, where the nerve snaps anteromedial to the medial epicondyle, may occur on lexion52,53 (Fig. 23.20). Patients with ulnar nerve subluxation or dislocation may experience pain or transient numbness, but this dynamic instability can also be seen in asymptomatic in healthy controls, and the association with neuropathy is debated.54,55

JOINT ASSESSMENT Ultrasound can play a helpful role in the diagnosis and follow-up of both inlammatory and noninlammatory arthropathy and may guide diagnostic and therapeutic procedures in patients with these disorders. Patients with inlammatory arthropathy such as rheumatoid arthritis present with joint pain, swelling, and stifness. Ultrasound plays a complementary role to clinical history, physical examination, radiographs, and serology tests such as acute phase reactants (e.g., C-reactive protein, erythrocyte sedimentation rate, rheumatoid factor, and antinuclear antibody). In this role, when used systematically, ultrasound can substantially increase diagnostic certainty in patients with suspected inlammatory arthropathy.56 Ultrasound also represents a great tool in the follow-up of these patients, allowing detection of subclinical relapse in patients with clinical remission and predicting relapse and joint deterioration.57

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be adjusted to just below a level where noise is visualized.59 Either color Doppler or power Doppler may be more sensitive to low in the evaluation of synovitis, depending on individual machine, so familiarity with the hardware being used is important.60 he quantity of synovial hyperemia can be graded as described by Szkudlarek et al.61: Grade I (low) hyperemia consists of the visualization of several single vessel dots. Grade II (moderate) hyperemia is shown when there are conluent vessel signals occupying less than half of the visualized synovial tissue. Grade III (high) represents conluent vessel signals in more than half of the synovium. Doppler ultrasound has shown high degrees of sensitivity and speciicity in the diagnosis of synovitis at the metacarpophalangeal joints in patients with rheumatoid arthritis when compared with dynamic contrast-enhanced MRI.61 Ultrasound has also been shown to have high interobserver and intraobserver reliability in detection of synovitis.62 Bone erosion in erosive inlammatory arthritis such as rheumatoid arthritis can be depicted on ultrasound as a cortical defect visible in two perpendicular planes63 (Fig. 23.23). Erosions may be graded as small (4 mm).64 Ultrasound is more sensitive than plain radiographs in the detection of bone erosion and thus may aid in diagnosis of early disease.65 In addition to cortical discontinuity, there may be acoustic enhancement of marrow subjacent to the inlammatory bony erosion.65 Patients with inlammatory arthropathy may also have associated tenosynovitis, enthesitis, and, in the case of rheumatoid arthritis, inlammatory periarticular nodules (rheumatoid nodules)66 (Fig. 23.24). Gout is a common inlammatory arthritis with a predilection for irst metatarsophalangeal joint involvement, caused by precipitation of uric acid crystals within joints. In patients with gout, there may be joint efusion, synovial hypertrophy and hyperemia, sot tissue swelling, and juxtaarticular erosions that can be large.67 Intraarticular crystals may be evidenced by the presence of a characteristic irregular hyperechoic line along the surface of the normally hypoechoic cartilage, termed the “double contour sign”68 (Fig. 23.25). his is distinct from

Joint efusions are frequently present in patients with inlam­ matory arthritis but are nonspeciic as they may also occur in patients with osteoarthritis, with infection, and in the setting of trauma or internal derangement (Fig. 23.21). he diagnosis of an efusion rests on the visualization of increased volume of joint luid. Joint luid is typically anechoic but can contain some mobile low-level echoes. In addition, joint luid is mobile and compressible.58 Normal joints contain just a trace of luid, so an increase in this luid volume constitutes a joint efusion. Synovitis is determined by the presence of intraarticular nondisplaceable hypoechoic to hyperechoic sot tissue, which usually demonstrates hyperemia on color Doppler assessment (Fig. 23.22). On Doppler assessment, the velocity ilter should be set to detect low amounts of low, and the gain settings should

FIG. 23.21 Simple Knee Joint Effusion. Anechoic luid is present within the suprapatellar recess of the knee (arrows). There is concomitant quadriceps tendinosis (*). F, Distal femur; P, patella.

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FIG. 23.22 Complex Ankle Joint Effusion in Rheumatoid Arthritis. (A) A long-axis image of the tibiotalar joint demonstrates a complex joint effusion (arrows) with both anechoic luid and echogenic, thickened synovium consistent with synovitis. (B) Color Doppler imaging of the tibiotalar joint demonstrates marked hyperemia within the echogenic synovium. T, Talus.

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FIG. 23.23 Bone Erosions in Two Different Patients Rheumatoid Arthritis. (A) Long-axis gray-scale image at the ifth metatarsophalangeal joint demonstrates bone erosion in the ifth metatarsal head (arrow) with associated cortical irregularity and synovial hypertrophy (arrowheads). M, Metatarsal, P, proximal phalanx. (B) Color Doppler imaging of the dorsal wrist in long-axis view demonstrates hyperemia within the synovium and erosion (arrow) of the scaphoid (S). R, Distal radius, T, trapezium.

FIG. 23.24 Achilles Tendon With Rheumatoid Nodules. Long-axis image of the Achilles tendon demonstrates hypoechoic nodular thickening (*) of the posterior tendon surface, consistent with rheumatoid nodules. No hyperemia was seen on color Doppler imaging (not shown).

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FIG. 23.25 Gout in Two Different Patients. (A) Long-axis gray-scale image of the irst metatarsal phalangeal joint demonstrates the “sugar icing” appearance where echogenic urate crystals are deposited along the synovial lining of the joint (arrowheads). The “double contour sign” is formed by the echogenic urate crystals (“sugar icing”) layering on the anechoic hyaline cartilage with the underlying echogenic cortex (arrows). (B) Long-axis gray-scale image of the ifth metatarsal phalangeal joint shows a large erosion (arrow) with a large amorphous tophus (arrowheads), part of which extends into the erosion. M, First metatarsal, P, irst proximal phalanx.

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FIG. 23.26 Osteoarthritis. Long-axis gray-scale image of the ifth metatarsophalangeal joint demonstrates osteophyte formation (arrows) at both sides of the joint. M, Metatarsal, P, proximal phalanx.

FIG. 23.27 Ganglion Cyst. Long-axis image of the radiocarpal joint at the radioscaphoid articulation demonstrates a lobulated, hypoechoic ganglion cyst (arrows) arising from the region of the scapholunate ligament. Note the neck (arrowhead) arising from the joint. R, Radius, S, scaphoid.

chondrocalcinosis in which cartilage calciication may be seen with an intracartilaginous echogenic line. Tophi are focal crystal accumulations, which occur around joints in some patients with gout, appearing as clumps of hyperechoic material, which may have a surrounding hypoechoic rim, an appearance has been referred to as “wet sugar clumps.”68 Bony erosions may be seen adjacent to these tophi. In osteoarthritis (nonerosive), cartilage thinning and irregularity may be seen in addition to osteophytes and typically mild synovitis (Fig. 23.26). Osteophytes appear as cortical protrusions at the margin of the articular surface, with posterior acoustic shadowing.69 Synovitis may be nodular or difuse. Joint efusions may also be demonstrated in osteoarthritis, and although they may occur in the absence of synovitis, the presence and size of efusion correlate with the presence of synovitis and the extent of synovial thickening. Joint efusion and synovitis also correlate with clinical and radiographic disease severity.70

SOFT TISSUE MASSES Palpable sot tissue masses are very common and represent a diagnostic dilemma for physicians. Although the vast majority of these masses are benign, discrimination between benign and malignant masses is not clinically possible. Ultrasound is a complementary modality to MRI in the workup of sot tissue masses. Although MRI has overall higher speciicity, several sot tissue masses can be characterized as benign with ultrasound.71,72 In indeterminate cases, contrast-enhanced MRI can be performed, and this two-tiered strategy may provide an overall cost savings to the health care system if appropriately implemented. Ganglion cysts are mucin-illed lesions most oten found at the wrist; they are usually closely related to a joint or tendon sheath. Approximately 10% of ganglion cysts occur secondary to trauma.73 he most common location is adjacent to the scapholunate articulation (Fig. 23.27). A neck extending from the lesion to an underlying joint or tendon sheath should be

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FIG. 23.28 Baker Cyst. (A) Short-axis image from the medial posterior knee shows a lobulated, septated, hypoechoic Baker cyst (arrows) communicating with the joint between the medial gastrocnemius muscle (M) and the semimembranosus tendon (S). F, Posterior medial femoral condyle. (B) In a different patient, long-axis image from the posterior medial knee demonstrates an ovoid, septated complex Baker cyst (arrows) with internal debris, lined with echogenic synovium. See also Video 23.5.

FIG. 23.29 Ruptured Baker Cyst. Longitudinal sonogram of the calf with extended ield of view shows a complex mass (arrows) that is connected to a small amount of luid in the popliteal fossa (arrowheads), representing the ruptured Baker cyst.

sought but is oten not deinable.74 hese lesions typically appear as well-circumscribed, oval or lobulated anechoic cystic masses, with accompanying through transmission.75 Ganglion cysts may demonstrate low-level internal echoes and may be septated.74 Ganglion cysts are typically noncompressible (as opposed to bursae, which are compressible). Ganglion cysts do not usually demonstrate internal low on color Doppler evaluation.76 Baker cysts, occurring in the medial aspect of the popliteal fossa, deserve special mention, as they are extremely common. A Baker cyst is caused by luid distention of the semimembranosus­ gastrocnemius bursa, occurring between the distal semimembranosus tendon and the medial head of the gastrocnemius muscle with a narrow neck arising from the underlying knee joint (Fig. 23.28, Video 23.5). his usually occurs in the setting of an underlying cause of joint efusion, including osteoarthritis, but also in the setting of posterior horn medial meniscal tear, inlammatory arthritis, and internal derangement. Although common, they are not reliably diagnosed clinically.77 Baker cysts are typically anechoic when uncomplicated, yet may have a variable appearance, with complex luid and hemorrhage, internal septations and debris, and thick, echogenic, hyperemic synovium lining the cyst. he narrow neck can act as a valve, and luid

accumulation within the cyst can lead to rupture, resulting in acute pain, swelling, and erythema behind the knee and in the proximal calf.78 When this occurs, the margin of the cyst is oten irregular caudally and there may be associated medial calf subcutaneous edema, with luid tracking distally about the medial head of the gastrocnemius (Fig. 23.29). he clinical presentation of this may mimic deep venous thrombosis or developing cellulitis.79 Lipomas are the most common palpable sot tissue masses (Table 23.1). hese may occur within the subcutaneous tissues, muscle, or deep sot tissues. Simple lipomas are usually homogeneously isoechoic, or slightly hyperechoic to fat, with welldeined margins and internal wavy septations mimicking the surrounding fat80 (Fig. 23.30). hey should be painless, mobile, and compressible with transducer pressure.81 Simple lipomas should not demonstrate internal complexity or hypervascularity; however, vessels may be seen passing through the lipoma. MRI with contrast should be performed to exclude underlying liposarcoma in the evaluation of any suspected lipoma with the following atypical features: deep acoustic shadowing, internal complexity or hypervascularity, size greater than 5 cm, deep or intramuscular location, pain, or history of enlargement.

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TABLE 23.1 Fat-Containing Soft Tissue Lesions Diagnosis

Sonographic Findings

Follow-Up

Simple lipoma

Similar echogenicity to subcutaneous fat Mobile Soft, compressible Painless Few, small vessels Complex echogenicity Deep acoustic shadowing Hypervascularity Size > 5 cm Deep or intramuscular location Pain History of enlargement Change in appearance over time or with Valsalva maneuver

Clinical follow-up suficient if classic sonographic appearance

Indeterminate lipomatous lesion

Fat-containing hernia

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MRI with contrast for further evaluation, with biopsy if needed

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FIG. 23.30 Lipoma. (A) A simple lipoma (arrows) is isoechoic to the adjacent subcutaneous fat and contains thin echogenic septations that parallel the skin surface. (B) Color Doppler imaging demonstrates two small vessels traversing the lipoma. There is no hyperemia.

A pitfall in the diagnosis of lipoma is that a fat-containing hernia can have some overlapping ultrasound appearances, including similar echogenicity to subcutaneous fat and internal wavy septations.80 Anatomic location, dynamic change in appearance, and movement with Valsalva maneuver can assist in the diagnosis of hernia. When appearances are typical for benign lipoma, periodic clinical follow-up can be performed rather than additional imaging or biopsy. Nerve sheath tumors are common, usually benign masses, although malignant nerve sheath tumors may uncommonly occur. Nerve sheath tumors are usually well-circumscribed solid hypoechoic masses, ovoid or fusiform in shape, and have faint deep acoustic enhancement.82 A contiguous nerve of origin of the lesion may be identiied, either centrally within the lesion in the case of neuroibroma or peripherally related to the lesion in a schwannoma (however, these indings are not absolute) (Fig. 23.31). An echogenic capsule may be seen, and occasionally cystic spaces can occur in a degenerated schwannoma. A split-fat sign, although not entirely speciic, is oten seen in association with benign peripheral nerve sheath tumors. his sign comprises the presence of a rim of fat about the end of the lesion, representing fat normally present about the neurovascular bundle from which the lesion arises.83 he imaging appearances of benign and malignant peripheral nerve sheath tumors overlap, but malignant lesions should be considered when a lesion is more poorly deined (relecting its iniltrative nature), is increasing in size, or is internally heterogeneous in appearance as a result of

internal necrosis and/or hemorrhage.84 If lesions typical for benign nerve sheath tumors on imaging are not biopsied or resected, then imaging and clinical follow-up are warranted. Various benign and malignant sot tissue lesions cannot be deinitively discriminated by ultrasound alone. Lesions that remain indeterminate by ultrasound may then be evaluated with contrastenhanced MRI. Lesions that remain worrisome for malignant neoplasm will typically undergo image-guided biopsy (most oten with ultrasound guidance). Primary sot tissue sarcomas typically appear solid, with irregular borders, variable internal necrosis, and hemorrhage (Fig. 23.32). hey may be partly calciied (especially synovial sarcomas).85 he lesions usually demonstrate internal vascularization and may show local invasion of adjacent tissues. Secondary lesions (metastases) should be considered when a solid vascularized sot tissue lesion is found in a patient with known underlying malignancy. An important pitfall in the diagnosis of sarcoma is the clinical presentation with a hemorrhagic tumor, which can be incorrectly diagnosed as a bland hematoma, potentially leading to delay in correct diagnosis.86 To further complicate the diagnosis, patients may report a history of trauma. A spontaneous hematoma in the absence of anticoagulant medication should be regarded with suspicion, as should an apparent hematoma disproportionate to the patient-reported trauma.73 Such lesions should be evaluated carefully for vascularized components, which should be targeted for biopsy. If none are found, then repeat imaging should be performed in 6 weeks to document resolution of the hematoma. Following surgical

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A

B

FIG. 23.31 Peripheral Nerve Sheath Tumor. (A) Long-axis image obtained at the site of a palpable mass shows an ovoid, hypoechoic mass with smooth borders, arising from the ulnar nerve. Note the ulnar nerve enters and exits the mass (arrows). (B) A short-axis image of the forearm demonstrates the mass in the expected location of the ulnar nerve. Color Doppler shows marked hyperemia within the mass. FCU, Flexor carpi ulnaris; FDS, lexor digitorum supericialis and profunda.

A

B

FIG. 23.32 Sarcoma. (A) A myxoid liposarcoma demonstrates mildly increased through transmission (arrows) due to the myxoid content. However, the mass is solid, with internal echoes. The supericial border is microlobulated. (B) Color Doppler imaging demonstrates increased blood low within the mass.

resection of sot tissue sarcoma, ultrasound has been shown to have acceptable diagnostic accuracy but may miss a small number of recurrences. Ultrasound could play a complementary role to MRI in follow-up of these cases.87,88

FOREIGN BODIES Embedded sot tissue foreign bodies are a common problem in both adult and pediatric populations. Whereas some materials, such as metal and glass, are radiopaque and can be seen on plain radiographs, other materials such as wood are not detected radiographically. In these cases, ultrasound is an efective means for diagnosis. Foreign bodies are typically highly echogenic and may have posterior acoustic shadowing (Fig. 23. 33). hey may be surrounded by a hypoechoic halo, representing an inlammatory reaction89 or hyperemia on color Doppler imaging. A large amount of associated luid should prompt consideration of a secondary abscess. From a practical standpoint, the patient can usually accurately direct the sonographer to the area of greatest concern, and observation of skin entry and/or exit sites is helpful to focus evaluation. Knowledge of the trajectory of foreign body entry is particularly helpful in assessment of thin linear objects such

as wooden splinters, because they are oten seen in nonanatomic oblique planes. Meticulous scanning is needed because small foreign bodies may be occult to cursory scanning in the hands and feet, where they may be obscured by adjacent ligaments, tendons, nerves, and vessels.90 It is also important to determine the relationship of the object to these anatomic structures and to determine if there is associated injury to them. In addition to the visualization of nonradiopaque foreign bodies, ultrasound may help guide surgical planning by providing accurate threedimensional localization of both radiopaque and nonradiopaque objects, and the overlying skin can be marked preprocedurally as an aid. Ultrasound can also be used to directly guide foreign body retrieval with real-time imaging.91,92

SOFT TISSUE INFECTION Infection of the skin and subcutaneous sot tissue, cellulitis, is a common clinical problem, which can be efectively treated with antibiotics. On ultrasound, the skin and subcutaneous tissues are thickened and hyperechoic early in the process. Later, there may be interdigitating reticular strands of hypoechogenicity representing interstitial inlammatory exudate,93 also known as the “cobblestone” appearance (Fig. 23.34).

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FIG. 23.33 Wood Foreign Body. A wood splinter is embedded within the dorsal soft tissues of the hand. The splinter (arrowheads) appears as a linear, echogenic structure.

A

C

B

D

FIG. 23.34 Cellulitis. (A) Normal subcutaneous fat in the lateral nonaffected ankle is juxtaposed with the (B) abnormal contralateral ankle in the same patient with cellulitis. Note the hypoechoic echotexture of the normal fat (left side of image) versus the echogenic, swollen subcutaneous fat with obscuration of the normal internal septations (right side of image). (C) Color Doppler imaging demonstrates increased blood low within the echogenic, swollen subcutaneous fat. (D) Gray-scale imaging in a different patient with cellulitis demonstrates anechoic luid (arrows) within the echogenic cellulitic tissue.

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FIG. 23.35 Forearm Abscess. (A) Short-axis image of a complex luid hypoechoic collection (arrows) with echogenic peripheral soft tissue rind and increased through transmission, consistent with an abscess. (B) Color Doppler image demonstrates hyperemia within the surrounding soft tissues. U, Ulna.

Cellulitis may progress to abscess formation. he development of an associated abscess is an important inding to diagnose, as this will typically not respond to antibiotics, instead requiring drainage, either surgical or image guided. Abscesses can have a variable appearance on ultrasound evaluation.94 An abscess border may be well deined or poorly deined and iniltrative (Fig. 23.35). here may be a surrounding rim of hyperemic, thickened sot tissue. he internal liqueied material may demonstrate an anechoic, hypoechoic, or complex echogenic appearance, with internal septations and low-level echoes. Foci of echogenic gas, with associated ill-deined shadowing, may be present within the abscess. With dynamic compression, swirling of the echogenic debris within the abscess can be seen. In cases of luid collection, several other entities may be considered and diferentiated from an abscess. A seroma can be distinguished from an abscess in that a seroma appears as a simple anechoic to hypoechoic luid collection without peripheral hyperemia, and there may be increased through transmission. A hematoma may appear as a mixed echogenicity luid collection, yet will have no internal color Doppler low and will have scant peripheral hyperemia. A sot tissue sarcoma will demonstrate solid, hyperemic internal components, as well as posterior acoustic shadowing. If the sonographic diagnosis of the luid collection is indeterminate, conirmation can be obtained with aspiration (sonographically guided, if needed) and microbiologic and histologic assessment of the aspirate.

CONCLUSION Ultrasound is a cost-efective means by which to provide an accurate diagnosis in many scenarios of musculoskeletal pathology, including tendon and ligament injury, arthritis, and characterization of infection and some sot tissue masses. In addition to ongoing technical developments, critical to the use of this technology in the future will be technologist and physician education and appropriate and consistent incorporation of new technology into patient care pathways.

REFERENCES 1. Nazarian LN. he top 10 reasons musculoskeletal sonography is an important complementary or alternative technique to MRI. AJR Am J Roentgenol. 2008;190(6):1621-1626. 2. Jamadar DA, Jacobson JA, Caoili EM, et al. Musculoskeletal sonography technique: focused versus comprehensive evaluation. AJR Am J Roentgenol. 2008;190(1):5-9. 3. Teh J. Applications of Doppler imaging in the musculoskeletal system. Curr Probl Diagn Radiol. 2006;35(1):22-34. 4. Klauser AS, Miyamoto H, Bellmann-Weiler R, et al. Sonoelastography: musculoskeletal applications. Radiology. 2014;272(3):622-633. 5. Ooi CC, Malliaras P, Schneider ME, Connell DA. “Sot, hard, or just right?” Applications and limitations of axial-strain sonoelastography and shear-wave elastography in the assessment of tendon injuries. Skeletal Radiol. 2014;43(1):1-12. 6. Botar Jid C, Damian L, Dudea SM, et al. he contribution of ultrasonography and sonoelastography in assessment of myositis. Med Ultrason. 2010;12(2): 120-126. 7. Magarelli N, Carducci C, Bucalo C, et al. Sonoelastography for qualitative and quantitative evaluation of supericial sot tissue lesions: a feasibility study. Eur Radiol. 2014;24(3):566-573. 8. Weng L, Tirumalai AP, Lowery CM, et al. US extended-ield-of-view imaging technology. Radiology. 1997;203(3):877-880. 9. Kavanagh EC, Koulouris G, Parker L, et al. Does extended-ield-of-view sonography improve interrater reliability for the detection of rotator cuf muscle atrophy? AJR Am J Roentgenol. 2008;190(1):27-31. 10. Harcke HT, Grissom LE, Finkelstein MS. Evaluation of the musculoskeletal system with sonography. AJR Am J Roentgenol. 1988;150(6):1253-1261. 11. Peetrons P. Ultrasound of muscles. Eur Radiol. 2002;12(1):35-43. 12. Draghi F, Zacchino M, Canepari M, et al. Muscle injuries: ultrasound evaluation in the acute phase. J Ultrasound. 2013;16(4):209-214. 13. Nguyen JT, Nguyen JL, Wheatley MJ, Nguyen TA. Muscle hernias of the leg: a case report and comprehensive review of the literature. Can J Plast Surg. 2013;21(4):243-247. 14. Strobel K, Hodler J, Meyer DC, et al. Fatty atrophy of supraspinatus and infraspinatus muscles: accuracy of US. Radiology. 2005;237(2): 584-589. 15. Dillehay GL, Deschler T, Rogers LF, et al. he ultrasonographic characterization of tendons. Invest Radiol. 1984;19(4):338-341. 16. Crass JR, van de Vegte GL, Harkavy LA. Tendon echogenicity: ex vivo study. Radiology. 1988;167(2):499-501. 17. Khan KM, Bonar F, Desmond PM, et al. Patellar tendinosis (jumper’s knee): indings at histopathologic examination, US, and MR imaging. Victorian Institute of Sport Tendon Study Group. Radiology. 1996;200(3):821-827.

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18. Ohberg L, Lorentzon R, Alfredson H. Neovascularisation in Achilles tendons with painful tendinosis but not in normal tendons: an ultrasonographic investigation. Knee Surg Sports Traumatol Arthrosc. 2001;9(4):233-238. 19. Connell D, Burke F, Coombes P, et al. Sonographic examination of lateral epicondylitis. AJR Am J Roentgenol. 2001;176(3):777-782. 20. Dones 3rd VC, Grimmer K, hoirs K, et al. he diagnostic validity of musculoskeletal ultrasound in lateral epicondylalgia: a systematic review. BMC Med Imaging. 2014;14:10. 21. Eder L, Barzilai M, Peled N, et al. he use of ultrasound for the assessment of enthesitis in patients with spondyloarthritis. Clin Radiol. 2013;68(3): 219-223. 22. Frediani B, Falsetti P, Storri L, et al. Ultrasound and clinical evaluation of quadricipital tendon enthesitis in patients with psoriatic arthritis and rheumatoid arthritis. Clin Rheumatol. 2002;21(4):294-298. 23. Martinoli C, Bianchi S, Dahmane M, et al. Ultrasound of tendons and nerves. Eur Radiol. 2002;12(1):44-55. 24. Breidahl WH, Staford Johnson DB, Newman JS, Adler RS. Power Doppler sonography in tenosynovitis: signiicance of the peritendinous hypoechoic rim. J Ultrasound Med. 1998;17(2):103-107. 25. Jefrey Jr RB, Laing FC, Schechter WP, et al. Acute suppurative tenosynovitis of the hand: diagnosis with US. Radiology. 1987;162(3):741-742. 26. Hodgson RJ, O’Connor PJ, Grainger AJ. Tendon and ligament imaging. Br J Radiol. 2012;85(1016):1157-1172. 27. Zbojniewicz AM. US for diagnosis of musculoskeletal conditions in the young athlete: emphasis on dynamic assessment. Radiographics. 2014;34(5): 1145-1162. 28. Ebrahim FS, De Maeseneer M, Jager T, et al. US diagnosis of UCL tears of the thumb and Stener lesions: technique, pattern-based approach, and differential diagnosis. Radiographics. 2006;26(4):1007-1020. 29. Noszian IM, Dinkhauser LM, Orthner E, et al. Ulnar collateral ligament: diferentiation of displaced and nondisplaced tears with US. Radiology. 1995;194(1):61-63. 30. Melville DM, Jacobson JA, Fessell DP. Ultrasound of the thumb ulnar collateral ligament: technique and pathology. AJR Am J Roentgenol. 2014;202(2):W168. 31. Finlay K, Lee R, Friedman L. Ultrasound of intrinsic wrist ligament and triangular ibrocartilage injuries. Skeletal Radiol. 2004;33(2):85-90. 32. Gondim Teixeira PA, Omoumi P, Trudell DJ, et al. High-resolution ultrasound evaluation of the trapeziometacarpal joint with emphasis on the anterior oblique ligament (beak ligament). Skeletal Radiol. 2011;40(7):897-904. 33. Chiavaras MM, Harish S, Oomen G, et al. Sonography of the anterior oblique ligament of the trapeziometacarpal joint: a study of cadavers and asymptomatic volunteers. AJR Am J Roentgenol. 2010;195(6):W428-W434. 34. Ferreira FB, Fernandes ED, Silva FD, et al. A sonographic technique to evaluate the anterior bundle of the ulnar collateral ligament of the elbow: imaging features and anatomic correlation. J Ultrasound Med. 2015;34(3): 377-384. 35. Bica D, Armen J, Kulas AS, et al. Reliability and precision of stress sonography of the ulnar collateral ligament. J Ultrasound Med. 2015;34(3):371-376. 36. Jacobson JA, Chiavaras MM, Lawton JM, et al. Radial collateral ligament of the elbow: sonographic characterization with cadaveric dissection correlation and magnetic resonance arthrography. J Ultrasound Med. 2014;33(6): 1041-1048. 37. Nazarian LN, McShane JM, Ciccotti MG, et al. Dynamic US of the anterior band of the ulnar collateral ligament of the elbow in asymptomatic major league baseball pitchers. Radiology. 2003;227(1):149-154. 38. Jacobson JA, Propeck T, Jamadar DA, et al. US of the anterior bundle of the ulnar collateral ligament: indings in ive cadaver elbows with MR arthrographic and anatomic comparison—initial observations. Radiology. 2003;227(2): 561-566. 39. Sasaki J, Takahara M, Ogino T, et al. Ultrasonographic assessment of the ulnar collateral ligament and medial elbow laxity in college baseball players. J Bone Joint Surg Am. 2002;84-A(4):525-531. 40. Hua Y, Yang Y, Chen S, Cai Y. Ultrasound examination for the diagnosis of chronic anterior taloibular ligament injury. Acta Radiol. 2012;53(10): 1142-1145. 41. De Maeseneer M, Vanderdood K, Marcelis S, et al. Sonography of the medial and lateral tendons and ligaments of the knee: the use of bony landmarks

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as an easy method for identiication. AJR Am J Roentgenol. 2002;178(6): 1437-1444. Fornage BD. Peripheral nerves of the extremities: imaging with US. Radiology. 1988;167(1):179-182. Bianchi S. Ultrasound of the peripheral nerves. Joint Bone Spine. 2008;75(6):643-649. Silvestri E, Martinoli C, Derchi LE, et al. Echotexture of peripheral nerves: correlation between US and histologic indings and criteria to diferentiate tendons. Radiology. 1995;197(1):291-296. Sole JS, Pingree MJ, Spinner RJ, et al. Saphenous neuropathy secondary to extraneural ganglion cyst 15 years ater reconstruction of the anterior cruciate ligament. PM R. 2014;6(5):451-455. Rawal A, Ratnam KR, Yin Q, et al. Compression neuropathy of common peroneal nerve caused by an extraneural ganglion: a report of two cases. Microsurgery. 2004;24(1):63-66. Elias DA, Lax MJ, Anastakis DJ. Musculoskeletal images. Ganglion cyst of Guyon’s canal causing ulnar nerve compression. Can J Surg. 2001;44(5):331-332. Klauser AS, Halpern EJ, De Zordo T, et al. Carpal tunnel syndrome assessment with US: value of additional cross-sectional area measurements of the median nerve in patients versus healthy volunteers. Radiology. 2009;250(1): 171-177. Wiesler ER, Chloros GD, Cartwright MS, et al. he use of diagnostic ultrasound in carpal tunnel syndrome. J Hand Surg Am. 2006;31(5): 726-732. Duncan I, Sullivan P, Lomas F. Sonography in the diagnosis of carpal tunnel syndrome. AJR Am J Roentgenol. 1999;173(3):681-684. Roll SC, Evans KD, Li X, et al. Screening for carpal tunnel syndrome using sonography. J Ultrasound Med. 2011;30(12):1657-1667. Ozturk E, Sonmez G, Colak A, et al. Sonographic appearances of the normal ulnar nerve in the cubital tunnel. J Clin Ultrasound. 2008;36(6):325-329. Okamoto M, Abe M, Shirai H, Ueda N. Morphology and dynamics of the ulnar nerve in the cubital tunnel. Observation by ultrasonography. J Hand Surg [Br]. 2000;25(1):85-89. Van Den Berg PJ, Pompe SM, Beekman R, Visser LH. Sonographic incidence of ulnar nerve (sub)luxation and its associated clinical and electrodiagnostic characteristics. Muscle Nerve. 2013;47(6):849-855. Campbell WW. Ulnar nerve subluxation. Muscle Nerve. 2013;48(6): 997-998. Rezaei H, Torp-Pedersen S, af Klint E, et al. Diagnostic utility of musculoskeletal ultrasound in patients with suspected arthritis—a probabilistic approach. Arthritis Res her. 2014;16(5):448. Ben Abdelghani K, Miladi S, Souabni L, et al. Role of ultrasound in assessing remission in rheumatoid arthritis. Diagn Interv Imaging. 2015;96(1): 3-10. Wakeield RJ, Balint PV, Szkudlarek M, et al. Musculoskeletal ultrasound including deinitions for ultrasonographic pathology. J Rheumatol. 2005;32(12):2485-2487. Szkudlarek M, Court-Payen M, Strandberg C, et al. Power Doppler ultrasonography for assessment of synovitis in the metacarpophalangeal joints of patients with rheumatoid arthritis: a comparison with dynamic magnetic resonance imaging. Arthritis Rheum. 2001;44(9):2018-2023. Torp-Pedersen S, Christensen R, Szkudlarek M, et al. Power and color Doppler ultrasound settings for inlammatory low: impact on scoring of disease activity in patients with rheumatoid arthritis. Arthritis Rheumatol. 2015;67(2):386-395. Szkudlarek M, Court-Payen M, Strandberg C, et al. Contrast-enhanced power Doppler ultrasonography of the metacarpophalangeal joints in rheumatoid arthritis. Eur Radiol. 2003;13(1):163-168. Cheung PP, Dougados M, Gossec L. Reliability of ultrasonography to detect synovitis in rheumatoid arthritis: a systematic literature review of 35 studies (1,415 patients). Arthritis Care Res (Hoboken). 2010;62(3):323-334. McGonagle D, Gibbon W, O’Connor P, et al. A preliminary study of ultrasound aspiration of bone erosion in early rheumatoid arthritis. Rheumatology (Oxford). 1999;38(4):329-331. Wright SA, Filippucci E, McVeigh C, et al. High-resolution ultrasonography of the irst metatarsal phalangeal joint in gout: a controlled study. Ann Rheum Dis. 2007;66(7):859-864.

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65. Weidekamm C, Koller M, Weber M, Kainberger F. Diagnostic value of high-resolution B-mode and Doppler sonography for imaging of hand and inger joints in rheumatoid arthritis. Arthritis Rheum. 2003;48(2): 325-333. 66. Fornage BD. Sot-tissue changes in the hand in rheumatoid arthritis: evaluation with US. Radiology. 1989;173(3):735-737. 67. Kang MH, Moon KW, Jeon YH, Cho SW. Sonography of the irst metatarsophalangeal joint and sonographically guided intraarticular injection of corticosteroid in acute gout attack. J Clin Ultrasound. 2015;43(3):179-186. 68. hiele RG, Schlesinger N. Diagnosis of gout by ultrasound. Rheumatology (Oxford). 2007;46(7):1116-1121. 69. Iagnocco A. Imaging the joint in osteoarthritis: a place for ultrasound? Best Pract Res Clin Rheumatol. 2010;24(1):27-38. 70. D’Agostino MA, Conaghan P, Le Bars M, et al. EULAR report on the use of ultrasonography in painful knee osteoarthritis. Part 1: prevalence of inlammation in osteoarthritis. Ann Rheum Dis. 2005;64(12):1703-1709. 71. Lakkaraju A, Sinha R, Garikipati R, et al. Ultrasound for initial evaluation and triage of clinically suspicious sot-tissue masses. Clin Radiol. 2009;64(6):615-621. 72. Hung EH, Griith JF, Ng AW, et al. Ultrasound of musculoskeletal sot-tissue tumors supericial to the investing fascia. AJR Am J Roentgenol. 2014;202(6):W532-W540. 73. Carra BJ, Bui-Mansield LT, O’Brien SD, Chen DC. Sonography of musculoskeletal sot-tissue masses: techniques, pearls, and pitfalls. AJR Am J Roentgenol. 2014;202(6):1281-1290. 74. Teefey SA, Dahiya N, Middleton WD, et al. Ganglia of the hand and wrist: a sonographic analysis. AJR Am J Roentgenol. 2008;191(3):716-720. 75. Bianchi S, Abdelwahab IF, Zwass A, Giacomello P. Ultrasonographic evaluation of wrist ganglia. Skeletal Radiol. 1994;23(3):201-203. 76. Wang G, Jacobson JA, Feng FY, et al. Sonography of wrist ganglion cysts: variable and noncystic appearances. J Ultrasound Med. 2007;26(10): 1323-1328. 77. Akgul O, Guldeste Z, Ozgocmen S. he reliability of the clinical examination for detecting Baker’s cyst in asymptomatic fossa. Int J Rheum Dis. 2014;17(2):204-209. 78. Rudikof JC, Lynch JJ, Phillips E, Clapp PR. Ultrasound diagnosis of Baker cyst. JAMA. 1976;235(10):1054-1055. 79. Cronan JJ, Dorfman GS, Grusmark J. Lower-extremity deep venous thrombosis: further experience with and reinements of US assessment. Radiology. 1988;168(1):101-107.

80. Wagner JM, Lee KS, Rosas H, Kliewer MA. Accuracy of sonographic diagnosis of supericial masses. J Ultrasound Med. 2013;32(8):1443-1450. 81. Jacobson JA. Fundamentals of musculoskeletal ultrasound: Expert ConsultOnline. Philadelphia: Elsevier Health Sciences; 2012. 82. Beggs I. Sonographic appearances of nerve tumors. J Clin Ultrasound. 1999;27(7):363-368. 83. Abreu E, Aubert S, Wavreille G, et al. Peripheral tumor and tumor-like neurogenic lesions. Eur J Radiol. 2013;82(1):38-50. 84. Murphey MD, Smith WS, Smith SE, et al. From the archives of the AFIP. Imaging of musculoskeletal neurogenic tumors: radiologic-pathologic correlation. Radiographics. 1999;19(5):1253-1280. 85. Widmann G, Riedl A, Schoepf D, et al. State-of-the-art HR-US imaging indings of the most frequent musculoskeletal sot-tissue tumors. Skeletal Radiol. 2009;38(7):637-649. 86. Brouns F, Stas M, De Wever I. Delay in diagnosis of sot tissue sarcomas. Eur J Surg Oncol. 2003;29(5):440-445. 87. Tagliaico A, Truini M, Spina B, et al. Follow-up of recurrences of limb sot tissue sarcomas in patients with localized disease: performance of ultrasound. Eur Radiol. 2015;25(9):2764-2770. 88. Choi H, Varma DG, Fornage BD, et al. Sot-tissue sarcoma: MR imaging vs sonography for detection of local recurrence ater surgery. AJR Am J Roentgenol. 1991;157(2):353-358. 89. Montechiarello S, Miozzi F, Martinelli M, Giovagnorio F. Ultrasound picture of a wooden splinter evolved in phlegmon of the hand. J Ultrasound. 2010;13(1):38-40. 90. Shiels WE 2nd, Babcock DS, Wilson JL, Burch RA. Localization and guided removal of sot-tissue foreign bodies with sonography. AJR Am J Roentgenol. 1990;155(6):1277-1281. 91. Bradley M, Kadzombe E, Simms P, Eyes B. Percutaneous ultrasound guided extraction of non-palpable sot tissue foreign bodies. Arch Emerg Med. 1992;9(2):181-184. 92. Callegari L, Leonardi A, Bini A, et al. Ultrasound-guided removal of foreign bodies: personal experience. Eur Radiol. 2009;19(5):1273-1279. 93. Bureau NJ, Chhem RK, Cardinal E. Musculoskeletal infections: US manifestations. Radiographics. 1999;19(6):1585-1592. 94. Loyer EM, DuBrow RA, David CL, et al. Imaging of supericial sot-tissue infections: sonographic indings in cases of cellulitis and abscess. AJR Am J Roentgenol. 1996;166(1):149-152.

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24

The Shoulder Colm McMahon and Corrie Yablon

SUMMARY OF KEY POINTS • In the diagnosis of full-thickness rotator cuff tears, ultrasound is of comparable accuracy to magnetic resonance imaging, although it may be less accurate in the diagnosis of partial-thickness tears. • The key to scanning the shoulder is meticulous technique using a protocol that systematically evaluates the entirety of the shoulder.

• Understanding of optimal patient positioning, probe orientation, and shoulder anatomy is critical to effective diagnostic shoulder ultrasound. • Ultrasound allows dynamic assessment of subacromial and subcoracoid impingement, biceps subluxation, and rotator cuff integrity.

CHAPTER OUTLINE CLINICAL PERSPECTIVE SHOULDER ANATOMY SCAN TECHNIQUE Biceps Tendon Evaluation Subscapularis Tendon Evaluation Supraspinatus Evaluation Infraspinatus, Teres Minor, and Posterior Shoulder Evaluation Rotator Cuff Musculature Evaluation

ROTATOR CUFF DEGENERATION AND TEARS Background Tendinosis Full-Thickness Rotator Cuff Tears Partial-Thickness Rotator Cuff Tears Postsurgical Rotator Cuff Muscle Atrophy Subacromial-Subdeltoid Bursa Calciic Tendinitis

CLINICAL PERSPECTIVE he human shoulder represents an intricate balanced anatomic system capable of exerting force in multiple directions, in multiple diferent positions, all possible because of a number of static and dynamic structures, which when functioning well provide for the competing needs of movement and stability. Proper function of the shoulder is critical for activities ranging from the most basic of daily life to many sporting pursuits including those of the throwing athlete. he shoulder is, however, prone to injury, related to anatomic factors such as subacromial impingement.1,2 Shoulder pain and limitation of motion are very common causes for quality-of-life impairment, medical resource use, and loss of workplace productivity.3-7 In fact, about 50% of adults have at least one episode of shoulder pain yearly.8 Clinical presentation varies from acute injury9,10 to more chronic dysfunction, which is more common with advancing age.11 Although shoulder pain and dysfunction are common clinical complaints, the underlying etiology is variable, with causes including rotator cuf pathology (degeneration, tears, calciic tendinosis), long head biceps pathology, subacromial

LONG HEAD BICEPS TENDON PATHOLOGY ARTHROPATHY Degenerative Inlammatory PITFALLS IN SHOULDER ULTRASOUND CONCLUSION

subdeltoid bursa pathology, arthropathy of the glenohumeral or acromioclavicular joint (which may be of inlammatory or degenerative cause), or osseous disease. Of these, subacromial subdeltoid bursitis and rotator cuf pathology are the most common causes of symptomatic shoulder disease.12 Correct diagnosis is crucial for treatment decision making, allowing appropriate management with surgical or nonsurgical treatment, which may diminish the personal and societal efect of shoulder problems.13,14 Of course, clinical history taking and examination are intrinsic parts of patient assessment, but the accuracy of clinical examination in diagnosis of the cause of shoulder pain is both modest and variable.15-20 In this clinical and socioeconomic setting, the advantages of ultrasound as a diagnostic test are myriad, as this technique is accurate, cost-efective, and well tolerated by patients. In the diagnosis of full-thickness rotator cuf tears, ultrasound is of comparable accuracy to magnetic resonance imaging (MRI), although it may be less accurate in the diagnosis of partialthickness tears.21-30 Ultrasound can also determine muscle atrophy, an important parameter in predicting successful surgical outcome of rotator cuf repair.31 Ultrasound is a good alternative to MRI in patients who are claustrophobic, are of large size, or have

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incompatible implanted metallic and electronic devices. Patients with shoulder pain tolerate ultrasound better than MRI owing to relatively increased patient comfort and diminished examination time.32 Ultrasound provides several beneits that MRI cannot. Ultrasound ofers the possibility of dynamic assessment of the rotator cuf, allowing the patient to be imaged while engaging in the motion that causes pain or clicking. Ultrasound can assess subacromial impingement, subcoracoid impingement, and biceps tendon subluxation dynamically, in real time, and cine clips can be obtained. If there is a question as to pathology versus a normal variant, comparison to the contralateral side can be easily made. Dynamic compression of rotator cuf tears can aid in the assessment of cuf integrity. Ultrasound is also more sensitive than MRI to the detection of calcium deposits within the tendon. Finally, patients can receive the results of their examination instantaneously, and this adds tremendously to patients’ satisfaction with the modality.33 It should be noted that ultrasound is not without limitations. In the clinical setting of instability, ligamentous injury, or suspected glenoid labral injury, MRI or MRI arthrography are preferred. Ultrasound is also of limited value in the evaluation of bony disorders, and plain radiography should be considered complementary in the assessment of patients with shoulder pain to further diagnosis of fracture, bone lesions, subacromial spurs, acromioclavicular osteophytes, acromiohumeral interval narrowing, glenohumeral and acromioclavicular alignment and joint space abnormality, and sot tissue calciication. In view of these considerations, ultrasound should be considered a irst-line investigation in patients with acute or chronic shoulder pain in whom rotator cuf tear is suspected. Imaging algorithms detailing the role of shoulder ultrasound in speciic common scenarios have been published in a consensus statement Acromion

by the Society of Radiologists in Ultrasound, a highly useful resource.34

SHOULDER ANATOMY he shoulder consists of the osseous shoulder girdle with associated muscles and ligamentous structures.35 Central to understanding the anatomy of the shoulder and scan technique is the anatomy of the scapula (Fig. 24.1). he scapula consists of a lat triangular bone with anterior and posterior surfaces in addition to the glenoid fossa laterally. he glenoid fossa is deepened by a ibrocartilaginous labrum, and lined with hyaline cartilage for articulation with the humerus at the synovial glenohumeral joint. he glenoid neck tapers to the latter triangular body of the scapula. At the anterior aspect of the scapular body is the subscapular fossa, a concavity with oblique ridges that gives origin to the subscapularis muscle. he posterior surface of the scapula is convex posteriorly and divided into superior and inferior portions by the scapular spine. Above the spine is the supraspinatus fossa, which provides origin to the supraspinatus muscle. Below the spine is the infraspinatus fossa, with the infraspinatus muscle originating from the medial two-thirds, and the teres minor originating along the medial border. Extending superolaterally from the scapular spine is the acromion, a lattened hooklike structure that curves from posterior to anterior where it articulates with the clavicle at the acromioclavicular joint. he acromion and scapular spine give origin to the deltoid muscle. he acromion is important functionally and for the purpose of ultrasound technique as it overlies the supraspinatus and infraspinatus in the neutral position, prohibiting accurate visualization unless speciic positioning maneuvers are undertaken. Also, osseous spurs (subacromial spurs) along the undersurface of the acromion may be a cause for subacromial

Clavicle

Humeral head

Humeral head

Greater tuberosity

Lesser tuberosity Glenoid

Glenoid

Humerus Scapula

Anterior View

Posterior View

FIG. 24.1 Illustration of the Scapula and Osseous Landmarks.

CHAPTER 24

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Coracoid process

Clavicle

Subscapularis

The Shoulder

879

Supraspinatus

Supraspinatus

Capsular ligament (cut)

Humerus

Teres minor

Scapula

Infraspinatus

Right Shoulder Anterior View

Right Shoulder Posterior View

FIG. 24.2 Illustration of Rotator Cuff Anatomy.

impingement. hese typically form at the attachment of the coracoacromial ligament. Furthermore, osteoarthritis at the acromioclavicular joint may result in osteophyte formation, which, when present inferiorly, may cause rotator cuf tendon impingement. he coracoid process is a ingerlike curved process extending anteriorly from the scapular neck, giving attachment to the short head of biceps, coracobrachialis, and pectoralis minor muscles in addition to the coracohumeral ligament, and also the coracoclavicular ligaments, which help stabilize the acromioclavicular joint. he rotator cuf consists of four muscles: the subscapularis, supraspinatus, infraspinatus, and teres minor muscles (Fig. 24.2). hese originate from the scapula and insert on the proximal humerus. Normal rotator cuf tendons are about 4 to 6 mm in thickness,36 tapering out smoothly from medial to lateral along the insertional footprint at the greater tuberosity. he subscapularis muscle is a multipennate structure that originates from the anterior surface of the scapula, which converges to a lat tendon laterally to insert on the lesser tuberosity. Of note, the inferior one-third of the subscapularis remains muscular to the level of the lesser tuberosity.37 he supraspinatus muscle originates from and occupies the supraspinatus fossa, with its tendon extending laterally to insert on the greater tuberosity of the humerus at its anterior aspect. he tendon has a more cordlike component anteriorly and is latter and more quadrilateral in short axis at its mid and posterior ibers. he infraspinatus muscle originates at the infraspinatus fossa and passes laterally to insert on the posterosuperior aspect of the greater tuberosity. he ibers of the supraspinatus and infraspinatus tendons merge at their posterior and anterior borders, respectively, forming a conjoint insertion. he teres minor originates along the lateral border of

the scapular body and inserts along the posterior aspect of the greater tuberosity, inferior to the infraspinatus. he long head of biceps tendon originates from a bony tubercle at the superior glenoid, the supraglenoid tubercle, and from the superior labrum. It passes inferolaterally between the subscapularis and supraspinatus tendons, which form the inferior and superior borders of the rotator interval (Fig. 24.3). Within the rotator interval, the tendon is stabilized by a ligamentous sling formed by the coracohumeral and superior glenohumeral ligaments. Passing inferolaterally out of the rotator interval, the long head of biceps tendon becomes extraarticular and extends inferiorly in the bicipital or intertubercular groove, which lies between the greater and lesser tuberosities. he biceps tendon is stabilized in the groove by the transverse ligament, formed by tendinous ibers at the subscapularis insertion.38 he subacromial-subdeltoid bursa is a synovium-lined lat, thin structure that lies between the rotator cuf tendons and the overlying deltoid muscle and acromion.39 It serves to reduce friction between the rotator cuf and the overlying structures, permitting smooth movement.

SCAN TECHNIQUE For consistent and accurate shoulder ultrasound performance, a standard protocol is suggested with comprehensive evaluation in every case, rather than targeted scanning (Table 24.1).40-44 he patient should be sitting upright if possible, either on a rotating stool or at the edge of a bed. A chair with a backrest should not be used, because this would interfere with patient positioning. Likewise, the sonographer should also sit on a rotating stool, with the seat position somewhat higher than the patient’s, so

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Acromion

Acromioclavicular Coracoid joint process Clavicle

Subscapularis

Supraspinatus Lesser tuberosity Greater tuberosity Bicipital tendon sheath Subscapularis tendon Bicipital tendon

Biceps muscle (long head)

Glenohumeral joint

Scapula FIG. 24.3 Illustration of the Long Head Biceps Tendon in the Rotator Interval and in the Bicipital Groove.

TABLE 24.1 Routine Shoulder Ultrasound Protocol Long head of biceps tendon Subscapularis tendon

Supraspinatus tendon

Infraspinatus tendon Teres minor tendon Supraspinatus and infraspinatus muscles Posterior shoulder Acromioclavicular joint

Long and short-axis static images Long and short-axis static images Dynamic evaluation for subcoracoid impingement Long and short-axis static images Dynamic evaluation for subacromial impingement Long and short-axis static images Long and short-axis static images Sagittal images—panorama if possible Axial plane image Coronal plane image

Biceps Tendon Evaluation Biceps tendon evaluation is best performed with the arm in a neutral position, resting the forearm on the patient’s ipsilateral thigh, with elbow lexed and the palm up (Fig. 24.4). In this position, the biceps tendon is seen anteriorly.45 he tendon can be imaged in its short axis within the bicipital groove by holding the probe transversely with respect to the upper arm and following the course of the tendon inferiorly where it passes deep to the pectoralis major tendon insertion on the humerus. In short axis, the tendon appears as a homogeneous, echogenic, round or ovoid structure that may be accompanied by a trace of luid within its tendon sheath. he normal biceps tendon is 2 to 4 mm thick.36 he tendon can be followed superiorly and medially into the rotator interval, by angling the probe more obliquely to remain orthogonal to its short axis. Finally, the probe can be rotated 90 degrees to view the tendon in its long axis where it should appear smooth and ibrillar.

Subscapularis Tendon Evaluation that the sonographer’s arm can be held in a natural, ergonomic position. If a patient is wheelchair-bound, it is helpful if possible to temporarily remove the backrest. If the patient cannot sit upright, more limited scanning is possible with the patient lying supine, with the afected shoulder at the edge of the bed. A high-frequency 12- to 15-MHz linear array transducer is used to permit high-resolution scanning. Occasionally, in larger patients, a lower-frequency probe (9 MHz) may be needed to achieve tissue penetration to the required depth, but this incurs a reduction in resolution. When scanning any tendon, care should be taken to maintain an angle of close to 90 degrees between the probe and the tendon of interest to avoid artifactual hypoechogenicity due to anisotropy. his is discussed in more detail later in the chapter.

he subscapularis is scanned with the patient’s arm at the side, in external rotation with the palm facing up44 (Fig. 24.5). he tendon should be evaluated in long axis, with the probe aligned with the subscapularis tendon, and in short axis, with the probe held perpendicular to the subscapularis tendon. he coracoid process of the scapula, medial to the subscapularis and palpable in many patients, is a useful anatomic landmark when locating the subscapularis tendon. he tendon ibers can be seen emanating from the broad multipennate muscle belly. he normal hypoechoic muscle should not be mistaken for luid. In this position the patient’s arm can be rotated from external rotation to neutral position, while observing the passage of the tendon ibers deep to the coracoid process to assess for subcoracoid impingement (Video 24.1). his dynamic maneuver is also useful to assess for long head biceps tendon subluxation from the bicipital groove.

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FIG. 24.4 Long Head Biceps Tendon (LHBT). (A) Photograph of the probe position for imaging the LHBT in short axis. The patient’s shoulder is externally rotated, with the elbow lexed and held tight to the body, with the forearm palm up, resting on the patient’s lap. This position rotates the LHBT anteriorly. (B) Short-axis image of LHBT (arrow). (C) Photograph of probe position for imaging the LHBT in long axis. The probe is rotated 90 degrees to the short-axis starting position. Patient position remains the same as for the short-axis image. (D) Long-axis image of LHBT (arrowheads).

Supraspinatus Evaluation In neutral position the supraspinatus tendon is largely obscured from view by the overlying acromion. To draw the tendon out from under the acromion, speciic maneuvers are needed. he position, originally described by Crass46 (Fig. 24.6), consists of asking the patient to place his or her hand behind the back, reaching toward the opposite back pocket with the back of the hand. his results in lexion, internal rotation, and adduction of the shoulder. In this position, the greater tuberosity is located anteriorly, so the supraspinatus tendon courses anterolaterally to its insertion and is drawn out from under the acromion, allowing visualization. Patients with shoulder pain oten ind this position diicult to achieve and maintain, so an alternative position is the “modiied Crass position” (Fig. 24.7) in which the patient puts the palm of the hand on the ipsilateral hip or buttock, with elbow lexed and directed posteriorly. In this position, the greater tuberosity is similarly positioned as in the original Crass position, but the maneuver is usually well tolerated by patients. he supraspinatus tendon will again course anterolaterally to the greater tuberosity. To visualize the supraspinatus in long axis, the probe should parallel the long-axis orientation of the tendon, resulting in an

oblique sagittal probe position relative to the patient, with the probe directed toward the patient’s ear (see Fig. 24.7A). he long head biceps tendon in long axis with the patient in the modiied Crass position is a useful landmark for locating the most anterior portion of the supraspinatus tendon (Fig. 24.8). If the probe in long axis is then moved posteriorly in the same plane, the entire supraspinatus will be assessed. Correctly imaged, the normal supraspinatus should appear smooth, echogenic, and ibrillar, tapering at its insertion or “footprint” with a so called “bird’s beak appearance.” Normal rotator cuf tendons possess a ibrocartilaginous interface at their bony attachment that may manifest as a thin hypoechoic band paralleling the insertional cortex, similar in echogenicity to hyaline cartilage.37 his should not be mistaken for a tear. he probe is then rotated 90 degrees to image the tendon in short axis. In this position, the more cordlike anterior ibers of the supraspinatus tendon are seen merging with the latter quadrilateral mid and posterior ibers. While visualizing the supraspinatus tendon in short axis, it is important to move the probe anteriorly so that the long head biceps tendon is imaged in short axis. his ensures that the entire anterior leading edge of the supraspinatus has been evaluated. In short axis, the rotator interval is well seen

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FIG. 24.5 Subscapularis Tendon. (A) Long-axis probe position. From the long head biceps tendon (LHBT) starting position, the patient now externally rotates the elbow, keeping the elbow tight to the body with the palm up. This position elongates the subscapularis tendon and rotates the tendon out from under the coracoid process, allowing visualization. The probe is placed across from the coracoid process. Note that the probe position is similar for imaging the LHBT in short axis, but the patient’s position is different. (B) Long-axis image of subscapularis tendon (arrowheads). (C) Short-axis probe position. From the long-axis starting position, the probe is simply turned 90 degrees to image the subscapularis in short axis, with the patient remaining in the same position. Note that the probe position is similar to the LHBT long-axis probe position, but the patient’s position is different. (D) Short-axis image of subscapularis tendon (arrowheads). See also Video 24.1.

anterior to the tendon, with the biceps tendon coursing through the interval, also in short axis, stabilized by the coracohumeral ligament and superior glenohumeral ligament. As with all tendons, the supraspinatus should be scanned through its entirety from anterior to posterior in long axis and medial to lateral in short axis. When the posterior ibers of the supraspinatus tendon are reached, the more posteriorly oriented ibers of the infraspinatus tendon are routinely encountered; this is a helpful landmark to ensure the entire supraspinatus tendon has been studied. It is important to note that as the transducer is moved posteriorly, the greater tuberosity changes shape, from ledgelike to lat. his area of transition is where the anterior infraspinatus ibers overlap the posterior supraspinatus ibers. A discrete overlap of ibers can be visualized at this juncture (Fig. 24.9, Video 24.2). Continuing posteriorly from this overlap, the infraspinatus ibers can be evaluated in their entirety, looking for the similar normal ibrillar pattern in the long axis, and the echogenic appearance in the short axis.

he rotator cable is a thin ibrous band contiguous with the coracohumeral ligament that passes along the deep surface of the supraspinatus and infraspinatus tendons.47 his bandlike structure is oriented perpendicular to the long axis of the rotator cuf, running in an anterior to posterior direction, and is felt to have a biomechanical role in stress distribution, likened to the cable of a suspension bridge.48 It can be visualized consistently with ultrasound, seen in its short axis where it appears elliptical, when scanning the long axis of the supraspinatus and infraspinatus (Fig. 24.10). It is located about 1 cm (average 9 mm, range 4-15 mm47) medial to the rotator cuf insertion at the greater tuberosity. Dynamic assessment for subacromial impingement of the supraspinatus can now be performed. he patient’s arm rests in a neutral position at his or her side, and the probe is positioned in a coronal plane, with the acromion at the medial aspect of the ield of view, and the greater tuberosity laterally. he patient then abducts the arm slowly, and the motion of the supraspinatus

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tendon under the acromion is observed. he motion should be smooth and uninterrupted, without deformation of the tendon under the acromion, deformation of the bursa, or pooling of bursal luid (Video 24.3). A useful alternative technique to assess the supraspinatus has been described by Turrin and Cappello.49 In this technique, the patient lies supine with the afected shoulder at the edge of the bed, but allows the arm to drop over the side of the bed, with the elbow extended and the forearm pronated. his can be particularly helpful in patients who are unable to sit—for example following cerebrovascular accident with hemiplegia, when associated shoulder pain is not uncommon, though of varied etiology (related to subluxation, spasticity, adhesive capsulitis, or rotator cuf tears), and standard positioning in the seated position may be diicult.50

FIG. 24.6 Crass Position. The patient places her arm behind her back with the dorsum of the hand resting on the contralateral back pocket. This position rotates the supraspinatus tendon from underneath the acromion.

A

C

Infraspinatus, Teres Minor, and Posterior Shoulder Evaluation Several methods of evaluation of the infraspinatus have been described. he patient can remain in the modiied Crass position, or with the arm hanging at the side, and scanning can simply

B

D

FIG. 24.7 Supraspinatus Tendon and Modiied Crass Position. Probe position for supraspinatus in long axis, with the patient in the modiied Crass position. The patient places her arm behind her back, palm on the ipsilateral back pocket, with the elbow straight back, as tight to the body as possible. This position rotates the supraspinatus from underneath the acromion. This position is usually better tolerated by patients who have a rotator cuff tear. (A) The probe is placed somewhat obliquely, directed toward the patient’s ear. (B) Long-axis image of the supraspinatus tendon (arrowheads). (C) Short-axis probe position. The patient remains in the modiied Crass position and the probe is rotated 90 degrees from the long-axis starting position. (D) Short-axis image of the supraspinatus tendon (arrowheads). Note that the long head of biceps tendon is visualized anterior to the supraspinatus tendon (arrow).

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be continued posteriorly from the supraspinatus both in long and short axis. An alternate position of scanning the infraspinatus has been described, in which the patient is asked to bring the arm forward across the chest, resting the hand on the contralateral shoulder.44,51 hese positions allow imaging of the infraspinatus tendon and muscle. he probe is held in an oblique transverse orientation, placed on the posterior shoulder to parallel the long axis of the infraspinatus tendon, using the inferior border of the scapular spine as a visual landmark (Fig. 24.11). In long axis the tendon appears similar to the supraspinatus in morphology, although having a more elongated tapered appearance at its insertion, lacking the bird’s beak appearance seen at the supraspinatus footprint. he probe is then rotated 90 degrees, to the short axis of the infraspinatus, and the tendon and muscle are evaluated. he normal muscle is hypoechoic and positioned below the scapular spine in the infraspinatus fossa.

Using the scapular spine as a visual landmark, the supraspinatus muscle in the supraspinatus fossa can be imaged by placing the probe perpendicular to the scapular spine (Fig. 24.12). his demonstrates the muscle in its short axis. he normal muscle should be hypoechoic and convex in contour, and should ill the

FIG. 24.8 Long-Axis Biceps Tendon Image, With Shoulder in the Modiied Crass Position. This is a good starting point for imaging the supraspinatus tendon in long axis. Once the long head biceps tendon is seen well in long axis (arrowheads), the probe can simply be moved posteriorly to image the supraspinatus tendon.

FIG. 24.9 Overlap of Posterior Supraspinatus (Arrow) and Anterior Infraspinatus Fibers (Arrowheads) Seen in Long Axis. See also Video 24.2.

A

he teres minor tendon is also evaluated in this position and is seen inserting at the posterior aspect of the greater tuberosity, inferior to the infraspinatus insertion. he teres minor muscle can be seen arising from the posterolateral scapula, inferior to the infraspinatus muscle. Also in this position, the posterior shoulder is seen, with visualization of glenohumeral joint luid and limited views of the posterior labrum and spinoglenoid notch. Scanning the posterior shoulder with external rotation may aid visualization of a glenohumeral efusion.52

Rotator Cuff Musculature Evaluation

B

FIG. 24.10 Rotator Cable. (A) The rotator cable (arrows) is visualized in short axis along the articular surface of the supraspinatus tendon, when this tendon is imaged in long axis. (B) The rotator cable (arrows) is visualized as a linear structure in its long axis (arrows) along the articular surface of the supraspinatus tendon, when this tendon is imaged in short axis. (Courtesy of Dr. Yoav Morag, Ann Arbor, MI.)

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FIG. 24.11 Infraspinatus Tendon. (A) Long-axis probe position. The patient can simply rest the arm at the side, with the forearm palm up in the lap. The probe is placed under the scapular spine and moved laterally to see the distal insertion on the greater tuberosity. (B) Long-axis image of infraspinatus tendon (arrowheads). (C) Short-axis probe position. The probe is rotated 90 degrees to the infraspinatus long-axis starting position. (D) Short-axis image of infraspinatus tendon (arrowheads).

A

B

C

FIG. 24.12 Rotator Cuff Musculature. (A) Probe position for supraspinatus muscle. The probe is placed at the top of the shoulder, medial to the acromioclavicular joint, and posterior to the clavicle. (B) Probe position for infraspinatus and teres minor muscles. The probe is placed 90 degrees to the scapular spine, just inferior to the scapular spine (arrowheads). (C) Extended ield-of-view image of supraspinatus (straight arrow), infraspinatus (arrowheads), and teres minor (curved arrow). Note the spine of the scapula (*) separating the supraspinatus and infraspinatus muscles.

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supraspinatus fossa. he central tendon should be visible within the muscle. To image the infraspinatus and teres minor muscles, the transducer is moved distal to the scapular spine, remaining perpendicular to the spine. A relative comparison and assessment of muscle volume and echogenicity can easily be made by using an extended ield-of-view scan technique.

ROTATOR CUFF DEGENERATION AND TEARS Background Rotator cuf dysfunction, either due to tear or to tendon degeneration, is the most common cause of referral for evaluation of the shoulder.53 Likewise, rotator cuf disease is the most frequent cause for referral for shoulder ultrasound. he supraspinatus tendon is the most commonly injured tendon in the rotator cuf.54 he incidence of rotator cuf tears rises as patients age. Up to 22% of patients age 65 and older have rotator cuf tears.55 It is interesting to note that 70% of imaged patients age 65 and older have asymptomatic rotator cuf defects.56 Rotator cuf tears in patients younger than 40 are uncommon, but they do occur in the setting of acute trauma or sports-related injuries. Rotator cuf tears in patients older than 40 are usually secondary to tendon degeneration.

Tendinosis Tendinosis of the rotator cuf is a degenerative process that may be associated with shoulder pain. Histologically, there is no inlammatory component (hence the term “tendinitis” is not appropriate for this condition), but rather mucoid degeneration and frequently chondroid metaplasia are present. On ultrasound, tendinosis appears heterogeneous or hypoechoic, with tendon thickening, and loss of the normal ibrillar pattern57 (Fig. 24.13). Although discrete defects or tears are not encompassed by this diagnosis, they may coexist.

Full-Thickness Rotator Cuff Tears Ultrasound is a reliable method for diagnosis of rotator cuf tears, with sensitivity and speciicity over 90%21,26,28,29,58,59 for full-thickness tears, and low interobserver variability.60,61 Fullthickness tears are visualized as a hypoechoic or anechoic gap within the rotator cuf (Fig. 24.14), which may also have a concave contour at its bursal border.30,62 Alternatively, a greatly retracted tear can result in nonvisualization of the rotator cuf tendon62 (Fig. 24.15). his occurs because the tendon may retract deep to the acromion, and is likely in cases in which the degree of retraction exceeds 3 cm.63 When a full-thickness tear is present, the gap between the retracted tendon end and the greater tuberosity or distal tendon stump may be illed with hypoechoic luid or echogenic debris (Fig. 24.16) and granulation tissue. Alternatively, the subacromial-subdeltoid bursa (frequently thickened) and the deep surface of the deltoid muscle may occupy the defect created by the tear.29 Small foci of debris within the tear gap may give the appearance of mobile or “loating” bright spots.59 Fluid within the tear gap my accentuate visualization of the underlying humeral head articular cartilage owing to enhanced through transmission of the ultrasound beam, referred to as the “cartilage interface sign”64 (Fig. 24.17). Occasionally one may be uncertain as to whether abnormal echotexture in the location of the rotator cuf represents a partial tear or a full-thickness tear with intervening granulation tissue and debris. Dynamic compression of the abnormal area may clarify this confusion by causing complex luid and debris to swirl within the rotator cuf tear. It may be helpful to ascertain if a tear is more likely to be acute or chronic because acute tears are felt to have a greater chance of successful surgical outcome. In this regard, the indings of glenohumeral and bursal efusions are more common in acute tears. In addition, midsubstance tears, medial to the bone-tendon junction, are more likely to be acute. On the other hand, severely retracted tears are more likely to be chronic.65 In chronic full-thickness tears, the tendon gap may be illed with

FIG. 24.13 Tendinosis of the Supraspinatus. Long-axis image of the supraspinatus tendon (arrowheads) demonstrates hypoechogenicity and diffuse loss of normal ibrillar echotexture.

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FIG. 24.14 Focal Full-Thickness Supraspinatus Tear. (A) Long-axis image of the anterior supraspinatus tendon demonstrates intact ibers (arrowheads). (B) Long-axis image of more posterior ibers of supraspinatus show a full-thickness tear with hypoechoic luid (arrow) within the gap between the torn tendon end (arrowheads) and the greater tuberosity (*). (C) Short-axis image of supraspinatus. Intact anterior ibers (white arrowhead) are shown, with a luid-illed gap (straight arrow) at the posterior supraspinatus tear. Intact anterior infraspinatus ibers (curved arrow) are visible posterior to the tear. Assisting in orientation, the long head biceps tendon (black arrowhead) appears anteriorly.

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FIG. 24.15 Full-Thickness Supraspinatus Tear With Retraction of the Tendon Beneath the Acromion. Image in the expected location of the supraspinatus tendon in long (A) and short (B) axis demonstrates absence of the tendon above the humeral head (*) and greater tuberosity (white arrow). Fluid and debris are seen in place of the normal tendon (arrowheads). Note the intact long head biceps tendon anteriorly (black arrow).

noncompressible, complex echogenic debris and granulation tissue that are contiguous with the subacromial subdeltoid bursa, and this may give the false impression of rotator cuf volume to the novice practitioner.

Partial-Thickness Rotator Cuff Tears As with full-thickness rotator cuf tears, partial-thickness tears occur in both younger and older patients. Partial tears

occur more commonly than full-thickness tears in younger patients, and most commonly occur in young athletes. Partial articular-sided supraspinatus tears are the most common subtype in the young athlete.66 In the older patient population, partial-thickness tears also most commonly occur in the supraspinatus tendon, but the most common cause is tendon degeneration, with increased incidence as patients age.

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FIG. 24.16 Focal Full-Thickness Tear of Supraspinatus Tendon. In this long-axis image of the supraspinatus tendon, there is a focal full-thickness tear, and the gap between the tendon retracted end and the greater tuberosity is illed with echogenic debris (arrow) and luid.

tuberosity.67,68 his type of tear is most commonly seen in athletes who engage in overhead-throwing activities. Partial-thickness tears vary from small, 1- to 2-mm tears to those involving more than 50% of tendon thickness. Although tears of 50% or greater have typically been referred for repair, patients with tears involving as little as 25% of the tendon may beneit from arthroscopic debridement.69,70 Surgical decisions, however, are made in the context of the individual patient performance status, limitation by the injury, comorbidities, and patient preference. Partial tears occur most commonly along the articular side of the tendon in younger patients.70 Care must be taken to adequately assess the anterior leading edge ibers of the supraspinatus tendon, where these tears can oten occur.71 Bursalsided partial-thickness tears may manifest as lattening of the bursal contour of the tendon of varying severity.29 his may lead to an hourglass-like diameter shit between areas of normal and attenuated tendon.28 An associated sign frequently observed in the setting of both partial- and full-thickness rotator cuf tears is the inding of cortical irregularity of the greater tuberosity, a inding with a 75% positive predictive value for the presence of an associated rotator cuf tear.72 his is more severe in full-thickness tears and represents bony remodeling with irregularity, pitting, and erosion.73 A second sign that can be seen in both partial articularsided and full-thickness tears is the “cartilage interface” sign, mentioned earlier. In analysis of partial- and full-thickness tears, it is important to quantify the extent of the tear in both its long and short axis (tear length and width); for example, in the case of a supraspinatus tendon tear, a measurement of the medial to lateral tear length should be made in long axis, and a measurement of the anterior to posterior tear width should be made on short-axis imaging.

Postsurgical Rotator Cuff FIG. 24.17 Full-Thickness Supraspinatus Tear With Associated Cartilage Interface Sign. A hyperechoic line (arrowheads) is seen along the surface of the normal hypoechoic cartilage (arrow), along the superior aspect of the humeral head (*).

Partial-thickness tears are characterized by a focal area of hypoechogenicity or mixed echogenicity involving one side of the tendon, but not extending through the entire thickness.58 here are several subtypes of partial-thickness tears of the rotator cuf (Figs. 24.18 and 24.19). Bursal-sided partial-thickness tears (Fig. 24.19A and B) occur supericially, just deep to the subacromial subdeltoid bursa. Articular-sided tears (see Fig. 24.19C and D) occur at the undersurface of the tendon in contiguity with the joint space. Intrasubstance tears (Fig. 24.19E) can occur either within the substance of the tendon footprint at the enthesis or longitudinally within the tendon ibers. hese tendons may not be identiied at arthroscopy because they do not communicate with either the bursal or the articular surfaces of the tendon. A speciic partial-thickness tear type is the “rim-rent” tear (see Fig. 24.19F), occurring at the articular side of the supraspinatus tendon, extending into the tendon footprint on the greater

Ater surgical rotator cuf repair, the appearance of the rotator cuf and surrounding sot tissues is abnormal, as can be expected, with loss of normal sot tissue planes and abnormal echotexture of the rotator cuf tendon. Because of loss of normal interface with the overlying subacromial bursa, dynamic assessment may aid in identiication and visualization of the supraspinatus tendon.74 Bony irregularity at the site of anchor placement is expected, and echogenic suture material within the tendon may contribute to the heterogeneous appearance of the postoperative rotator cuf tendon (Fig. 24.20, Video 24.4). A gap within the tendon and nonvisualization of the tendon owing to retraction are the most reliable signs for a recurrent tear.75,76 A thinned tendon or one with subtle contour abnormality is considered intact.

Muscle Atrophy Ultrasound may also be used to assess for rotator cuf muscle atrophy, which may occur in the setting of a subacute or chronic rotator cuf tear. his is characterized by decreased muscle bulk and increased muscle echogenicity (related to increased fat interposed among muscle ibers77 (Fig. 24.21). Ultrasound appearances also include lack of clarity of the muscle contour, and loss of visibility of the central tendon within the myotendinous

CHAPTER 24

The Shoulder

889

Classification of Partial Tears based on depth of defect Articular surface

Bursal surface

Grade 1 10 MHz). Transducers with a small footprint (“hockey stick”) are particularly well suited to supericial injections. hese factors should be assessed before skin preparation. he immiscible nature of the steroid anesthetic mixture may likewise produce temporary contrast efect (Fig. 25.2, Video 25.1). In vitro experiments suggest that this property is caused by alterations in acoustic impedance by the scattering material, formed by the suspension of steroid in an aqueous background; this results in an increase in echo intensity of about 20 dB.19 his contrast efect has the advantage of increasing the conspicuity of the delivered agent during real time, enabling the operator to better deine the distribution of delivered agent during ultrasoundguided therapy.

INJECTION TECHNIQUE FIG. 25.1 Needle as Specular Relector With Reverberation Artifact. A 25-gauge needle (N) has been positioned into the retrocalcaneal bursa deep to the Achilles tendon (T). Note that the needle is a specular relector with a characteristic reverberation artifact (arrows). BASELINE

We use a sterile technique; the area in question is cleaned with iodine-based solution and draped with a sterile drape. he transducer is cleaned with iodine-based or alcohol-based solutions EARLY

LATE

FIG. 25.2 Contrast Effect. A suspension of anesthetic and triamcinolone has been injected into a cyst phantom. Baseline: Before injection, anechoic “cyst” is shown in a scattering medium, with baseline pixel intensities listed. Early: The early mixing phase is obtained immediately after injection. A contrast effect is evident, in which the cyst becomes almost isoechoic to the background. Late: 20 minutes after injection. In the late phase, apparent gravitational effect results in settling of the suspension toward the dependent portions of the cyst phantom and development of a contrast gradient.

900

PART III

Small Parts, Carotid Artery, and Peripheral Vessel Sonography PRE-INJECTION

POST-INJECTION

N

fh fn

A

B

FIG. 25.3 Long-Axis Approach: Injection of Left Hip. The long-axis approach is suitable for deep joint injections, such as the hip or shoulder. (A) Before injection, 22-gauge spinal needle (N) has been positioned at the femoral head-neck junction in a 50-year-old woman with a labral tear demonstrated on magnetic resonance imaging (not shown), to assess relief after therapeutic injection. (B) After injection, conirmation of intraarticular deposition of injected material is obtained by the presence of microbubbles (arrows) deep to the joint capsule. fh, Femoral head; fn, femoral neck. See also Video 25.1. PRE-INJECTION

POST-INJECTION C N

N

M

P

A

B

FIG. 25.4 Short-Axis Approach for Injection of First Metatarsophalangeal (MTP) Joint. (A) Long-axis view shows 25-gauge needle positioned in MTP joint of 53-year-old woman with plantar plate injury; needle (N) is seen in cross section. M, Metatarsal head; P, proximal phalanx. (B) While monitoring the injection in real time, the joint capsule distends and ills with echogenic material. C, Capsule.

and surrounded by a sterile drape. A drape is also placed over portions of the ultrasound unit. A sonographer or radiologist positions the transducer; a radiologist positions the needle and performs the procedure. We use 1% lidocaine and bupivacaine (0.25%-0.75%) for local anesthesia. Once the needle is in position, the procedure is undertaken while imaging in real time. Depending on anatomic location, a 1.5-inch or spinal needle with stylet is used to administer the anesthetic-corticosteroid mixture, generally consisting of local long-acting anesthetic and one of the standard injectable corticosteroid derivatives (e.g., triamcinolone). Two approaches to performing injections are long axis and short axis, which relate needle orientation to the structure being injected.9 he long-axis approach refers to needle placement in the plane parallel to the structure of interest (Fig. 25.3). For example, longitudinal imaging of the hip to display a hip efusion might be used as the plane to direct the needle for ultrasoundguided aspiration. Alternatively, the short-axis approach refers to needle entry in the plane perpendicular to the long axis of a structure (Fig. 25.4). For example, injection of the retrocalcaneal bursa or metatarsophalangeal (MTP) joint might use a lateral

approach. In my experience, the short-axis approach works well when performing injections or aspirations in small joints and tendon sheaths of the hand and foot. he long-axis approach appears better suited for deep joint injections, such as in the hip or shoulder. It is important to recognize, however, that such approaches serve merely as guidelines and that no single method necessarily applies to any speciic injection.

INJECTION MATERIALS Most injections involve use of a long-acting corticosteroid in combination with a local anesthetic in relatively small volumes. Injectable steroids usually come in either a crystalline form, associated with a slower rate of absorption, or a soluble form, characterized by rapid absorption.20-22 Crystalline agents include triamcinolone and methylprednisolone acetate (Depo-Medrol). A common soluble agent is Celestone, which includes a rapidly absorbed betamethasone salt. A reactive inlammatory response or lushing response may occur with crystalline steroids, but typically not with soluble agents.13

Musculoskeletal Interventions

CHAPTER 25 he most signiicant complications associated with injectable steroid use in the musculoskeletal system relate to chondrolysis (when used in weight-bearing joints), depigmentation, fat necrosis, and impaired healing response (when used in sot tissues).11-14 Impaired healing has been associated with tendon, ligament, and plantar fascia rupture. he most frequently used mixtures contain insoluble particles, so a systemic injection could theoretically result in an “embolic phenomenon,” which has been implicated as a mechanism for neurologic complications associated with transforaminal epidural injections. We have not encountered this as a complication when performing injections in the appendicular skeletal system. he most common anesthetics are lidocaine (Xylocaine) and bupivacaine (Marcaine).22,23 Both are characterized as “local injectable anesthetics” but difer in the onset of efect and duration. Lidocaine is characterized by early onset (seconds) and short duration (1-2 hours). Bupivacaine becomes efective in 5 to 10 minutes, and its efects generally last 4 to 6 hours. In addition to allergic reactions, potential adverse efects include neurotoxicity and cardiotoxicity; these are generally rare when small doses are used under image guidance, taking care to avoid an intravascular injection. Bupivacaine has also been associated with chondrolysis when used for intraarticular applications, but only with constant infusions during arthroscopy and in vitro.24 Chondrolysis is probably not an issue with the small, ixed volumes of bupivacaine typically used during injections in the musculoskeletal system.

C

901

N

R CA

L

FIG. 25.5 Long-Axis Approach for Therapeutic Radiocarpal Joint Injection. A 25-gauge needle (N) has been positioned deep to the dorsal capsule (C) and above the lunate bone (L) of a 19-year-old female patient with chronic wrist pain, to assess relief. CA, Capitate; R, radius.

D N I

G

H

Left shoulder

INJECTION OF JOINTS A high-frequency linear transducer is used for hand, wrist, elbow, foot, and ankle injections. A short-axis approach is oten technically easier for small joint injections. he needle should enter the skin parallel to the plane of the joint space. Supericial joints usually appear as separations between the normally continuous specular echoes produced by cortical surfaces. As in other luidcontaining structures, the presence of an efusion is a helpful feature in visualizing the needle as it enters the joint, because it provides a luid standof. he short-axis approach entails scanning across the joint and looking for the transition from one cortical surface to the next, marking the skin (with a surgical marker), and then placing a needle into the joint using ultrasound guidance. When imaging the joint in long axis, the needle will be seen in cross section (Fig. 25.5). Needle placement is conirmed by injecting a small amount of 1% lidocaine, which should display distention of the joint, as well as echoes illing the joint. Small joint injections generally require 0.5 to 1 mL of the therapeutic mixture. In my experience, this approach works well in the metatarsophalangeal (MTP) or metacarpophalangeal (MCP) and interphalangeal (IP) joints, midfoot, ankle, and elbow. Occasionally a long-axis approach may be eicacious, as in the radiocarpal joint or lateral gutter of the ankle. Ultrasound guidance allows the clinician to negotiate osteophytes and joint bodies. It allows identiication of capsular outpouching, thereby afording a more convenient, indirect approach into a joint than slipping a needle into a small joint space.

FIG. 25.6 Long-Axis Approach for Glenohumeral Joint Injection. A 22-gauge needle (N) has been positioned deep to the posterior capsule (arrows) during a glenohumeral joint injection in 42-year-old woman with adhesive capsulitis. Mild luid distention of the posterior recess of the joint is evident. D, Deltoid muscle; G, glenoid; H, humeral head; I, infraspinatus muscle.

A long-axis approach and a spinal needle are used when performing injections of large joints such as the hip or shoulder (Fig. 25.6). A greater volume is usually injected, typically 5 mL of the steroid-anesthetic mixture. In the case of adhesive capsulitis, signiicantly larger volumes of local anesthetic (5-10 mL) may be added to provide additional joint distention. We generally approach the glenohumeral joint using a posterior approach, with the patient in a decubitus position and the arm placed in crossadduction. An intermediate-frequency, linear or curvilinear transducer will suice in most cases. A linear transducer oten results in better anatomic detail than curved arrays. he interface of the glenohumeral joint is usually seen with the patient in the decubitus position, as well as the hypoechoic articular cartilage overlying the humeral head. We perform this injection using a long-axis approach, with the needle directed toward the joint along the articular cartilage and deep to the posterior capsule. A test injection with 1% lidocaine should show bright echoes illing the posterior recess or distributed along the articular cartilage. he hip is approached similarly in long axis, with the transducer placed over the proximal anterior thigh at the level of the joint25 (see Fig. 25.3, Video 25.1). he approach is similar to that

902

PART III

Small Parts, Carotid Artery, and Peripheral Vessel Sonography

C

A

CL

AC JT FIG. 25.7 Short-Axis Approach to Injection of Acromioclavicular (AC) Joint. A 25-gauge needle (long thin arrow) is seen in cross section in a distended hypertrophic AC joint during therapeutic injection in 73-year-old woman with pain centered over AC joint. The joint appears widened, containing echogenic material caused by the contrast effect (short thick arrow) of the therapeutic agent. A, Acromion; C, distended capsule; CL, clavicle.

used in evaluating the joint for an efusion. Ideally, the anterior capsule is imaged at the head-neck junction of the femur. In this approach the scan plane is lateral to the neurovascular bundle. he needle may be directed into the joint while maintaining its position in the scan plane of the transducer. A test injection of 1% lidocaine conirms the intraarticular needle position, and the therapeutic injection follows. Fibrous joints, such as the acromioclavicular (AC) joint, can likewise be injected using ultrasound guidance (Fig. 25.7). A short-axis technique is employed similar to that used in the foot. he majority of these injections can be performed using a 1.5-inch needle with a small volume (0.5-1.0 mL) of therapeutic mixture. In addition to the AC joint, this approach is useful in the sternoclavicular joint and pubic symphysis.

SUPERFICIAL PERITENDINOUS AND PERIARTICULAR INJECTIONS Peritendinous injection of anesthetic and long-acting corticosteroid is an efective means to treat tenosynovitis, bursitis, and ganglion cysts in the hand, foot, and ankle. hese structures are supericially located and well delineated on sonography. Ultrasound-guided injections are an efective means to ensure correct localization of therapeutic agents.

Foot and Ankle In my experience, peritendinous injections in the foot and ankle are most oten requested for patients with chronic achillodynia or those with medial or lateral ankle pain caused by posterior tibial or peroneal tendinosis or tenosynovitis. Less oten, patients are referred to help diferentiate pain from posterior impingement and stenosing tenosynovitis of the lexor hallucis longus (FHL) tendon.26 his distinction can be diicult, sometimes requiring diagnostic and therapeutic injection of the corresponding tendon sheath. Patients with plantar foot pain caused by plantar fasciitis and forefoot pain resulting from painful neuromas are also frequently referred for ultrasound-guided injections.27,28 he large majority of patients with achillodynia have pain referable to the enthesis, with associated retrocalcaneal bursitis

and Achilles tendinosis. Enthesis is the site of attachment of a muscle or ligament to bone where the collagen ibers are mineralized and integrated into bone. A retrocalcaneal bursal injection may help alleviate local pain and inlammation (Fig. 25.8). I scan the patient in a prone position with the ankle in mild dorsilexion, using a linear transducer of 10 MHz or higher frequency. A 1.5-inch needle usually suices in these patients, with placement using a short-axis approach. he deep retrocalcaneal bursa is usually well seen. A small amount of anesthetic will help conirm position by active distention of the bursa in real time. We similarly approach posterior tibial or peroneal tendons in short axis (Fig. 25.9). Patients with pain in this distribution have been shown to beneit from local tendon sheath injections. he presence of preexisting tendon sheath luid can facilitate needle visualization. However, careful scanning should be done before the procedure to assess the needle trajectory relative to adjacent neurovascular structures. Use of color or power Doppler imaging can facilitate visualization of the neurovascular bundle. he posterior tibial nerve is closely related to adjacent vascular structures and is usually well seen before bifurcating into medial and lateral plantar branches. Fluid frequently is seen in relation to the posterior tibial tendon, in the submalleolar region. he location of the peroneal tendon is less predictable. Use of power Doppler sonography in conjunction with real-time guidance can help localize areas of inlammation for guided injection. In stenosing tenosynovitis the tendons may be surrounded only by a thickened retinaculum, proliferative synovium, or scar tissue. In this case, use of a test injection of local anesthesia can be invaluable to conirm the distribution of the therapeutic agent within the tendon sheath in real time. he lexor hallucis longus (FHL) tendon poses a more challenging problem because of its close relation to the neurovascular bundle of the posterior medial ankle. One helpful feature in performing FHL tendon sheath injections is that tendon sheath efusions tend to localize at the posterior recess of the tibiotalar joint. he neurovascular bundle is easily circumvented by placing the needle lateral to the Achilles tendon while scanning medially (Fig. 25.10). his approach allows lexibility in needle placement while maintaining the needle perpendicular to the insonating beam. Ultrasound diagnosis of plantar fasciitis includes thickening of the medial band of the plantar fascia and fat pad edema. One treatment option for severe plantar fasciitis is regional corticosteroid injection, typically performed using anatomic landmarks. However, “blind” injections into the heel have been associated with rupture of the plantar fascia and failure of the longitudinal arch.13 Ultrasound can be used to guide a needle along the plantar margin of the fascia, thus avoiding direct intrafascial injection.26 he plantar fascia is imaged with the patient prone and the foot mildly dorsilexed, using a long-axis approach. he transducer is centered over the medial band, which is most oten implicated in these patients. A mark is placed over the posterior aspect of the heel and the needle advanced supericial to the plantar fascia, approximately to the margin of the medial tubercle (Fig. 25.11). I perform a perifascial injection using this approach, monitoring the distribution of injected material in real time.

T

T N

A

B

FIG. 25.8 Retrocalcaneal Bursa Injection. (A) Short-axis view shows Achilles tendon (T) in 59-year-old man with retrocalcaneal pain and history of Haglund deformity. A 25-gauge needle (N) enters perpendicular to the tendon’s long axis and terminates in a small, retrocalcaneal bursal effusion. (B) Rotating transducer 90 degrees results in the more typical short-axis view, with the needle (arrow) seen in cross section. (C) Under observation in real time, the bursa distends (arrows) and ills with echogenic material (contrast effect). The needle is still evident within the distended bursa.

C PRE-INJECTION

POST-INJECTION

N T

B

A

FIG. 25.9 Tendon Sheath Injection Using Short-Axis Approach. A 17-year-old female patient with medial ankle pain was referred for ultrasound-guided injection of posterior tibial tendon sheath. (A) Preinjection view shows 25-gauge needle (N) within a small tendon sheath effusion (long arrow) in the inframalleolar portion of the tendon (T). The tendon, which is inhomogeneous, is seen in cross section. (B) Postinjection view shows that the tendon sheath is distended, conirming appropriate deposition of the injected material. Note that the tendon margins are better delineated because of a tenosonographic effect of the injected luid. The vascular pedicle (short arrow) of the tendon is evident. PRE-INJECTION

POST-INJECTION

N TA

A

T

B

FIG. 25.10 Flexor Hallucis Longus (FHL) Tendon Sheath Injection. Short-axis approach with ultrasound guidance in 31-year-old professional dancer with posteromedial ankle pain during plantar lexion. (A) Preinjection image depicts the tendon (T) at the level of the posterior sulcus of the talus (TA). The arrows show relationship of the tendon to the neurovascular structures. (B) Postinjection image depicts 25-gauge needle (N) situated within the distended tendon sheath (arrows) below the neurovascular structures.

904

PART III

Small Parts, Carotid Artery, and Peripheral Vessel Sonography

Interdigital (Morton) neuromas, a common cause of forefoot pain especially in women, have been described at sonography as hypoechoic masses replacing the normal hyperechoic fat in the interdigital web spaces. Occasionally a dilated hypoechoic tubular structure can be seen associated with the neuroma, relecting the enlarged feeding interdigital nerve. he second and third web spaces are most oten involved. I generally inject Morton neuromas using a dorsal approach while imaging the neuroma in long axis28 (Fig. 25.12). his approach is well tolerated by the majority of patients. In certain patients, however, a plantar approach to injecting the nodule is preferred, such as those with severe subluxation at the MTP joint. In either case, the needle is positioned directly within the neuroma and/or adjacent intermetatarsal bursa (if present) and a small volume of therapeutic mixture injected, similar to that used for a small joint injection (0.5-0.75 mL).

administration of antiinlammatory agents (Fig. 25.13). Injections are also frequently requested for patients with rheumatoid arthritis or psoriatic arthritis. hese patients typically experience severe tenosynovitis, which can lead to secondary tendon rupture and deformity. he approach is similar to that used for supericial structures in the foot and ankle. A short-axis approach avoids the surrounding neurovascular structures, and the corresponding tendon sheaths are injected.

INJECTION OF DEEP TENDONS Frequently requested deep tendon injections include those for the bicipital tendon sheath, iliopsoas tendon, gluteal tendon insertion onto the greater trochanter, and hamstring tendon origin.

Biceps Tendon

Hand and Wrist

Anterior shoulder pain with radiation into the arm may be secondary to bicipital tendinitis or tenosynovitis.29 he biceps tendon can be palpated, but if nondistended, the sheath may ofer less than 2 mm of clearance to place a needle. his is complicated by the caudal extension of the subacromial subdeltoid bursa, which may overlie the bicipital tendon sheath. A nonimageguided injection could therefore result in delivery into an extratendinous synovial space, or possibly result in an intratendinous injection. Ultrasound guidance enables localization of therapeutic agent to the biceps tendon sheath.10 he patient is placed recumbent with the forearm supinated and the shoulder mildly elevated. he bicipital groove is oriented anteriorly. A linear transducer, typically 7.5 MHz, is used with a lateral approach and 25- or 22-gauge needle (Fig. 25.14). he long head of the biceps tendon is scanned in short axis. When luid distends the bicipital tendon sheath, the tip is directed into the luid. Otherwise, the needle is directed along the supericial margin of the tendon, and a test injection of local anesthetic is used to conirm local distention of the sheath, which is then followed by administration of the long-acting corticosteroid. he

In the hand and wrist, de Quervain tendinosis is a frequently encountered tendinopathy involving the abductor pollicis longus and extensor pollicis brevis tendons that respond to local

N

PF calc

FIG. 25.11 Plantar Fascia Injection. The proximal medial band of the plantar fascia (PF) is thickened and inhomogeneous in a 36-year-old man with hindfoot pain. calc, Calcaneus. A 25-gauge needle (N) has been positioned supericial to this plantar fascia and a perifascial injection performed. The injected material (arrows) loculates along the supericial margin of the medial band.

PRE-INJECTION

POST-INJECTION

N

A

B

FIG. 25.12 Morton Neuroma Injection. (A) Preinjection image shows 25-gauge needle (N) positioned in a third web space neuroma using a dorsal approach in 45-year-old woman with forefoot pain. Neuroma appears as a heterogeneous hypoechoic nodule (arrows) within the normal echogenic fat. (B) After injection and needle removal, the nodule appears expanded and echogenic (arrows). The injected material often decompresses into an adjacent adventitial bursa, which frequently accompanies these nodules.

CHAPTER 25 PRE-INJECTION

Musculoskeletal Interventions

905

POST-INJECTION

N T

ra

B

A

FIG. 25.13 Injection of First Dorsal Compartment of Wrist. This 70-year-old woman with de Quervain tendinosis had clinical symptoms of wrist pain radiating along the extensor surface of the forearm. (A) Preinjection image shows 25-gauge needle (N) positioned in the irst dorsal compartment tendon sheath under ultrasound guidance. The tendons (T) are inhomogeneous, with a small effusion evident (arrows) in the dependent part of the tendon sheath. (B) After injection and needle removal, the injected material distends the sheath (arrows), producing a tenosonographic effect; the intrinsic tendon abnormalities become more conspicuous. ra, Radial artery. PRE-INJECTION

POST-INJECTION

N

A

bg

B

bg

FIG. 25.14 Biceps Tendon Sheath Injection. Biceps tendinosis was clinically suspected and a biceps tendon sheath injection requested for this 41-year-old man with development of anterior shoulder pain after arthroscopic surgery for labral tear. (A) Preinjection image shows 25-gauge needle (N) placed supericial to the long head of the biceps tendon (arrow). (B) After injection and needle removal, there is distention of the tendon sheath by luid (arrows) containing low-level echoes caused by contrast effect. bg, Bicipital groove.

presence of luid distention of the sheath with supericially located microbubbles helps to conirm a successful injection. A technique to obviate the need to directly approach the tendon sheath, which can sometimes be challenging in the absence of an efusion, entails direct positioning of the needle within the rotator interval adjacent to the intraarticular portion of the biceps tendon and deep to the biceps pulley mechanism.30 Stone and Adler reported 100% success in distending the sheath in their series.30 herapeutic mixture was also noted to distribute within the rotator interval (Fig. 25.15, Video 25.2).

Iliopsoas Tendon he iliopsoas tendon lies supericial to and along the medial margin of the anterior capsule of the hip. he tendon inserts onto the lesser trochanter. A bursa that frequently communicates with the hip is present in this location and may be distended because of underling joint pathology or a primary iliopsoas bursitis. Alternatively, iliopsoas tendinosis may occur in the absence of a preexisting bursitis for which a peritendinous injection is requested.31 A lateral approach to the tendon oten requires use of a lower-frequency transducer and curved linear

or sector geometry. he neurovascular bundle lies medial and supericial to the tendon, so it is advantageous to approach from the lateral margin of the tendon and perform a small test injection to conirm needle position. A successful injection will show the appearance of luid or microbubbles distending a bursa that follows the course of the long axis of the tendon (Fig. 25.16).

Abductor and Hamstring Tendons he most commonly requested peritendinous injections in my experience are about the abductor tendon insertion and hamstring tendon origin. In the irst two of these injections, the needle is directed to the greater trochanteric bursa. hese injections can be fairly straightforward when the bursa is distended. hey become more challenging when there is no preexisting bursal distention. One must then employ anatomic landmarks and test injections with anesthetic for localization (Figs. 25.17 and 25.18). Injections at the hamstring origin are generally peritendinous because no true anatomic bursa exists. An adventitial bursa may be present over the ischium. A lateral approach while scanning the tendons in short axis is preferred for each of these injections, directing

A

B

C

D

FIG. 25.15 Biceps Tendon Sheath Injection: Rotator Interval Approach. A 44-year-old woman with anterior shoulder pain. (A) Gray-scale ultrasound image obtained slightly oblique to the intraarticular biceps tendon (arrow). The greater tuberosity (gt), humeral head (hh), and deltoid (D) are labeled. (B) A 25-gauge needle is positioned using a short-axis lateral approach adjacent to the margin of the biceps tendon within the rotator interval. The tip of the needle is indicated (arrow). A test injection with anesthetic is performed to ensure appropriate needle position. Fluid should not accumulate by the needle tip and the needle position should be adjusted accordingly. (C) Short-axis view of the biceps tendon within the sheath before needle placement and injection. The tendon (arrow) and bicipital groove (BG) are labeled. (D) Postinjection image at approximately the same anatomic level as (C) depicting the distended biceps tendon sheath. See also Video 25.2. PRE-INJECTION

fa

POST-INJECTION

fn

N T

e

A

B

FIG. 25.16 Ultrasound-Guided Iliopsoas Bursa Injection for Pain Relief. This 66-year-old woman with a total hip arthroplasty had developed pain with hip lexion. (A) Preinjection image shows 22-gauge spinal needle (N) positioned deep to the tendon (T) at the level of the iliopectineal eminence (e), using a short-axis approach. fa, Femoral artery; fn, femoral nerve. (B) After injection and needle removal, luid surrounds the tendon within the distended iliopsoas bursa (arrow).

CHAPTER 25

A

B

C

D

Musculoskeletal Interventions

907

FIG. 25.17 Ultrasound-Guided Greater Trochanteric Bursal Injection. A 53-year-old woman with right lateral hip pain. (A) Axial T2-weighted fat-suppressed image depicts the greater trochanter (GT) and abductor tendon complex (T). The image is oriented similar to the manner in which it would be viewed during an injection with the patient in a lateral decubitus position. A trace amount of T2-bright luid (arrow) is present in the bursa. (B) A 22-gauge spinal needle (arrow) is positioned near the posterior margin of the greater trochanter, supericial to the gluteus medius tendon and deep to the gluteus maximus. A test injection with local anesthetic helps ensure appropriate needle placement, which is followed by injection of the therapeutic mixture. (C) Short-axis postinjection image at the greater trochanter shows anterior extension of the greater trochanteric bursa (B) at the level of the anterior facet. (D) Postinjection short-axis image centered more posteriorly over the lateral and posterior facets depicts the posterior extension of the bursa (B) abutting the posterior facet of the greater trochanter, also referred to as the “bare area” of the greater trochanter. I usually inject a large volume (10 mL).

the needle toward the posterior facet of the greater trochanter in the case of a trochanteric bursal injection, or adjacent to the margin of the hamstring origin if a peritendinous injection is requested.

BURSAL, GANGLION CYST, AND PARALABRAL INJECTIONS Distended bursae around tendinous insertions provide anatomic localization for therapeutic agents. Injection of these areas is oten requested for the patient with localized bursitis and

abnormality of the adjacent tendon. Examples include the retrocalcaneal, iliopsoas, greater trochanteric, and ischial bursae (Fig. 25.19). Alternatively, the presence of a bursitis, distended synovial cyst, or ganglion cyst may cause mechanical impingement of adjacent tendons. he decompression of these cysts with subsequent administration of a therapeutic agent may alleviate these symptoms32 (Fig. 25.20). Ganglion cysts typically contain clear gelatinous material, most oten occurring in the hand, wrist, foot, and ankle. Not infrequently they may come in close proximity to neurovascular structures and may extend along nerves as perineural ganglia. his occurs most oten in the knee, at the

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FIG. 25.18 Ultrasound-Guided Hamstring Peritendinous Injection. A 50-year-old female runner with left buttock pain. (A) Axial fat-suppressed T2-weighted sequence positioned in a manner similar to that viewed by a sonographer. The hamstring origin (T) and ischium (I) are labeled. The sciatic nerve (arrow) appears as a mildly hyperintense ellipse lateral to the ischium and supericial to the quadratus femoris. F, Femur. (B) A 22-gauge spinal needle (N) is positioned in short axis, using a lateral approach, adjacent to the margin of the hamstring tendon origin (T). The sciatic nerve (arrow) and ischium (I) are labeled.

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FIG. 25.19 Ultrasound-Guided Aspiration and Injection of Multiloculated Iliopsoas Bursa. (A) Image shows 22-gauge spinal needle (N) positioned into the lateral component of the bursa in a 65-year-old woman with groin pain. e, Iliopectineal eminence; fh, femoral head. (B) After aspiration of the lateral component, the needle has been advanced into the medial component for aspiration and subsequent injection with therapeutic mixture. nv, Neurovascular structures.

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FIG. 25.20 Ultrasound-Guided Aspiration and Injection of Clinically Suspected Baker Cyst. (A) Preinjection image shows 22-gauge needle (N) positioned in the cyst (C) under ultrasound guidance in 59-year-old woman with posterior knee pain and swelling. mhg, Medial head of gastrocnemius muscle. (B) After cyst aspiration and injection of the therapeutic mixture, the anechoic luid is replaced by echogenic luid resulting from contrast effect (arrows).

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FIG. 25.21 Ultrasound-Guided Aspiration and Injection of Multiloculated Ganglion Cyst. (A) Baseline sonogram shows a multiloculated cyst (c) within the vastus lateralis muscle of the left knee and supericial to the lateral margin of the femur (f) in a 41-year-old woman. (B) A 20-gauge spinal needle (N) was initially positioned into the proximal component of the cyst. (C) Subsequently the needle was redirected into the distal component. Multiple lavages and aspiration enabled complete decompression of the cyst (not shown).

tibioibular joint.33,34 Ultrasound guidance allows the clinician to avoid intratendinous injections as well as adjacent neurovascular structures. Furthermore, the needle may be redirected as necessary in the presence of a multiloculated cyst (Fig. 25.21). We ind that performing a lavage technique similar to that employed in treating calciic tendinosis results in progressive dilution of the cyst contents, thereby permitting complete aspiration. In the upper extremity, where cosmesis may also be an issue, use of a rapidly absorbed corticosteroid may reduce potential complications, such as depigmentation and local atrophy. Similar considerations apply when aspirating and injecting parameniscal and paralabral cysts. hese cysts occur at sites of torn and/or degenerated ibrocartilage and are most oten present in the knee, hip, and shoulder. hese cysts are similar to ganglion cysts in consistency but oten contain additional echogenic debris. In the shoulder, paralabral cysts have been associated with development of a compressive neuropathy, because they can occur in close proximity to the suprascapular nerve.35 he approach used in aspirating these cysts is variable, depending on location and orientation, as well as location of adjacent neurovascular structures (Figs. 25.22 and 25.23, Video 25.3).

Calciic Tendinitis he presence of symptomatic intratendinous calciication involves the deposition of calcium hydroxyapatite. his oten appears as a nodular echogenic mass within the tendon, which may or may not display posterior acoustic shadowing.36 Although most oten afecting the shoulder, this may occur elsewhere in the musculoskeletal system. Ultrasound-guided fragmentation and

lavage, also known as barbotage, has been described as an excellent method to fenestrate the calciication and reduce the level of calciication and to deposit therapeutic agents.37-40 Singleand dual-needle techniques have been described and appear to be comparably efective. I currently use a single-needle technique, with the needle acting as inlow for anesthetic and sterile saline and as an outlow for the calcium solution (Fig. 25.24). he elasticity of the pseudocapsule encasing the calciication is suficient to decompress the calciic mass in the majority of cases (Video 25.4). Ater multiple lavages, the needle is used to inject the anesthetic and antiinlammatory mixture. he injected mixture is distributed within the adjacent subdeltoid bursa in most cases. If the calciication is too small or fragmented, precluding lavage and decompression, the single needle is used to fenestrate the calcium deposit, and a peritendinous therapeutic injection has been shown to be efective.

INTRATENDINOUS INJECTIONS: PERCUTANEOUS TENOTOMY Image guidance can be useful for performing percutaneous tenotomy and intratendinous injections with either autologous blood or platelet-rich plasma (PRP).41-45 hese methods are associated with secondary release of local growth factors, such as platelet-derived growth factor, which in turn may produce a direct healing response.44 Preliminary data show signiicant promise in promoting ultrasound-guided tendon repair. “Dry needling” techniques have been employed successfully in patients with lateral epicondylitis refractory to other conservative

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measures.41 Likewise, autologous blood injections and PRP injections have been successfully used in both the elbow and the knee42-44 (Figs. 25.25 and 25.26, Video 25.5). he advantage of performing these injections under ultrasound guidance becomes evident when the clinician wants to generalize such techniques to include tendons close to neurovascular structures, such as the hamstring tendon origin. Newer technology is now available that allows sonographically directed emulsiication of focal tendinosis, calciications, and enthesopathic spurs followed by removal during the course of the procedure.46 he technique employs a coaxial system with a mechanically active hollow tip that disrupts the tissue and is connected to vacuum suction, while the outer tube supplies sterile water to cool the tip and remove debris as part of the suctioned material (Fig. 25.27, Video 25.6). his technique is relatively new, and no deinitive long-term trials are available to assess eicacy, but preliminary results appear promising.

FIG. 25.22 Ultrasound-Guided Aspiration of Paralabral Cyst in the Hip. A 54-year-old woman with left hip pain. (A) Sagittal luid–sensitive image of the hip showing a multiloculated paralabral cyst (arrow) associated with a tear of the anterior superior labrum (not shown). (B) The same cyst (arrow) shown on ultrasound as a septated hypoechoic collection overlying the anterior joint margin. The acetabulum (a), femoral head (fh), and labrum (L) are labeled. (C) Ultrasoundguided aspiration of the cyst is depicted. A 22-gauge spinal needle (N) is positioned within the cyst (c) for purposes of aspiration and injection. The needle tip is depicted (arrow).

PERINEURAL INJECTIONS Ultrasound has shown promise in evaluating and treating patients with painful lesions of peripheral nerves due to compressive neuropathies, such as in carpal or cubital tunnel syndromes, or in cases of posttraumatic or postsurgical neuromas.35 hese injections can include nerve blocks with long-acting anesthetic, therapeutic injections using an injectable steroid, or neurolytic therapy with an agent that promotes cellular death such as absolute ethanol.47,48 A rapidly absorbed injectable steroid, such as dexamethasone, may be preferable for supericial lesion to minimize potential complications, such as depigmentation or atrophy of the subcutaneous fat. A thorough knowledge of the normal sonographic appearances of nerves and their anatomic course is a prerequisite.35,36 In the case of small sensory nerves, which can be diicult to visualize, knowledge of the anatomic relationships of the nerves to adjacent

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FIG. 25.23 Ultrasound-Guided Paralabral Cyst Aspiration in the Spinoglenoid Notch of the Shoulder. Spinoglenoid Notch Cyst Aspiration. (A) Axial fatsuppressed proton-density image that has been inverted for purposes of comparison with ultrasound. The cyst (C) is depicted appearing as a homogeneously T2-bright structure. The cyst produces bony remodeling of the adjacent glenoid. (B) Anechoic cyst (C) remodeling the spinoglenoid notch (sgn). The humeral head (hh) is labeled. (C) A 20-gauge spinal needle (arrow) is positioned within the cyst. See also Video 25.3.

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FIG. 25.24 Ultrasound-Guided Aspiration and Injection for Calciic Tendinosis. (A) Image shows 20-gauge spinal needle (N) positioned into the calciication (arrow) under ultrasound guidance in 42-year-old man with shoulder pain. D, Deltoid; H, humeral head. (B) Series of repeat lavage and aspirations of the calciication are performed, with the calciication eventually largely replaced by luid contents within the surrounding pseudocapsule of the calciic mass. T, Rotator cuff tendons. Note that the degree of posterior acoustic shadowing has diminished and that the center of the calciication (arrow on A) is partially replaced by luid. After numerous lavages, the calciication is typically fenestrated, and a therapeutic mixture is injected and often decompresses into the subdeltoid bursa (not shown).

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FIG. 25.25 Ultrasound-Guided Injection of Autologous Blood to Induce Healing Response. (A) Coronal inversion-recovery magnetic resonance imaging scan of the affected elbow in a 43-year-old man with medial epicondylitis shows increased signal intensity (arrow) of the common lexor tendon mass and adjacent collateral ligament. (B) Long-axis ultrasound image of the tendon (T) and adjacent medial epicondyle (me) shows that tendon is predominantly hypoechoic, relecting underlying tendinosis. (C) Image shows 22-gauge needle (N) placed within the common lexor tendon mass, for purposes of mechanical fenestration, and injection of 5 mL of autologous blood, obtained from an antecubital vein. Tendon echogenicity (small arrow) is increased by microbubbles within the injected blood.

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me

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FIG. 25.26 Baseline Image Before Autologous Blood Injection. Common extensor tendon mass (T) in 50-year-old woman with partial tear of the deep portion of the tendon (short arrow, extensor carpi radialis brevis) as it inserts on the medial epicondyle (me); rc, radiocapitellar joint; long arrow, plane of needle entry for percutaneous tenotomy and autologous blood injection. See also Video 25.5.

Ultrasound allows direct targeting of the perineural sot tissue or a neuroma for injection (Fig. 25.28, Video 25.7). he nerve is best approached in short axis, usually with a 1.5-inch 25-gauge needle or occasionally a spinal needle. In the case of a perineural injection, it is helpful to position the needle in close proximity to the nerve, injecting small amounts of anesthetic until a clear-cut luid plane outlining the epineurium is evident. When this is achieved, the therapeutic mixture can be instilled. he same procedure is used when performing ultrasound-guided neurolytic therapy. I typically inject a mixture of long-acting anesthetic (0.75% bupivacaine) with a total of 0.5 to 1 mL of absolute ethanol for peripheral nerve lesions. In my experience, absolute ethanol may require multiple injections and can produce a marked postinjection inlammatory response that can last for several days. he volume injected can be variable and in general does not exceed 1 mL. Multiple small injections have been advocated to be eicacious for Morton neuromas (0.25-0.5 mL).

CONCLUSION anatomic compartments is of value. Nerves are best visualized in short axis as clusters of hypoechoic fascicles with echogenic septations (internal epineurium), which have a surrounding echogenic epineurial sleeve (external epineurium). An enlarged hypoechoic nerve may indicate neuritis, whereas a focal hypoechoic nodule seen in relationship to the nerve may represent a neuroma in the appropriate clinical setting.

Ultrasound ofers distinct advantages in providing guidance for delivery of therapeutic injections. Most important, ultrasound allows the operator to visualize the needle and make adjustments in real time, to ensure that medication is delivered to the appropriate location. Current ultrasound technology provides excellent depiction of relevant musculoskeletal anatomy. he needle has a unique sonographic appearance and can be monitored with

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FIG. 25.27 Percutaneous Tenotomy Using Tenex Device. A 47-year-old man with lateral epicondylitis. (A) Coronal fat-suppressed proton-density image depicting a partial torn and degenerated common extensor tendon and radial collateral ligament (arrow). The lateral epicondyle (le) is labeled. (B) The common extensor mechanism (arrow) is shown in long axis. Hypoechoic areas within the tendon represent interstitial tearing. In addition, punctate echogenic foci within the tendon substance are characteristic for dystrophic calciication. The lateral epicondyle (le) is labeled. See also Video 25.6.

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FIG. 25.28 A 58-Year-Old Woman With Postoperative Sural Nerve Entrapment and Neuropathic Pain. (A) A 1.5-inch 25-gauge needle is positioned adjacent to the outer epineurium of the sural nerve (arrow). (B) Hypoechoic luid consisting of anesthetic and corticosteroid surrounds the nerve. Ideally, luid hydrodissection of the epineurial fat from the adjacent perineural soft tissues is achieved. See also Video 25.7.

real-time imaging, as can the steroid-anesthetic mixture. Given these advantages, ultrasound guidance should become the method of choice to perform a large variety of guided musculoskeletal interventions. REFERENCES 1. Christensen RA, Van Sonnenberg E, Casola G, Wittich GR. Interventional ultrasound in the musculoskeletal system. Radiol Clin North Am. 1988;26(1):145-156. 2. Cunnane G, Brophy DP, Gibney RG, FitzGerald O. Diagnosis and treatment of heel pain in chronic inlammatory arthritis using ultrasound. Semin Arthritis Rheum. 1996;25(6):383-389. 3. Brophy DP, Cunnane G, Fitzgerald O, Gibney RG. Technical report: ultrasound guidance for injection of sot tissue lesions around the heel in chronic inlammatory arthritis. Clin Radiol. 1995;50(2):120-122.

4. Cardinal E, Chhem RK, Beauregard CG. Ultrasound-guided interventional procedures in the musculoskeletal system. Radiol Clin North Am. 1998;36(3):597-604. 5. Koski JM. Ultrasound guided injections in rheumatology. J Rheumatol. 2000;27(9):2131-2138. 6. Grassi W, Farina A, Filippucci E, Cervini C. Sonographically guided procedures in rheumatology. Semin Arthritis Rheum. 2001;30(5): 347-353. 7. Soka CM, Collins AJ, Adler RS. Use of ultrasonographic guidance in interventional musculoskeletal procedures: a review from a single institution. J Ultrasound Med. 2001;20(1):21-26. 8. Soka CM, Adler RS. Ultrasound-guided interventions in the foot and ankle. Semin Musculoskelet Radiol. 2002;6(2):163-168. 9. Adler RS, Soka CM. Percutaneous ultrasound-guided injections in the musculoskeletal system. Ultrasound Q. 2003;19(1):3-12. 10. Adler RS, Allen A. Percutaneous ultrasound-guided injections in the shoulder. Tech Shoulder Elbow Surg. 2004;5(2):122-133.

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11. Unverferth LJ, Olix ML. he efect of local steroid injections on tendon. J Sports Med. 1973;1(4):31-37. 12. Ford LT, DeBender J. Tendon rupture ater local steroid injection. South Med J. 1979;72(7):827-830. 13. Gottlieb NL, Riskin WG. Complications of local corticosteroid injections. JAMA. 1980;243(15):1547-1548. 14. Oxlund H, Manthorpe R. he biochemical properties of tendon and skin as inluenced by long term glucocorticoid treatment and food restriction. Biorheology. 1982;19(5):631-646. 15. Stapczynski JS. Localized depigmentation ater steroid injection of a ganglion cyst on the hand. Ann Emerg Med. 1991;20(7):807-809. 16. Shrier I, Matheson GO, Kohl 3rd HW. Achilles tendonitis: are corticosteroid injections useful or harmful? Clin J Sport Med. 1996;6(4):245-250. 17. Boufard JA, Eyler WR, Introcaso JH, van Holsbeeck M. Sonography of tendons. Ultrasound Q. 1993;11:259-286. 18. Koski JM, Saarakkala SJ, Heikkinen JO, Hermunen HS. Use of air-steroidsaline mixture as contrast medium in greyscale ultrasound imaging: experimental study and practical applications in rheumatology. Clin Exp Rheumatol. 2005;23(3):373-378. 19. Luchs JS, Soka CM, Adler RS. Sonographic contrast efect of combined steroid and anesthetic injections: in vitro analysis. J Ultrasound Med. 2007;26(2):227-231. 20. Curatolo M, Bogduk N. Pharmacologic pain treatment of musculoskeletal disorders: current perspectives and future prospects. Clin J Pain. 2001;17(1):25-32. 21. Caldwell JR. Intra-articular corticosteroids. Guide to selection and indications for use. Drugs. 1996;52(4):507-514. 22. Kannus P, Jarvinen M, Niittymaki S. Long- or short-acting anesthetic with corticosteroid in local injections of overuse injuries? A prospective, randomized, double-blind study. Int J Sports Med. 1990;11(5):397-400. 23. Cox B, Durieux ME, Marcus MA. Toxicity of local anaesthetics. Best Pract Res Clin Anaesthesiol. 2003;17(1):111-136. 24. Gomoll AH, Kang RW, Williams JM, et al. Chondrolysis ater continuous intra-articular bupivacaine infusion: an experimental model investigating chondrotoxicity in the rabbit shoulder. Arthroscopy. 2006;22: 813-819. 25. Soka CM, Saboeiro G, Adler RS. Ultrasound-guided adult hip injections. J Vasc Interv Radiol. 2005;16(8):1121-1123. 26. Mehdizade A, Adler RS. Sonographically guided lexor hallucis longus tendon sheath injection. J Ultrasound Med. 2007;26(2):233-237. 27. Tsai WC, Wang CL, Tang FT, et al. Treatment of proximal plantar fasciitis with ultrasound-guided steroid injection. Arch Phys Med Rehabil. 2000;81(10):1416-1421. 28. Soka CM, Adler RS, Ciavarra GA, Pavlov H. Ultrasound-guided interdigital neuroma injections: short-term clinical outcomes ater a single percutaneous injection—preliminary results. HSS J. 2007;3:44-49. 29. Middleton WD, Reinus WR, Totty WG, et al. US of the biceps tendon apparatus. Radiology. 1985;157(1):211-215.

30. Stone TJ, Adler RS. Ultrasound-guided biceps peritendinous injections in the absence of a distended tendon sheath: a novel rotator interval approach. J Ultrasound Med. 2015;34(12):2287-2292. 31. Adler RS, Buly R, Ambrose R, Sculco T. Diagnostic and therapeutic use of sonography-guided iliopsoas peritendinous injections. Am J Roentgenol. 2005;185(4):940-943. 32. Breidahl WH, Adler RS. Ultrasound-guided injection of ganglia with corticosteroids. Skeletal Radiol. 1996;25(7):635-638. 33. Martinoli C, Bianchi S, Derchi LE. Tendon and nerve sonography. Radiol Clin North Am. 1999;37(4):691-711, viii. 34. Bianchi S. Ultrasound of the peripheral nerves. Joint Bone Spine. 2008;75(6):643-649. 35. Tung GA, Entzian D, Stern JB, Green A. MR imaging and MR arthrography of paraglenoid labral cysts. AJR Am J Roentgenol. 2000;174(6): 1707-1715. 36. Farin PU, Jaroma H. Sonographic indings of rotator cuf calciications. J Ultrasound Med. 1995;14(1):7-14. 37. Farin PU, Jaroma H, Soimakallio S. Rotator cuf calciications: treatment with US-guided technique. Radiology. 1995;195(3):841-843. 38. Farin PU, Rasanen H, Jaroma H, Harju A. Rotator cuf calciications: treatment with ultrasound-guided percutaneous needle aspiration and lavage. Skeletal Radiol. 1996;25(6):551-554. 39. Aina R, Cardinal E, Bureau NJ, et al. Calciic shoulder tendinitis: treatment with modiied US-guided ine-needle technique. Radiology. 2001;221(2): 455-461. 40. Lin JT, Adler RS, Bracilovic A, et al. Clinical outcomes of ultrasound-guided aspiration and lavage in calciic tendinosis of the shoulder. HSS J. 2007;3(1): 99-105. 41. McShane JM, Nazarian LN, Harwood MI. Sonographically guided percutaneous needle tenotomy for treatment of common extensor tendinosis in the elbow. J Ultrasound Med. 2006;25(10):1281-1289. 42. James SL, Ali K, Pocock C, et al. Ultrasound guided dry needling and autologous blood injection for patellar tendinosis. Br J Sports Med. 2007;41(8):518-521. 43. Connell DA, Ali KE, Ahmad M, et al. Ultrasound-guided autologous blood injection for tennis elbow. Skeletal Radiol. 2006;35(6):371-377. 44. Mishra A, Pavelko T. Treatment of chronic elbow tendinosis with bufered platelet-rich plasma. Am J Sports Med. 2006;34(11):1774-1778. 45. Gamradt SC, Rodeo SC, Warren RF. Platelet-rich plasma in rotator cuf repair. Tech Orthop. 2007;22:26-33. 46. Barnes D. Ultrasonic energy in tendon treatment. Oper Tech Orthop. 2013;23(2):78-83. 47. Tagliaico A, Seraini G, Lacelli F, et al. Ultrasound-guided treatment of meralgia paresthetica (lateral femoral cutaneous neuropathy): technical description and results of treatment in 20 consecutive patients. J Ultrasound Med. 2011;30(10):1341-1346. 48. Lee J, Lee YS. Percutaneous chemical nerve block with ultrasound-guided intraneural injection. Eur Radiol. 2008;18(7):1506-1512.

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The Extracranial Cerebral Vessels Edward I. Bluth, Stephen I. Johnson, and Laurie Troxclair

SUMMARY OF KEY POINTS • The combination of gray-scale, color-low Doppler, and Doppler spectral analysis is highly accurate in determining plaque characterization and degree of carotid stenosis. • Accurate diagnosis of carotid stenosis is critical for patients who would beneit from surgical and interventional treatment. • Clinicians can accurately follow changes in noncritical carotid stenosis or plaque using ultrasound. • The assessment of the vertebral arteries is an integral component of the carotid ultrasound examination. However, the degree of stenosis of the vertebral arteries cannot be accurately assessed.

• Carotid atherosclerotic plaque with resultant stenosis usually involves the internal carotid artery within 2 cm of the carotid bifurcation. • Homogenous plaque, which is stable, has uniform echo pattern with a smooth surface. The amount of sonolucency is less than 50%. • Heterogeneous plaque, which can be unstable, has a more complex echo pattern with sonolucent areas of more than 50%. • Either the consensus table by the Society of Radiologists in Ultrasound or other standard reporting tables and criteria can be used to grade carotid stenosis as long as there is appropriate quality outcome feedback for accuracy.

CHAPTER OUTLINE INTRODUCTION: INDICATIONS FOR CAROTID ULTRASOUND EXAMINATION CAROTID ARTERY ANATOMY CAROTID ULTRASOUND EXAMINATION CAROTID ULTRASOUND INTERPRETATION Visual Inspection of Gray-Scale Images Vessel Wall Thickness and IntimaMedia Thickening Plaque Characterization Ultrasound Plaque Classiication System Plaque Ulceration Gray-Scale Evaluation of Stenosis Doppler Spectral Analysis Standard Examination

Spectral Broadening Pitfalls in Interpretation High-Velocity Blood Flow Patterns Color Doppler Ultrasound Optimal Settings for Low-Flow Vessel Evaluation Advantages and Pitfalls Power Doppler Ultrasound Pitfalls and Adjustments Internal Carotid Artery Occlusion Follow-Up of Stenosis Preoperative Strategies for Patients With Carotid Artery Disease Postoperative Ultrasound Carotid Artery Stents and Revascularization Grading Carotid Intrastent Restenosis

INTRODUCTION: INDICATIONS FOR CAROTID ULTRASOUND EXAMINATION Stroke secondary to atherosclerotic disease is the third leading cause of death in the United States. Many stroke victims survive the catastrophic event with some degree of neurologic impairment depending on collateral low.1,2 Annually, stroke kills more than

NONATHEROSCLEROTIC CAROTID DISEASE Pulsatile Neck Masses in the Carotid Region TRANSCRANIAL DOPPLER SONOGRAPHY VERTEBRAL ARTERY Anatomy Sonographic Technique and Normal Examination Subclavian Steal Stenosis and Occlusion INTERNAL JUGULAR VEINS Sonographic Technique Thrombosis Acknowledgment

130,000 people in the United States with an incidence of more than 795,000 cases of cerebrovascular accident (CVA).3,4 Ischemia from severe, low-limiting stenosis caused by atherosclerotic disease involving the extracranial carotid arteries is implicated in 20% to 30% of strokes with a decreasing incidence due to improved control of hypertension and hyperlipidemia with medications.3,5 An estimated 80% of CVAs are thromboembolic in origin, oten with carotid plaque as the embolic source.6 Cardioembolic stroke carries a higher risk of death, recurrent

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stroke, hospital readmission, and severe disability than other types of stroke.6 Carotid atherosclerotic plaque with resultant stenosis usually involves the internal carotid artery (ICA) within 2 cm of the carotid bifurcation. his location is readily amenable to examination by sonography as well as surgical intervention. Carotid endarterectomy (CEA) initially proved to be more beneicial than medical therapy in symptomatic patients with carotid stenoses of more than 70%, as reported in the North American Symptomatic Carotid Endarterectomy Trial (NASCET) and the European Carotid Surgery Trial (ECST).7,8 Subsequent NASCET results for moderate stenoses have shown a net beneit for surgical intervention with carotid narrowing between 50% and 69% of vessel diameter. A 15.7% reduction in the 5-year ipsilateral stroke rate was seen in patients treated surgically versus 22.2% stroke reduction in those treated medically. hese results are not as compelling as those for the higher degree of stenosis seen in the earlier NASCET trial. he beneit from surgery was greatest in men, patients with recent stroke, and those with hemispheric symptoms. In addition, the NASCET trials dealing with moderate carotid stenoses required rigorous surgical expertise, such that the risks for disabling stroke or death should not exceed 2% to achieve the statistical surgical beneit.9 he Asymptomatic Carotid Atherosclerosis Study (ACAS) trials published in 1995 reported a reduction in ipsilateral stroke in asymptomatic patients with greater than 60% ICA stenoses who undergo CEA.3 However, these results were less clear-cut than the NASCET trials. According to the Carotid Revascularization Endarterectomy Versus Stenting Trial (CREST), carotid artery stenting has been shown to be comparable to CEA with respect to rates of ipsilateral stroke and death. However, there are increased adverse efects in women and elevated stroke rates and deaths in older patients.10 With implementation of new medical management regimens—including aspirin, clopidogrel, statins, antihypertensive medications, diabetic management, smoking cessation, and lifestyle changes—future trials may change how carotid disease is treated.10 Accurate diagnosis of carotid stenosis clearly is critical to identify patients who would beneit from surgical treatment. In addition, ultrasound can assess plaque morphology, such as determining heterogeneous or homogeneous plaque, known to be an independent risk factor for stroke and transient ischemic attack (TIA). Carotid sonography is the principal screening method for suspected extracranial carotid atherosclerotic disease. Gray-scale examination, color Doppler, power Doppler, and pulsed Doppler imaging techniques are routinely employed in the evaluation of patients with neurologic symptoms and suspected extracranial cerebral disease.11,12 Ultrasound is an inexpensive, noninvasive, and highly accurate method of diagnosing carotid stenosis. Magnetic resonance angiography (MRA) and computed tomography angiography (CTA) are additional noninvasive screening tools for the identiication of carotid bifurcation disease as well as for clariication of ultrasound indings. Angiography is oten now reserved for those patients for whom the ultrasound or MRA was equivocal or inadequate.

Other carotid ultrasound applications include the evaluation of carotid bruits, monitoring the progression of known atherosclerotic disease,11,13,14 assessment during or ater CEA or stent placement,15 screening before major vascular surgery, and evaluation ater the detection of retinal cholesterol emboli.11 Also, nonatherosclerotic carotid diseases can be evaluated, including follow-up of carotid dissection,16-21 examination of ibromuscular dysplasia or Takayasu arteritis,22-24 assessment of malignant carotid artery invasion,25,26 and workup of pulsatile neck masses and carotid body tumors.27-29

Indications for Carotid Ultrasound Evaluation of patients with hemispheric neurologic symptoms, including stroke, transient ischemic attack, and amaurosis fugax Evaluation of patients with a carotid bruit Evaluation of pulsatile neck masses Evaluation of patients scheduled for major cardiovascular surgical procedures Evaluation of nonhemispheric or unexplained neurologic symptoms Follow-up of patients with proven carotid disease Evaluation of patients after carotid revascularization, including stenting Intraoperative monitoring of vascular surgery Evaluation of suspected subclavian steal syndrome Evaluation of a potential source of retinal emboli Follow-up of carotid dissection Follow-up of radiation therapy to the neck in select patients

CAROTID ARTERY ANATOMY he irst major branch of the aortic arch is the innominate or brachiocephalic artery, which divides into the right subclavian artery and right common carotid artery (CCA). he second major branch is the let CCA, which is generally separate from the third major branch, the let subclavian artery (Fig. 26.1). he right and let CCAs ascend into the neck posterolateral to the thyroid gland and lie deep to the jugular vein and sternocleidomastoid muscle. he CCAs have diferent proximal conigurations, with the right originating at the bifurcation of the innominate (brachiocephalic) artery into the common carotid and subclavian arteries. he let CCA usually originates directly from the aortic arch but oten arises with the brachiocephalic trunk. his is known as a “bovine arch” coniguration. he CCA usually has no branches in its cervical region. Occasionally, however, it may give of the superior thyroid artery, vertebral artery, ascending pharyngeal artery, and occipital or inferior thyroid artery. At the carotid bifurcation, the CCA divides into the external carotid artery (ECA) and the internal carotid artery (ICA). he ICA usually has no branching vessels in the neck. he ECA, which supplies the facial musculature, has multiple branches in the neck. he ICA may demonstrate an ampullary region of mild dilation just beyond its origin.

CHAPTER 26

CAROTID ULTRASOUND EXAMINATION Carotid artery ultrasound examinations are performed with the patient supine, the neck slightly extended, and the head turned away from the side being examined. Some operators prefer to perform the examination at the patient’s side, whereas others prefer to sit at the patient’s head. he examination sequence also varies with operator preference. his sequence includes the gray-scale examination, Doppler spectral analysis, and color

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FIG. 26.1 Branches of Aortic Arch and Extracranial Cerebral Arteries. A, Aortic arch; C, common carotid artery; E, external carotid artery; I, internal carotid artery; In, innominate artery; L, left side; R, right side; S, subclavian artery; V, vertebral artery.

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Doppler blood low interrogations. Power Doppler sonography may or may not be employed. A 5- to 12-MHz transducer is used for gray-scale imaging and a 3- to 7-MHz transducer for Doppler sonography; the choice depends on the patient’s body habitus and technical characteristics of the ultrasound machine. Color Doppler low imaging and power Doppler imaging may be performed with 5- to 10-MHz transducers. In cases of critical stenosis, the Doppler parameters should be optimized to detect extremely slow low. Gray-scale sonographic examination begins in the transverse projection. Scans are obtained along the entire course of the cervical carotid artery, from the supraclavicular notch cephalad to the angle of the mandible (Fig. 26.2). Inferior angulation of the transducer in the supraclavicular area images the CCA origin. he let CCA origin is deeper and more diicult to image consistently than the right. he carotid bulb is identiied as a mild widening of the CCA near the bifurcation. Transverse views of the carotid bifurcation establish the orientation of the external and internal carotid arteries and help deine the optimal longitudinal plane in which to perform Doppler spectral analysis (Video 26.1). When the transverse ultrasound images demonstrate occlusive atherosclerotic disease, the percentage of “diameter stenosis” or “area stenosis” can be calculated directly using electronic calipers and sotware analytic algorithms available on most duplex equipment. Ater transverse imaging, longitudinal scans of the carotid artery are obtained. he examination plane necessary for optimal longitudinal scans is determined by the course of the vessels demonstrated on the transverse study. In some patients, the optimal longitudinal orientation will be nearly coronal, whereas in others it will be almost sagittal. In most cases, the optimal longitudinal scan plane will be oblique, between sagittal and coronal. In approximately 60% of patients, both vessels above the carotid bifurcation and the CCA can be imaged in the same plane (Fig. 26.3); in the remainder, only a single vessel will be imaged in the same plane as the CCA. Images are obtained to display the relationship of both branches of the carotid bifurcation to the visualized plaque disease, and the cephalocaudal extent

B

FIG. 26.2 Carotid Sonographic Anatomy. (A) Transverse image of the left internal carotid artery (I) and external carotid artery (E). The internal carotid artery is lateral and larger in relation to the external carotid artery. (B) Color Doppler image of the left internal carotid artery (I) and the external carotid artery (E). Note normal color-low separation in the internal carotid artery.

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PART III

of the plaque is measured. Several anatomic features diferentiate the ICA from the ECA. In about 95% of patients, the ICA is posterior and lateral to the ECA. his may vary considerably, and the ICA may be medial to the ECA in 3% to 9% of people.15 he ICA frequently has an ampullary region of dilation just beyond its origin and is usually larger than the ECA. One reliable distinguishing feature of the ECA is that it has branching vessels (Fig. 26.4A). A useful method to identify the ECA is the tapping of the ipsilateral supericial temporal artery in the preauricular area, the temporal tap. he pulsations are transmitted back to the ECA where they cause a sawtooth appearance on the spectral waveform (Fig. 26.4B). Although the tap helps identify the ECA, this tap delection may be transmitted into the CCA and even the ICA in certain rare situations. he superior thyroid artery is oten seen as the irst branch of the ECA ater the bifurcation of the CCA. Occasionally, an aberrant superior thyroid artery branch will arise from the distal CCA. he ICA usually has no branches in the neck, although

&

( ,

FIG. 26.3 Carotid Bifurcation. Longitudinal image demonstrates common carotid artery (C); external carotid artery (E); and large, posterior internal carotid artery (I).

A

in rare cases the ICA gives rise to the ascending pharyngeal, occipital, facial, laryngeal, or meningeal arteries. In some patients, a considerable amount of the ICA will be visible, but in others, only the immediate origin of the vessel will be accessible. Very rarely, the bifurcation may not be visible at all.28 Rarely, the ICA may be hypoplastic or congenitally absent.30,31

CAROTID ULTRASOUND INTERPRETATION Each facet of the carotid sonographic examination is valuable in the inal determination of the presence and extent of disease. In most cases, the gray-scale, color Doppler, and power Doppler sonographic images and assessments will agree. However, when there are discrepancies between Doppler ultrasound imaging indings and measured velocities, every attempt should be made to discover the source of the disagreement. he more closely the image and spectral Doppler indings correlate, the higher the degree of conidence in the diagnosis. Generally, gray-scale and color or power Doppler images better demonstrate and quantify low-grade stenoses, whereas high-grade occlusive disease is more accurately deined by Doppler spectral analysis. For plaque characterization, assessment must be made in gray-scale only, without color or power Doppler ultrasound.

Visual Inspection of Gray-Scale Images Vessel Wall Thickness and Intima-Media Thickening Longitudinal views of the layers of the normal carotid wall demonstrate two nearly parallel echogenic lines, separated by a hypoechoic to anechoic region (Fig. 26.5). he irst echo, bordering the vessel lumen, represents the lumen-intima interface; the second echo is caused by the media-adventitia interface. he media is the anechoic/hypoechoic zone between the echogenic lines. he distance between these lines represents the combined thickness of the intima and media (I-M complex). he far wall of the CCA is measured. Many consider measurement of

B

FIG. 26.4 Normal External Carotid Artery (ECA). (A) Color Doppler ultrasound of bifurcation demonstrates two small arteries originating from the ECA. (B) ECA spectral Doppler shows the relected temporal tap (TT) as a serrated (sawtooth) low disturbance.

CHAPTER 26 intima-media thickness (IMT) to be a surrogate marker for atherosclerotic disease in the whole arterial system, not only the cerebrovascular system.32,33 Some believe that thickening of the I-M complex greater than 0.8 mm is abnormal and may represent the earliest changes of atherosclerotic disease. However, because thickness of the I-M increases with age, absolute measurements of IMT for any given person may not be a reliable indicator of atherosclerotic risk factors34 (Fig. 26.6). Carotid artery IMT is an independent predictor of new cardiovascular events in persons without a history of cardiovascular disease.35 Numerous studies support the relationship between IMT and increased risk for myocardial infarction

FIG. 26.5 Normal Intima-Media (I-M) Complex of Common Carotid Artery. The I-M complex (arrows) is seen in a left common carotid artery.

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The Extracranial Cerebral Vessels

919

or stroke in asymptomatic patient populations.19,36-43 Assessment of IMT has been advocated as a means of assessing efectiveness of medical interventions to reduce the progression of I-M thickening or even reverse carotid wall thickening. However, because of concerns regarding minimal impact on prediction models and diiculty in standardizing measurement technique, the 2013 American College of Cardiology/American Heart Association (ACC/AHA) Guideline on the Assessment of Cardiovascular Risk does not recommend the carotid IMT test.44

Plaque Characterization Atheromatous carotid plaques should be carefully evaluated to determine plaque extent, location, surface contour, and texture, as well as to assess luminal stenosis.45 he plaque should be scanned and evaluated in both the sagittal and the transverse projections.46 he most common cause of TIAs is embolism, not low-limiting stenosis; less than half of patients with documented TIA have hemodynamically signiicant stenosis. It is important to identify low-grade atherosclerotic lesions that may contain hemorrhage or ulceration, which can serve as a nidus for emboli that cause both TIAs and stroke.1 Polak et al.47 showed that plaque is an independent risk factor for developing a stroke. Of patients with hemispheric stroke symptoms, 50% to 70% demonstrate hemorrhagic or ulcerated plaque. Plaque analysis of CEA specimens has implicated intraplaque hemorrhage as an important factor in the development of neurologic symptoms.48-55 However, the relationship between sonographic plaque morphology and the onset of symptoms is controversial. Currently, substantial gaps in knowledge of the mechanisms involved in atherosclerotic plaque rupture exist and this is a critical barrier to developing methodologies for the prevention of myocardial infarction and stroke. Myocardial infarction and stroke, complications of atherosclerosis, are the most common causes of death in developed countries and are caused by inlammation-driven rupture of atherosclerotic plaques. Stable plaques are characterized by a necrotic core with an overlying ibrous cap composed of vascular smooth muscle cells in a

B

FIG. 26.6 Abnormal Intima-Media (I-M) Complex of Common Carotid Artery (CCA). (A) Early I-M hyperplasia with loss of the hypoechoic component of the I-M complex and thickening (arrows). (B) Thickening of the I-M complex with hyperplasia (arrows).

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collagen-rich matrix.56,57 In vulnerable/ruptured plaques, the ibrous cap has thinned, exhibiting fewer vascular smooth muscle cells, decreased collagen, and increased inlammatory cells. Heterogeneous plaque has been suggested as unstable and vulnerable, in contrast to homogeneous plaque. Some have suggested that environmental factors and toxins cause abnormal low patterns, damaging the internal structure of the vessels.58 his can lead to intimal proliferation and potential wall ischemia and the degradation of the vasa vasorum.58 Because the vasa vasorum do not have a muscular media, these vessels are subsequently at risk to rupture, perhaps leading, in part, to intraplaque hemorrhage.58 Others have suggested that a bacterial infection etiology may play a role in inlammatory angiogenesis.58 Recently, several groups have demonstrated that microRNAs play a key role in the development and thinning of the ibrous cap.59-69 MicroRNAs are a class of noncoding RNAs (ncRNAs) that are approximately 21 nucleotides in length and are potent

efectors of gene expression, doing so by binding to messenger RNA and inhibiting protein translation. A role for ncRNA in cardiovascular diseases is emerging, including microRNAs (miRNAs) and their inhibition by circular RNA (circRNAs). MicroRNA-221 and microRNA-222 (miR-221/miR-222) are short ncRNAs that inhibit the expression of the cyclin-dependent kinase inhibitor p27Kip1, promoting vascular smooth muscle cell proliferation and intimal thickening. Bazan et al. recently demonstrated an important role for the downregulation of miR-221/222 in the shoulder region of carotid plaques shortly ater rupture70 through increased p27Kip1 and propose that vascular smooth muscle cell volume is lost, leading to intimal thinning.

Ultrasound Plaque Classiication System Plaque texture is generally classiied as homogeneous or heterogeneous.14,38,41,45,46,48-50,71-75 he accurate evaluation of plaque can only be made with gray-scale ultrasound, without the use of

A

B

C

D

FIG. 26.7 Spectrum of Patterns of Homogeneous Plaque. (A) Sagittal and (B) transverse images show homogeneous plaque in left common carotid artery (type 4). Note the uniform echo texture. (C) Sagittal and (D) transverse images show homogeneous plaque in proximal left internal carotid artery (type 3). Note the focal hypoechoic area within the plaque, estimated at less than 50% of plaque volume.

CHAPTER 26

E

F

G

H

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FIG. 26.7, cont’d (E) Sagittal and (F) transverse images demonstrate homogeneous plaque (type 3). Associated calciications best seen on image E obscure uniformity of plaque. (G) Sagittal and (H) transverse images demonstrate homogeneous plaque (type 3) in the carotid bifurcation. The sonolucent areas are less than 50% of the volume of the plaque.

color or power Doppler. he plaque must be evaluated in both sagittal and transverse planes.46 Homogeneous plaque has a generally uniform echo pattern and a smooth surface (Fig. 26.7). Sonolucent areas may be seen, but the amount of sonolucency is less than 50% of the plaque volume. he uniform acoustic texture corresponds pathologically to dense ibrous connective tissue (Videos 26.2 through 26.4). Calciied plaque produces posterior acoustic shadowing and is common in asymptomatic individuals (Fig. 26.8, Video 26.5). Heterogeneous plaque has a more complex echo pattern and contains one or more focal sonolucent areas corresponding to more than 50% of the plaque volume (Fig. 26.9, Videos 26.6 through 26.11). Heterogeneous plaque is characterized pathologically by containing intraplaque hemorrhage and deposits of lipid, cholesterol, and proteinaceous material.15,73 Homogeneous plaque is identiied much more oten than heterogeneous plaque, occurring in 80% to 85% of patients examined.47 Sonography accurately determines the presence or absence of intraplaque hemorrhage (sensitivity, 90%-94%; speciicity, 75%-88%).48,54,73,76-80 Some sources suggest classifying plaque according to four types. Plaque types 1 and 2, similar to heterogeneous plaque and much more likely to be associated with intraplaque hemorrhage and ulceration, are considered unstable and subject to abrupt increases in plaque size ater hemorrhage or embolization.14,46,74,81-84 Types 1 and 2 plaque are typically found in

FIG. 26.8 Calciied Plaque. The calciied plaque creates a shadow that obscures characterization of plaque in the left internal carotid artery.

symptomatic patients with stenoses greater than 70% of diameter. Plaque types 3 and 4 are generally composed of ibrous tissue and calciication. hese plaque types are similar to homogeneous plaque. hese are generally more benign, stable plaques typically seen in asymptomatic individuals (see Fig. 26.8).

922

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D

G

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Small Parts, Carotid Artery, and Peripheral Vessel Sonography

C

B

E

F

H

FIG. 26.9 Spectrum of Patterns of Heterogeneous Plaque in the Internal Carotid Artery (ICA). (A) Sagittal and (B) transverse images show plaque (arrows) virtually completely sonolucent, consistent with heterogeneous plaque (type 1). Note smooth plaque surface. (C) Sagittal and (D) transverse images show focal sonolucent areas within the plaque greater than 50% of plaque volume, corresponding to heterogeneous plaque (type 2). Note the irregular surface of the plaque. (E) Sagittal image demonstrates heterogeneous plaque in the carotid bulb and homogeneous plaque in the internal carotid artery (type 2). (F) Transverse image demonstrates heterogeneous plaque (type 2). (G) and (H) Sagittal and transverse images demonstrate subtle heterogeneous plaque (type 2).

Ultrasound Types of Plaque Morphology Type 1: Predominantly echolucent, with a thin echogenic cap Type 2: Substantially echolucent with small areas of echogenicity (>50% sonolucent) Type 3: Predominantly echogenic with small areas of echolucency (95%), the velocity measurements may actually decrease, and the waveform becomes dampened.99,108

CHAPTER 26

929

B

A

C

The Extracranial Cerebral Vessels

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E

FIG. 26.20 Internal Carotid Artery (ICA) Stenosis. (A) ICA stenosis of 50% to 69% diameter shows a peak systolic velocity (PSV) of 187 cm/ sec. (B) Left ICA demonstrates a visible high-grade stenosis on color Doppler with end diastolic velocities (EDVs) of greater than 180 cm/sec and PSVs that alias at greater than 350 cm/sec. This is consistent with a very high-grade stenosis. (C) Right carotid bulb seen in longitudinal projection with color Doppler demonstrates a high-grade narrowing and spectral broadening with an approximately 500 cm/sec velocity in peak systole and 250 cm/sec in end diastole, consistent with an 80% to 95% stenosis. (D) and (E) Power transverse and long images demonstrate high-grade stenosis of the ICA.

In these cases, correlation with color or power Doppler imaging is essential to diagnose correctly the severity of the stenoses. Velocity increases are focal and most pronounced in and immediately distal to a stenosis, emphasizing the importance of sampling directly in these regions. Moving further distal from a stenosis, low begins to reconstitute and assume a more normal pattern, provided a tandem lesion does not exist distal to the initial site of stenosis. Spectral broadening results in the jets of high-velocity low associated with carotid stenosis; however, correlation with gray-scale and color Doppler images can deine other causes of spectral broadening. An awareness of normal low spectra combined with appropriate Doppler techniques can obviate many potential diagnostic pitfalls. he degree of carotid stenosis that is considered clinically signiicant in the symptomatic or asymptomatic patient is in evolution. Initially, it was thought that lesions causing 50% diameter stenosis were signiicant; this perception changed as more information was gathered from two large clinical trials. As noted earlier, NASCET demonstrated that CEA was more beneicial than medical therapy in symptomatic patients with 70% to 99% ICA stenosis.7 ECST demonstrated a CEA beneit when the degree of stenosis was greater than 60%.8 Interestingly, the method used to grade stenoses in the ECST study was

substantially diferent than that used in the NASCET trials. he NASCET trials compared the severity of the ICA stenosis on arteriogram with the residual lumen of a presumably more normal distal ICA. he ECST methodology entailed assessment of the severity of stenosis with a “guesstimation” of the lumen of the carotid artery at the level of the stenosis. he ECST assessment is more comparable to ultrasound’s visible assessment of the degree of narrowing, whereas velocity tables currently in use have been derived to correspond to the NASCET angiographic determinations for stenosis. he ECST method for grading carotid artery stenosis tends to give a more severe assessment of narrowing than the NASCET technique (Fig. 26.21). he initial NASCET trials retrospectively compared velocity data obtained on the Doppler examination with angiographic measurements of stenosis. No standardized ultrasound protocol was employed by the numerous centers involved in the trials. Despite the lack of uniformity, moderate sensitivity and speciicity ranging from 65% to 77% were obtained for grading ICA stenoses using Doppler velocities. If ultrasound technique is standardized and criteria are validated in a given laboratory, peak systolic velocity (PSV) and peak systolic ratios have proved to be an accurate method for determining carotid stenosis.109 he ECST group compared three diferent angiographic measurement

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PART III ICA C

B

ECA

A Measurement Methodology

ECST =

B–A

x 100

B NASCET = 1– ACAS

A

x 100

C

CCA FIG. 26.21 Comparative Measurement Methodology. Different methodologies for grading internal carotid artery stenoses, from the North American Symptomatic Carotid Endarterectomy Trial (NASCET), Asymptomatic Carotid Atherosclerosis Study (ACAS), and European Carotid Surgery Trial (ECST). CCA, Common carotid artery; ECA, external carotid artery; ICA, internal carotid artery.

techniques: the NASCET, the ECST, and a technique comparing distal CCA measurements with those of ICA stenosis. Researchers concluded that the ECST and NASCET techniques were similar in their prognostic value, whereas the CCA/stenosis measurement was the most reproducible of the three techniques. hey also concluded that the CCA method, although reproducible, would be invalidated by the presence of CCA disease.110 Virtually all investigators advocate using the NASCET angiographic measurement technique. he results of these trials, as well as the more recent ACAS and moderate NASCET studies, have generated reappraisals of the Doppler velocity criteria that most accurately deine 70% or greater stenosis and, more recently, greater than 50% diameter stenoses.111 Attempts have been made to determine the Doppler parameters or combination of parameters that most reliably identify a certain-diameter stenosis. Most sources agree that the best parameter is the PSV of the ICA in the region of a stenosis.108 Using multiple parameters can improve diagnostic conidence, particularly when combined with color and power Doppler imaging (see Video 26.19). he degree of stenosis is best assessed using the gray-scale and pulsed Doppler parameters, including ICA PSV, ICA end diastolic velocity (EDV), CCA PSV, CCA EDV, peak systolic ICA/CCA ratio, and peak end diastolic ICA/CCA ratio (EDR)108,109,112 (Videos 26.21 and 26.22).108,109,112 PSV has proved accurate for quantifying high-grade stenoses.98,109 he relationship of PSV to the degree of luminal narrowing is well deined and easily measured.113,114 Although Doppler velocities have proved reliable for deining 70% or greater stenosis, Grant et al.109 showed less favorable results for substenosis classiication between 50% to 69% using PSV and ICA/CCA PSV ratios. In

our experience, however, using all four parameters and determining a correct category for the degree of stenosis is the most eicacious way to ensure accuracy. Agreement for all four parameters for a clinical situation is most common. When there is an outlying parameter, further assessment and careful attention to technique and detail are required. EDV and EDR are particularly useful in distinguishing between high grades of stenosis. Additionally, correlating the visual estimation of the degree of stenosis and the velocity numbers will help in correctly grading stenosis, particularly when the degree of stenosis is “near occlusion” (Figs. 26.22 and 26.23; see also Fig. 26.20D and E). On rare occasions, alternate imaging methodologies (e.g., MRA, CTA) may need to be recommended. No criteria for grading external carotid artery stenoses have been established. A good general rule is that if the ECA velocities do not exceed 200 cm/sec, no signiicant stenosis is present. However, we usually rely on a visible assessment of the degree of narrowing associated with velocity changes. Occlusive plaque involving the ECA is less common than in the ICA and is rarely clinically signiicant. Similarly, velocity criteria used to grade common carotid artery stenoses have not been well established.115,116 However, if one is able to visualize 2 cm proximal and 2 cm distal to a visible CCA stenosis, a PSV ratio obtained 2 cm proximal to the stenosis (vs. in region of greatest visible stenosis) can be used to grade the “percent diameter stenosis” in a manner similar to that used in peripheral artery studies. A doubling of the PSV across a lesion would correspond to at least a 50% diameter stenosis, and a velocity ratio in excess of 3.5 corresponds to a greater than 75% stenosis. One persistent problem with duplex Doppler with gray-scale ultrasound evaluation of the carotid arteries is that diferent institutions use PSVs ranging from 130 cm/sec117 to 325 cm/ sec111 to diagnose greater than 70% ICA stenosis.118,119 Factors adding to these discrepancies include technique and equipment.120 While there is a strong level of correlation between techniques and criteria, the choice of criteria has a signiicant impact on which patients go to surgery.119 his wide range of PSVs reinforces the need for individual ultrasound laboratories to determine which Doppler parameters are most reliable in their own institution.120 Correlation of the velocity ranges obtained by ultrasound with angiographic and surgical results is necessary to achieve accurate, reproducible examinations in a particular ultrasound laboratory.121 he Society of Radiologists in Ultrasound, representing multiple medical and surgical specialties, held a consensus conference in 2002 to consider carotid Doppler ultrasound.122 In addition to guidelines for performing and interpreting carotid ultrasound examinations, panelists devised a set of criteria widely applicable among vascular laboratories (Table 26.1).122 Although the conference did not recommend all established laboratories with internally validated velocity charts alter their practices, they suggested physicians establishing new laboratories consider using the consensus criteria; those with preexisting charts might consider comparing in-house criteria with those provided by the consensus conference. Velocity criteria corresponding to speciic degrees of vascular stenosis are listed in the tables. Our

CHAPTER 26

The Extracranial Cerebral Vessels

B

A

D

931

C

FIG. 26.22 Abnormal High-Resistance Waveforms. High-resistance waveforms: (A) CCA, (B) proximal ICA, and (C) distal ICA. Color-low Doppler imaging of the carotid bulb in (D) transverse and (E) sagittal projections demonstrates a signiicantly narrowed ICA. These indings are consistent with a greater than 95% stenosis of the ICA and a distal tandem stenosis of the intracranial carotid artery.

E

TABLE 26.1 Diagnostic Criteria for Carotid Ultrasound Examinations

Normal 90 >2.15 ≥2.7 ≥4.15 >2 >125 2.45 4.3

ICA/CCA PSV Ratio

≥3.8 >4

>4

CCA, Common carotid artery; EDV, end diastolic velocity; ICA, internal carotid artery; PSV, peak systolic velocity. Modiied from Chahwan S, Miller MT, Pigott JP, et al. Carotid artery velocity characteristics after carotid artery angioplasty and stenting. J Vasc Surg. 2007;45(3):523-526206; Fleming SE, Bluth EI, Milburn J. Role of sonography in the evaluation of carotid artery stents. J Clin Ultrasound. 2005;33(7):321-328.198

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C

B

FIG. 26.39 Fibromuscular Dysplasia. (A) Longitudinal color Doppler image of the middle to distal portion of the ICA shows velocity elevation and signiicant stenosis. (B) Same patient’s proximal portion of the ICA shows no stenosis. (C) Angiogram demonstrates typical appearance of ibromuscular dysplasia in the mid and distal ICA. Note the beaded appearance resulting from focal bands (arrow) of thickened tissue that narrow the lumen.

carotid dissection or subsequent thromboembolic events (Fig. 26.39). Arteritis resulting from autoimmune processes (e.g., Takayasu arteritis, temporal arteritis) or radiation changes can produce difuse concentric thickening of carotid walls, which most frequently involves the CCA23,216,217 (Fig. 26.40). Cervical trauma can produce carotid dissections or aneurysms. Carotid artery dissection results from a tear in the intima, allowing blood to dissect into the wall of the artery, which produces a false lumen. he false lumen may be blind ended or may reenter the true lumen. he false lumen may occlude or narrow the true lumen, producing symptoms similar to carotid plaque disease. Dissections may arise spontaneously or secondary

to trauma or to intrinsic disease with elastic tissue degeneration (e.g., Marfan syndrome) or may be related to atherosclerotic plaque disease.20 he ultrasound examination of a carotid dissection may reveal a mobile or ixed echogenic intimal lap, with or without thrombus formation.218 Frequently, there is a striking image/Doppler mismatch with a paucity of gray-scale abnormalities seen in association with marked low abnormalities (Fig. 26.41). Color or power Doppler ultrasound can readily clarify the source of this mismatch by demonstrating abrupt tapering of the patent, illed lumen to the point of an ICA occlusion. When the ICA is occluded, the proximal ipsilateral CCA will demonstrate

CHAPTER 26

A

C

Internal Carotid Artery Dissection: Spectrum of Findings INTERNAL CAROTID ARTERY Absent low or occlusion Echogenic intimal lap, with or without thrombus Hypoechoic thrombus, with or without luminal narrowing Normal appearance COMMON CAROTID ARTERY High-resistance waveform Dampened low Normal appearance

a high-resistance waveform. When the ICA is severely narrowed (secondary to hemorrhage and a thrombus in the area of the false lumen), low in the ICA may demonstrate high velocities. In these nonoccluded ICA cases, low velocity waveforms in the CCA may be normal. Although conventional angiography, MRA,

The Extracranial Cerebral Vessels

947

B

FIG. 26.40 Long-Segment Stenosis of CCA Caused by Takayasu Arteritis. Power Doppler images of (A) left and (B) right CCA shows long-segment concentric narrowing caused by greatly thickened walls of the artery (arrows). (C) Spectral Doppler waveform shows a mildly tardus-parvus waveform.

or CTA can be used initially to diagnose a dissection, ultrasound can be used to follow patients to assess the therapeutic response to anticoagulation. Repeat sonographic evaluation of patients with ICA dissection ater anticoagulation therapy reveals recanalization of the artery in as many as 70% of cases.219-221 It is important to consider the diagnosis of dissection as a cause of neurologic symptoms, particularly when the clinical presentation, age, and patient history are atypical for that of atherosclerotic disease or hemorrhagic stroke.

Pulsatile Neck Masses in the Carotid Region he most common CCA aneurysm occurs in the region of the carotid bifurcation. hese aneurysms may result from atherosclerosis, infection, trauma, surgery, or contagious disease, such as syphilis. he normal CCA usually measures no more than 1 cm in diameter. Carotid body tumors, one of several paragangliomas that involve the head and neck, are usually benign,

948

Small Parts, Carotid Artery, and Peripheral Vessel Sonography

PART III

A

C

B

D

E

FIG. 26.41 Carotid Artery Dissection. (A) Abnormal high-resistance waveforms (arrow) at the origin of the right ICA with no evidence of low distal to this point (curved arrow). (B) Gray-scale evaluation of the vessel in the area of the occlusion demonstrates only a small, linear echogenic structure (arrow) without evidence of signiicant atherosclerotic narrowing. (C) Subsequent angiogram demonstrates the characteristic tapering to the point of occlusion (arrow) associated with carotid artery dissection and thrombotic occlusion. (D) Transverse and (E) longitudinal images of another patient show an intimal lap (arrow) in an ECA. I, Internal carotid artery.

well-encapsulated masses located at the carotid bifurcation.29 hese tumors may be bilateral, particularly in the familial variant, and are very vascular, oten producing an audible bruit.29 Some of these tumors produce catecholamines, leading to sudden changes in blood pressure during or ater surgery. Color Doppler ultrasound demonstrates an extremely vascular sot tissue mass at the carotid bifurcation29 (Fig. 26.42). Color Doppler ultrasound can also be used to monitor embolization or surgical resection of carotid body tumors. A classic nonmass is the ectatic innominate/proximal CCA, frequently occurring as a pulsatile supraclavicular mass in older women. he request to rule out a carotid aneurysm almost invariably shows the classic normal features of these tortuous vessels (Fig. 26.43). Extravascular masses (e.g., lymph node masses [Fig. 26.44], hematomas, abscesses) that compress or displace the carotid arteries can be readily distinguished from primary vascular masses, such as aneurysms or pseudoaneurysms. Posttraumatic pseudoaneurysms can usually be distinguished from true carotid aneurysms by the characteristic to-and-fro

waveforms in the neck of the pseudoaneurysm, as well as the internal variability (yin-yang) characteristic of a pseudoaneurysm (Fig. 26.45).

TRANSCRANIAL DOPPLER SONOGRAPHY In transcranial Doppler (TCD) ultrasound, a low-frequency 2-MHz transducer is used to evaluate blood low within the intracranial carotid and vertebrobasilar system and the circle of Willis. Access is achieved through the orbits, foramen magnum, or, most oten, the region of temporal calvarial thinning (transtemporal window).222,223 However, many patients (up to 55% in one series224) may not have access to an interpretable TCD examination. Women, particularly African American women, have a thick temporal bone through which it is diicult to insonate the basal cerebral arteries.224,225 his diiculty limits the feasibility of TCD imaging as a routine part of the noninvasive cerebrovascular workup.223,224

CHAPTER 26

The Extracranial Cerebral Vessels

949

ECA

ICA

A

B

FIG. 26.42 Carotid Body Tumor. (A) Transverse image of the carotid bifurcation shows a mass (arrows) splaying the internal carotid artery (ICA) and external carotid artery (ECA). (B) Pulsed Doppler traces of the carotid body tumor show typical arteriovenous shunt (low-resistance) waveform.

,

(

,

FIG. 26.43 Ectatic CCA. Color Doppler image shows ectatic proximal common carotid artery (CCA) arising from the innominate artery (I) and responsible for a pulsatile right supraclavicular mass. FIG. 26.44 Pathologic Lymph Node Near Carotid Bifurcation. Power Doppler image shows a malignant lymph node (arrow) lateral to the carotid bifurcation. E, External carotid artery; I, internal carotid artery.

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PART III

Small Parts, Carotid Artery, and Peripheral Vessel Sonography

By using spectral analysis, various parameters are determined, including mean velocity, PSV, EDV, and the pulsatility and resistive indices of the blood vessels. Color or power Doppler ultrasound can improve velocity determination by providing better angle theta determination and localizing the course of vessels.222 TCD applications include (1) evaluation of intracranial stenoses and collateral circulation, (2) detection and follow-up of vasoconstriction from subarachnoid hemorrhage, (3) determination of brain death, (4) evaluation of patients with sickle cell disease, and (5) identiication of arteriovenous malformation.219-223,226,227 TCD is

most reliable in diagnosing stenoses of the middle cerebral artery, with sensitivities as high as 91% reported. TCD is less reliable for detecting stenoses of the intracranial vertebrobasilar system, anterior and posterior cerebral arteries, and terminal ICA. However, TCD is helpful in assessing vertebral artery patency and low direction when no low is detected in the extracranial vertebral artery (Fig. 26.46). Diagnosis of an intracranial stenosis is based on an increase in the mean velocity of blood low in the afected vessel compared to that of the contralateral vessel at the same location.223-225 Advantages of TCD ultrasound also include its availability for monitoring patients in the operating room or angiographic suite for potential cerebrovascular complications.225 Intraoperative TCD monitoring can be performed with the transducer strapped over the transtemporal window, allowing evaluation of blood low in the middle cerebral artery during CEA. he adequacy of cerebral perfusion can be assessed while the carotid artery is clamped.225,228 TCD is also capable of detecting intraoperative microembolization, which produces high-amplitude spikes (high-intensity transient signals [“HITS”]) on the Doppler spectrum.223,224,227,229-231 he technique can be used for the serial evaluation of vasospasms. his diagnosis is usually based on serial examinations of the relative increase in blood low velocity and resistive index changes resulting from a decrease in the lumen of the vessel caused by vasospasms.225 More description of transcranial Doppler is in Chapter 47.

VERTEBRAL ARTERY FIG. 26.45 Pseudoaneurysm of the Common Carotid Artery (CCA). Transverse image of the right CCA demonstrates a jet of low into a pseudoaneurysm, which resulted from an attempted central venous line placement.

A

he vertebral arteries supply the majority of the posterior brain circulation. hrough the circle of Willis, the vertebral arteries also provide collateral circulation to other portions of the brain

B

FIG. 26.46 Transcranial Doppler Imaging. (A) Transcranial duplex scan of the posterior fossa in a patient with an incomplete left subclavian steal syndrome demonstrates retrograde systolic low (arrow) and antegrade diastolic low (curved arrow). The scan is obtained in a transverse projection from the region of the foramen magnum (open arrowhead). (B) Color Doppler image obtained in the same patient demonstrates that there is retrograde low not only within the left vertebral artery but also within the basilar artery (arrow).

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FIG. 26.47 Vertebral Artery Course. Lateral diagram of vertebral artery (arrows) shows its course through the cervical spine transverse foramina en route to joining the contralateral vertebral artery to form the basilar artery (B). C, Carotid artery; S, subclavian artery.

in patients with carotid occlusive disease. Evaluation of the extracranial vertebral artery seems a natural extension of carotid duplex and color Doppler imaging.232,233 Historically, however, these arteries have not been studied as intensively as the carotids. Symptoms of vertebrobasilar insuiciency also tend to be rather vague and poorly deined compared with symptoms referable to the carotid circulation. It is oten diicult to make an association conidently between a lesion and symptoms. Furthermore, interest in surgical correction of vertebral lesions has been limited. he anatomic variability, small size, deep course, and limited visualization resulting from overlying transverse processes make the vertebral artery more diicult to examine accurately with ultrasound.232,234-236 he clinical utility of vertebral artery duplex scanning in diagnosing subclavian steal and presteal phenomena is well established.237-239 Less clear-cut is the use of vertebral duplex scanning in evaluating vertebral artery stenosis, dissection, or aneurysm.240

Anatomy he vertebral artery is usually the irst branch of the subclavian artery (Fig. 26.47). However, variation in the origin of the vertebral arteries is common. In 6% to 8% of people, the let vertebral artery arises directly from the aortic arch proximal to the let subclavian artery.234,241 In 90%, the proximal vertebral artery ascends superomedially, passing anterior to the transverse process

FIG. 26.48 Normal Vertebral Artery and Vein. Longitudinal color Doppler image shows a normal vertebral artery (A) and vein (V) running between the transverse processes of the second to sixth cervical vertebrae (C2-C6), which are identiied by their periodic acoustic shadowing (S).

of the seventh cervical vertebra (C7), and enters the transverse foramen at the C6 level. he rest of the vertebral arteries enter into the transverse foramen at the C5 or C7 level and, rarely, at the C4 level. he size of vertebral arteries is variable, with the let larger than the right in 42%, the two vertebral arteries equal in size in 26%, and the right larger than the let in 32% of cases.242 One vertebral artery may even be congenitally absent. Usually, the vertebral arteries join at their conluence to form the basilar artery. Rarely, the vertebral artery may terminate in a posterior inferior cerebellar artery.

Sonographic Technique and Normal Examination Vertebral artery visualization with Doppler low analysis can be obtained in 92% to 98% of vessels232,243 (Fig. 26.48). Vertebral artery duplex examinations are performed by irst locating the CCA in the longitudinal plane. he direction of low in the CCA and jugular vein is determined. A gradual sweep of the transducer laterally demonstrates the vertebral artery and vein running between the transverse processes of C2 to C6, which are identiied by their periodic acoustic shadowing. Angling the transducer caudad allows visualization of the vertebral artery origin in 60% to 70% of the arteries, in 80% on the right side, and in 50% on the let. his discrepancy may relate to the let vertebral artery origin being deeper and arising directly from the aortic arch in 6% to 8% of cases.234,241 he presence and direction of low should be established. Visible plaque should be assessed. he vertebral artery usually has a low-resistance low pattern similar to that of the CCA, with continuous low in systole and diastole; however, wide variability in waveform shape has been noted in angiographically

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FIG. 26.49 Normal Vertebral Artery Waveform. Normal lowresistance waveform of the vertebral artery with illing of the spectral window. S

normal vessels.244 Because the vessel is small, low tends to demonstrate a broader spectrum. he clear spectral window seen in the normal carotid system is oten illed in the vertebral artery102 (Fig. 26.49). he vertebral vein (oten a plexus of veins) runs parallel and adjacent to the vertebral artery. Care must be taken not to mistake its low for that of the adjacent artery, particularly if the venous low is pulsatile. Comparison with jugular venous low during respiration should readily distinguish between vertebral artery and vein. At times, the ascending cervical branch of the thyrocervical trunk can be mistaken for the vertebral artery. his can be avoided by looking for landmark transverse processes that accompany the vertebral artery and by paying careful attention to the waveform of the visualized vessel. he ascending cervical branch has a high-impedance waveform pattern similar to that of the ECA.237 TCD sonographic examination of the vertebrobasilar artery system can be performed as an adjunct to the extracranial evaluation. he examination is conducted with a 2-MHz transducer with the patient sitting, using a suboccipital midline nuchal approach, or with the patient supine, using a retromastoidal approach. Color or power Doppler facilitates TCD imaging of the vertebrobasilar system.245

Subclavian Steal he subclavian steal phenomenon occurs when there is highgrade stenosis or occlusion of the proximal subclavian or innominate arteries with patent vertebral arteries bilaterally. he artery of the ischemic limb “steals” blood from the vertebrobasilar circulation through retrograde vertebral artery low, which may result in symptoms of vertebrobasilar insuiciency (Fig. 26.50). Symptoms are usually most pronounced during exercise of the

FIG. 26.50 Hemodynamic Pattern in Subclavian Steal Syndrome. Proximal left subclavian artery occlusive lesion (arrowhead) decreases low to the distal subclavian artery (S). This produces retrograde low (large arrows) down the left vertebral artery (L) and stealing from the right vertebral artery (R) and other intracranial vessels through the circle of Willis (W).

upper extremity but can be produced by changes in head position. However, there is oten poor correlation between vertebrobasilar symptoms and the subclavian steal phenomenon. In most cases, low within the basilar artery is unafected unless severe stenosis of the vertebral artery supplying the steal exists.245 Also, surgical or angioplastic restoration of blood low may not result in relief of symptoms.246 he subclavian steal phenomenon is most oten caused by atherosclerotic disease, although traumatic, embolic, surgical, congenital, and neoplastic factors have also been implicated. Although the proximal subclavian stenosis or occlusion may be diicult to image, particularly on the let, the vertebral artery waveform abnormalities correlate with the severity of the subclavian disease. Doppler evaluation of the vertebral artery reveals four distinct abnormal waveforms that correlate with subclavian or vertebral

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FIG. 26.51 Reversal of Vertebral Artery Flow in Subclavian Steal. Subclavian steal causes reversed low in vertebral artery. Spectral Doppler (A) demonstrates complete vertebral artery low reversal due to right subclavian artery occlusion. Color-low Doppler (B) demonstrates low toward the transducer.

Abnormal Vertebral Artery Waveforms COMPLETE SUBCLAVIAN STEAL Reversal of low within vertebral artery ipsilateral to stenotic or occluded subclavian or innominate artery INCOMPLETE OR PARTIAL SUBCLAVIAN STEAL Transient reversal of vertebral artery low during systole May be converted into a complete steal using provocative maneuvers Suggests stenotic, not occlusive, lesion PRESTEAL PHENOMENON “Bunny” waveform: systolic deceleration less than diastolic low May be converted into partial steal by provocative maneuvers Seen with proximal subclavian stenosis TARDUS-PARVUS (DAMPENED) WAVEFORM Seen with vertebral artery stenosis FIG. 26.52 Incomplete Subclavian Steal. Flow in early systole is antegrade, low in peak systole is retrograde, and low in late systole and diastole (arrow) is again antegrade.

artery pathology on angiography. hese include the complete subclavian steal, partial or incomplete steal, presteal phenomenon, and tardus-parvus vertebral artery waveforms.239,244 In a complete subclavian steal, low within the vertebral artery is completely reversed (Fig. 26.51). Incomplete steal or partial steal demonstrate transient reversal of vertebral low during systole239,245

(Fig. 26.52). Incomplete steal suggests high-grade stenosis of the subclavian or innominate artery rather than occlusion. Provocative maneuvers, such as exercising the arm for 5 minutes or 5-minute inlation of a sphygmomanometer on the arm to induce rebound hyperemia on the side of the subclavian or innominate lesion, can enhance the sonographic indings and convert an incomplete steal to a complete steal.155,185

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FIG. 26.53 Incomplete Subclavian Steal and Provocative Maneuver. (A) Presteal left vertebral artery waveform. Flow decelerates in peak systole but does not reverse. (B) After provocative maneuver, there is reversal of low in peak systole in response to a decrease in peripheral arterial pressure.

he presteal (“bunny”) waveform shows antegrade low but with a striking deceleration of velocity in peak systole to a level less than EDV. his is seen in patients with proximal subclavian stenosis, which is usually less severe than in those with partial steal waveform.239 he bunny waveform can be converted into a partial steal or complete steal waveform by provocative maneuvers (Fig. 26.53). A tardus-parvus waveform (also called a dampened waveform) can be seen in patients with high-grade proximal vertebral stenosis.238,239 With a subclavian steal, color Doppler may show two similarly color-encoded vessels between the transverse processes, representing the vertebral artery and vein.129 Transverse images of the vertebral artery with color Doppler show reversed low compared with those of the CCA. A Doppler spectral waveform must be produced in all such cases to avoid mistaking low reversal within an artery for low in a pulsatile vertebral vein.129,237

Stenosis and Occlusion Diagnosis of vertebral artery stenosis is more diicult than diagnosis of low reversal. Most hemodynamically signiicant stenoses occur at the vertebral artery origin, situated deep in the upper thorax and seen in only 60% to 70% of patients.234,243,241 Even if the vertebral artery origin is visualized, optimal adjustments of the Doppler angle for accurate velocity measurements may

be diicult because of the deep location and vessel tortuosity. No accurate reproducible criteria for evaluating vertebral artery stenosis exist. Because low is normally turbulent within the vertebral artery, spectral broadening cannot be used as an indicator of stenosis. Velocity measurements are not reliable as criteria for stenosis because of the wide normal variation in vertebral artery diameter. Although velocities greater than 100 cm/ sec oten indicate stenosis, they can occur in angiographically normal vessels. For example, high-low velocity may be present in a vertebral artery that is serving as a major collateral pathway for cerebral circulation in cases of carotid occlusion34,188,247 (Fig. 26.54). hus only a focal increase in velocity of at least 50%, visible stenosis on gray-scale or color Doppler, or a striking tardus-parvus vertebral artery waveform is likely to indicate signiicant vertebral stenosis. he variability of resistive indices in normal and abnormal vertebral arteries precludes the use of this parameter as an indicator of vertebral disease.244 Diagnosis of vertebral artery occlusion is also diicult. Oten, the inability to detect arterial low results from a small or congenitally absent vertebral artery or a technically diicult examination. he diferentiation of severe stenosis from occlusion is diicult for the same reasons. Extremely dampened blood low velocity in high-grade stenoses may result in a Doppler

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FIG. 26.54 Increased Flow Velocity in Vertebral Artery. Pulsed Doppler spectral trace from a left vertebral artery demonstrates strikingly high velocities and disturbed low (arrow). Although this degree of velocity elevation and low disturbance could be associated with a focal stenosis, in this case there was increased velocity throughout the vertebral artery from bilateral internal carotid artery occlusion and increased collateral low into the vertebral artery.

signal with amplitude too low to be detected.235 Power Doppler imaging may prove useful in this situation. Visualization of only a vertebral vein may indicate vertebral artery occlusion or congenital absence.

INTERNAL JUGULAR VEINS he internal jugular veins are the major vessels responsible for the return of venous blood from the brain. he most common clinical indication for duplex and color Doppler low ultrasound of the internal jugular vein is the evaluation of suspected jugular venous thrombosis.248-256 hrombus formation may be related to central venous catheter placement. Other indications include a diagnosis of jugular venous ectasia254,255,257,258 and guidance for internal jugular or subclavian vein cannulation,259-265 particularly in diicult situations where vascular anatomy is distorted.

Sonographic Technique he normal internal jugular vein is easily visualized. he vein is scanned with the neck extended and the head turned to the contralateral side. Longitudinal and transverse scans are obtained with light transducer pressure on the neck to avoid collapsing the vein. A coronal view from the supraclavicular fossa is used to image the lower segment of the internal jugular vein and the medial segment of the subclavian vein as they join to form the brachiocephalic vein. he jugular vein lies lateral and anterior to the CCA, lateral to the thyroid gland, and deep to the sternocleidomastoid muscle. he vessel has sharply echogenic walls and a hypoechoic or

FIG. 26.55 Normal Jugular Vein. Complex venous pulsations in a normal jugular vein (J) relect the cycle of events in the right atrium.

anechoic lumen. Normally, a valve can be visualized in its distal portion.251,260,266 he right internal jugular vein is usually larger than the let.259 Real-time ultrasound demonstrates venous pulsations related to right heart contractions, as well as changes in venous diameter that vary with changes in intrathoracic pressure. Doppler examination graphically depicts these low patterns (Fig. 26.55). On inspiration, negative intrathoracic pressure causes low toward the heart and the jugular veins to decrease in diameter. During expiration and during Valsalva maneuver, increased intrathoracic pressure causes a decrease in the blood return, and the veins enlarge, with minimal or no low noted. he walls of the normal jugular vein collapse completely when moderate transducer pressure is applied. Sudden patient sniing reduces intrathoracic pressure, causing momentary collapse of the vein on real-time ultrasound, accompanied by a brief increase in venous low toward the heart as shown by Doppler.250,252,254

Thrombosis Clinical features of jugular venous thrombosis include a tender, poorly deined, nonspeciic neck mass or swelling. he correct diagnosis may not be immediately obvious.251 hrombosis of the internal jugular vein can be completely asymptomatic because of the deep position of the vein and the presence of abundant collateral circulation.254 Internal jugular thrombosis most oten results from complications of central venous catheterization.249,253,254 Other causes include intravenous drug abuse, mediastinal tumor, hypercoagulable states, neck surgery, and local inlammation or adenopathy.251 Some cases are idiopathic or spontaneous.251 Possible complications of jugular venous thrombosis include suppurative thrombophlebitis, clot propagation, and pulmonary embolism.251,255 Real-time examination reveals an enlarged, noncompressible vein, which may contain a visible echogenic intraluminal thrombus. An acute thrombus may be anechoic and

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FIG. 26.56 Internal Jugular Vein (IJV) Thrombosis: Spectrum of Appearances. (A) Transverse image of an acute left internal jugular vein thrombus (arrow). The vein is distended and noncompressible. C, Common carotid artery. (B) Longitudinal image of a different patient demonstrates a hypoechoic thrombus and no Doppler signal. (C) Longitudinal color Doppler image shows a small amount of thrombus arising from the posterior wall of the IJV. (D) Transverse image shows an echogenic thrombus, indicating chronic thrombus in IJV. (E) Longitudinal image demonstrates a thrombus (arrow) around jugular vein catheter. (F) Longitudinal images show a thrombus arising from anterior wall. This thrombus probably results from previous catheter placement in this region.

indistinguishable from lowing blood; however, the characteristic lack of compressibility and absent Doppler or color Doppler low in the region of a thrombus quickly lead to the correct diagnosis. In addition, there is visible loss of vein response to respiratory maneuvers and venous pulsation. Spectral and color Doppler interrogations reveal absent low (Fig. 26.56). Collateral veins may be identiied, particularly in cases of chronic internal jugular vein thrombosis. Central liquefaction or other heterogeneity of the thrombus also suggests chronicity. Chronic thrombi may be diicult to visualize because they tend to organize and are diicult to separate from echogenic perivascular fatty tissue.260 he absence of cardiorespiratory plasticity in a patent jugular or subclavian vein can indicate a more central, nonocclusive thrombus (Fig. 26.57). he conirmation of bilateral loss of venous pulsations strongly supports a more central thrombus, which can be documented by angiographic or magnetic resonance venography. A thrombus that is related to catheter insertion is oten demonstrated at the tip of the catheter, although it may be seen

anywhere along the course of the vein. he catheter can be visualized as two parallel echogenic lines separated by an anechoic region. Flow is not usually demonstrated in the catheter, even if the catheter itself is patent. Sonography is a reliable means of diagnosing jugular and subclavian vein thrombosis. Sonography has limited access and cannot image all portions of the jugular and subclavian veins, especially those located behind the mandible or below the clavicle, although knowledge of the full extent of a thrombus is not typically a critical factor in treatment planning.251,255 Serial sonographic examination to evaluate response to therapy ater the initial assessment can be performed safely and inexpensively. Sonography can also document venous patency before vascular line placement, facilitating safer and more successful catheter insertion.

Acknowledgment hanks to Kathleen McFadden and Barbara Siede for their assistance with manuscript preparation.

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FIG. 26.57 Normal and Abnormal Venous Waveforms in Three Patients. (A) Brachiocephalic vein has normal cardiorespiratory change in the venous waveforms, implying a patent superior vena cava. (B) Near-occlusive left central brachiocephalic vein stenosis caused by a prior central venous catheter. Pulsed Doppler waveform shows reversed nonpulsatile low in the internal jugular vein (IJV). (C) Left subclavian vein shows monophasic low with respiratory phasicity upon snifing.

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PART III

Small Parts, Carotid Artery, and Peripheral Vessel Sonography

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CHAPTER 26 154. AbuRahma AF, Richmond BK, Robinson PA, et al. Efect of contralateral severe stenosis or carotid occlusion on duplex criteria of ipsilateral stenoses: comparative study of various duplex parameters. J Vasc Surg. 1995;22(6):751-761. 155. van Everdingen KJ, van der Grond J, Kappelle LJ. Overestimation of a stenosis in the internal carotid artery by duplex sonography caused by an increase in volume low. J Vasc Surg. 1998;27(3):479-485. 156. Preiss JE, Itum DS, Reeves JG, et al. Carotid duplex criteria for patients with contralateral occlusion. J Surg Res. 2015;193(1):28-32. 157. Blackshear WM, Phillips DJ, Chikos PM, et al. Carotid artery velocity patterns in normal and stenotic vessels. Stroke. 1980;11(1):67-71. 158. Rubens DJ, Bhatt S, Nedelka S, Cullinan J. Doppler artifacts and pitfalls. Radiol Clin North Am. 2006;44(6):805-835. 159. Grubb Jr RL, Derdeyn CP, Fritsch SM, et al. Importance of hemodynamic factors in the prognosis of symptomatic carotid occlusion. JAMA. 1998;280(12):1055-1060. 160. Berman SS, Devine JJ, Erdoes LS, Hunter GC. Distinguishing carotid artery pseudo-occlusion with color-low Doppler. Stroke. 1995;26(3): 434-438. 161. Gortler M, Niethammer R, Widder B. Diferentiating subtotal carotid artery stenoses from occlusions by colour-coded duplex sonography. J Neurol. 1994;241(5):301-305. 162. AbuRahma AF, Pollack JA, Robinson PA, Mullins D. he reliability of color duplex ultrasound in diagnosing total carotid artery occlusion. Am J Surg. 1997;174(2):185-187. 163. Kliewer MA, Freed KS, Hertzberg BS, et al. Temporal artery tap: usefulness and limitations in carotid sonography. Radiology. 1996;201(2):481484. 164. Bebry AJ, Hines GL. Total occlusion of the common carotid artery with a patent internal carotid artery; identiication by duplex ultrasonography: report of a case. J Vasc Surg. 1989;10(4):469-470. 165. Blackshear Jr WM, Phillips DJ, Bodily KC, Strandness Jr DE. Ultrasonic demonstration of external and internal carotid patency with common carotid occlusion: a preliminary report. Stroke. 1980;11(3):249-252. 166. Lee DH, Gao FQ, Rankin RN, et al. Duplex and color Doppler low sonography of occlusion and near occlusion of the carotid artery. AJNR Am J Neuroradiol. 1996;17(7):1267-1274. 167. Alexandrov AV, Bladin CF, Maggisano R, Norris JW. Measuring carotid stenosis. Time for a reappraisal. Stroke. 1993;24(9):1292-1296. 168. Beach KW, Leotta DF, Zierler RE. Carotid Doppler velocity measurements and anatomic stenosis: correlation is futile. Vasc Endovascular Surg. 2012;46(6):466-474. 169. Gupta A, Baradaran H, Schweitzer AD, et al. Carotid plaque MRI and stroke risk: a systematic review and meta-analysis. Stroke. 2013;44(11): 3071-3077. 170. Saam T, Hetterich H, Hofmann V, et al. Meta-analysis and systematic review of the predictive value of carotid plaque hemorrhage on cerebrovascular events by magnetic resonance imaging. J Am Coll Cardiol. 2013;62(12):1081-1091. 171. McLaughlin MS, Hinckley PJ, Treiman SM, et al. Optimal prediction of carotid intraplaque hemorrhage using clinical and lumen imaging markers. AJNR Am J Neuroradiol. 2015;36(12):2360-2366. 172. Yuan C, Parker DL. hree-dimensional carotid plaque MR imaging. Neuroimaging Clin N Am. 2016;26(1):1-12. 173. Brinjikji W, Rabinstein AA, Lanzino G, et al. Ultrasound characteristics of symptomatic carotid plaques: a systematic review and meta-analysis. Cerebrovasc Dis. 2015;40(3-4):165-174. 174. Randoux B, Marro B, Koskas F, et al. Carotid artery stenosis: prospective comparison of CT, three-dimensional gadoliniumenhanced MR, and conventional angiography. Radiology. 2001;220(1): 179-185. 175. Nonent M, Serfaty JM, Nighoghossian N, et al. Concordance rate diferences of 3 noninvasive imaging techniques to measure carotid stenosis in clinical routine practice: results of the CARMEDAS multicenter study. Stroke. 2004;35(3):682-686. 176. Polak JF, Kalina P, Donaldson MC, et al. Carotid endarterectomy: preoperative evaluation of candidates with combined Doppler sonography and MR angiography. Work in progress. Radiology. 1993;186(2):333-338.

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177. Johnston DC, Goldstein LB. Clinical carotid endarterectomy decision making: noninvasive vascular imaging versus angiography. Neurology. 2001;56(8):1009-1015. 178. Kuntz KM, Skillman JJ, Whittemore AD, Kent KC. Carotid endarterectomy in asymptomatic patients—is contrast angiography necessary? A morbidity analysis. J Vasc Surg. 1995;22(6):706-714. 179. DeMarco JK, Spence JD. Plaque assessment in the management of patients with asymptomatic carotid stenosis. Neuroimaging Clin N Am. 2016;26(1):111-127. 180. Spence JD. Management of asymptomatic carotid stenosis. Neurol Clin. 2015;33(2):443-457. 181. Mattos MA, Hodgson KJ, Faught WE, et al. Carotid endarterectomy without angiography: is color-low duplex scanning suicient? Surgery. 1994;116(4):776-782. 182. Cartier R, Cartier P, Fontaine A. Carotid endarterectomy without angiography. he reliability of Doppler ultrasonography and duplex scanning in preoperative assessment. Can J Surg. 1993;36(5):411-416. 183. husay MM, Khoury M, Greene K. Carotid endarterectomy based on duplex ultrasound in patients with and without hemispheric symptoms. Am Surg. 2001;67(1):1-6. 184. Welch HJ, Murphy MC, Ratery KB, Jewell ER. Carotid duplex with contralateral disease: the inluence of vertebral artery blood low. Ann Vasc Surg. 2000;14(1):82-88. 185. Chen JC, Salvian AJ, Taylor DC, et al. Can duplex ultrasonography select appropriate patients for carotid endarterectomy? Eur J Vasc Endovasc Surg. 1997;14(6):451-456. 186. Johnson BL, Gupta AK, Bandyk DF, et al. Anatomic patterns of carotid endarterectomy healing. Am J Surg. 1996;172(2):188-190. 187. Kagawa R, Okada Y, Shima T, et al. B-mode ultrasonographic investigations of morphological changes in endarterectomized carotid artery. Surg Neurol. 2001;55(1):50-56. 188. Jackson MR, D’Addio VJ, Gillespie DL, O’Donnell SD. he fate of residual defects following carotid endarterectomy detected by early postoperative duplex ultrasound. Am J Surg. 1996;172(2):184-187. 189. Ricotta JJ, DeWeese JA. Is routine carotid ultrasound surveillance ater carotid endarterectomy worthwhile? Am J Surg. 1996;172(2):140142. 190. Lal BK. Recurrent carotid stenosis ater CEA and CAS: diagnosis and management. Semin Vasc Surg. 2007;20(4):259-266. 191. Kallmayer M, Tsantilas P, Zieger C, et al. Ultrasound surveillance ater CAS and CEA: what’s the evidence? J Cardiovasc Surg (Torino). 2014;55(2 Suppl. 1):33-41. 192. Goodney PP, Lucas FL, Travis LL, et al. Changes in the use of carotid revascularization among the Medicare population. Arch Surg. 2008;143(2): 170-173. 193. Murad MH, Shahrour A, Shah ND, et al. A systematic review and metaanalysis of randomized trials of carotid endarterectomy vs stenting. J Vasc Surg. 2011;53(3):792-797. 194. Ricotta JJ, Aburahma A, Ascher E, et al. Updated Society for Vascular Surgery guidelines for management of extracranial carotid disease: executive summary. J Vasc Surg. 2011;54(3):832-836. 195. Chaer RA, Derubertis BG, Trocciola SM, et al. Safety and eicacy of carotid angioplasty and stenting in high-risk patients. Am Surg. 2006;72(8): 694-698. 196. Wolf T, Guirguis-Blake J, Miller T, et al. Screening for carotid artery stenosis: an update of the evidence for the U.S. Preventive Services Task Force. Ann Intern Med. 2007;147(12):860-870. 197. Diethrich EB, Pauliina Margolis M, Reid DB, et al. Virtual histology intravascular ultrasound assessment of carotid artery disease: the Carotid Artery Plaque Virtual Histology Evaluation (CAPITAL) study. J Endovasc her. 2007;14(5):676-686. 198. Fleming SE, Bluth EI, Milburn J. Role of sonography in the evaluation of carotid artery stents. J Clin Ultrasound. 2005;33(7):321-328. 199. Peterson BG, Longo GM, Kibbe MR, et al. Duplex ultrasound remains a reliable test even ater carotid stenting. Ann Vasc Surg. 2005;19(6): 793-797. 200. Roi M, Greutmann M, Eberli FR, et al. Starting a carotid artery stenting program is safe. Catheter Cardiovasc Interv. 2008;71(4):469-473.

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Small Parts, Carotid Artery, and Peripheral Vessel Sonography

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226. Kwiatkowski J. Ultrasound screening helps prevent stroke in children with sickle cell disease. Science Centric. 2008;7. 227. Kalanuria A, Nyquist PA, Armonda RA, Razumovsky A. Use of transcranial Doppler (TCD) ultrasound in the neurocritical care unit. Neurosurg Clin N Am. 2013;24(3):441-456. 228. Lupetin AR, Davis DA, Beckman I, Dash N. Transcranial Doppler sonography. Part 2. Evaluation of intracranial and extracranial abnormalities and procedural monitoring. Radiographics. 1995;15(1):193-209. 229. Lin SK, Ryu SJ, Chu NS. Carotid duplex and transcranial color-coded sonography in evaluation of carotid-cavernous sinus istulas. J Ultrasound Med. 1994;13(7):557-564. 230. Mast H, Mohr JP, hompson JL, et al. Transcranial Doppler ultrasonography in cerebral arteriovenous malformations: diagnostic sensitivity and association of low velocity with spontaneous hemorrhage and focal neurological deicit. Stroke. 1995;26:1024-1027. 231. Gaunt ME, Martin PJ, Smith JL, et al. Clinical relevance of intraoperative embolization detected by transcranial Doppler ultrasonography during carotid endarterectomy: a prospective study of 100 patients. Br J Surg. 1994;81(10):1435-1439. 232. Bendick PJ, Glover JL. Hemodynamic evaluation of vertebral arteries by duplex ultrasound. Surg Clin North Am. 1990;70(1):235-244. 233. Lewis BD, James EM, Welch TJ. Current applications of duplex and color Doppler ultrasound imaging: carotid and peripheral vascular system. Mayo Clin Proc. 1989;64(9):1147-1157. 234. Visona A, Lusiani L, Castellani V, et al. he echo-Doppler (duplex) system for the detection of vertebral artery occlusive disease: comparison with angiography. J Ultrasound Med. 1986;5(5):247-250. 235. Davis PC, Nilsen B, Braun IF, Hofman Jr JC. A prospective comparison of duplex sonography vs angiography of the vertebral arteries. AJNR Am J Neuroradiol. 1986;7(6):1059-1064. 236. Yurdakul M, Tola M. Doppler criteria for identifying proximal vertebral artery stenosis of 50% or more. J Ultrasound Med. 2011;30(2): 163-168. 237. Bluth EI, Merritt CR, Sullivan MA, et al. Usefulness of duplex ultrasound in evaluating vertebral arteries. J Ultrasound Med. 1989;8(5):229-235. 238. Walker DW, Acker JD, Cole CA. Subclavian steal syndrome detected with duplex pulsed Doppler sonography. AJNR Am J Neuroradiol. 1982;3(6):615-618. 239. Kliewer MA, Hertzberg BS, Kim DH, et al. Vertebral artery Doppler waveform changes indicating subclavian steal physiology. Am J Roentgenol. 2000;174(3):815-819. 240. Gottesman RF, Sharma P, Robinson KA, et al. Imaging characteristics of symptomatic vertebral artery dissection: a systematic review. Neurologist. 2012;18(5):255-260. 241. Ackerstaf RG, Grosveld WJ, Eikelboom BC, Ludwig JW. Ultrasonic duplex scanning of the prevertebral segment of the vertebral artery in patients with cerebral atherosclerosis. Eur J Vasc Surg. 1988;2(6):387-393. 242. Elias DA, Weinberg PE. Angiography of the posterior fossa. In: Taverask JM, Ferrucci JT, editors. Radiology: diagnosis-imaging-intervention. Philadelphia: Lippincott; 1989. 243. Bendick PJ, Jackson VP. Evaluation of the vertebral arteries with duplex sonography. J Vasc Surg. 1986;3(3):523-530. 244. Carroll BA, Holder CA. Vertebral artery duplex sonography (abstract). J Ultrasound Med. 1990;9:S27-S28. 245. de Bray JM, Zenglein JP, Laroche JP, et al. Efect of subclavian syndrome on the basilar artery. Acta Neurol Scand. 1994;90(3):174-178. 246. homassen L, Aarli JA. Subclavian steal phenomenon. Clinical and hemodynamic aspects. Acta Neurol Scand. 1994;90(4):241-244. 247. Nicolau C, Gilabert R, Garcia A, et al. Efect of internal carotid artery occlusion on vertebral artery blood low: a duplex ultrasonographic evaluation. J Ultrasound Med. 2001;20(2):105-111. 248. Williams CE, Lamb GH, Roberts D, Davies J. Venous thrombosis in the neck. he role of real time ultrasound. Eur J Radiol. 1989;9(1):3236. 249. Hubsch PJ, Stiglbauer RL, Schwaighofer BW, et al. Internal jugular and subclavian vein thrombosis caused by central venous catheters. Evaluation using Doppler blood low imaging. J Ultrasound Med. 1988;7(11): 629-636.

CHAPTER 26 250. Gaitini D, Katori JK, Pery M, Engel A. High-resolution real-time ultrasonography. Diagnosis and follow-up of jugular and subclavian vein thrombosis. J Ultrasound Med. 1988;7(11):621-627. 251. Albertyn LE, Alcock MK. Diagnosis of internal jugular vein thrombosis. Radiology. 1987;162(2):505-508. 252. Falk RL, Smith DF. hrombosis of upper extremity thoracic inlet veins: diagnosis with duplex Doppler sonography. Am J Roentgenol. 1987;149(4):677-682. 253. Weissleder R, Elizondo G, Stark DD. Sonographic diagnosis of subclavian and internal jugular vein thrombosis. J Ultrasound Med. 1987;6(10): 577-587. 254. de Witte BR, Lameris JS. Real-time ultrasound diagnosis of internal jugular vein thrombosis. J Clin Ultrasound. 1986;14(9):712-717. 255. Wing V, Scheible W. Sonography of jugular vein thrombosis. Am J Roentgenol. 1983;140(2):333-336. 256. Chin EE, Zimmerman PT, Grant EG. Sonographic evaluation of upper extremity deep venous thrombosis. J Ultrasound Med. 2005;24(6): 829-838. 257. Gribbin C, Raghavendra BN, Ginsburg HB. Ultrasound diagnosis of jugular venous ectasia. N Y State J Med. 1989;89(9):532-533.

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258. Hughes PL, Qureshi SA, Galloway RW. Jugular venous aneurysm in children. Br J Radiol. 1988;61(731):1082-1084. 259. Jasinski RW, Rubin JM. CT and ultrasonographic indings in jugular vein ectasia. J Ultrasound Med. 1984;3(9):417-420. 260. Stevens RK, Fried AM, Hood Jr TR. Ultrasonic diagnosis of jugular venous aneurysm. J Clin Ultrasound. 1982;10(2):85-87. 261. Lee W, Leduc L, Cotton DB. Ultrasonographic guidance for central venous access during pregnancy. Am J Obstet Gynecol. 1989;161(4):1012-1013. 262. Bond DM, Champion LK, Nolan R. Real-time ultrasound imaging aids jugular venipuncture. Anesth Analg. 1989;68(5):700-701. 263. Machi J, Takeda J, Kakegawa T. Safe jugular and subclavian venipuncture under ultrasonographic guidance. Am J Surg. 1987;153(3):321-323. 264. Oh C, Lee S, Seo JM, Lee SK. Ultrasound guided percutaneous internal jugular vein access in neonatal intensive care unit patients. J Pediatr Surg. 2016;51(4):570-572. 265. Vezzani A, Manca T, Vercelli A, et al. Ultrasonography as a guide during vascular access procedures and in the diagnosis of complications. J Ultrasound. 2013;16(4):161-170. 266. Dresser LP, McKinney WM. Anatomic and pathophysiologic studies of the human internal jugular valve. Am J Surg. 1987;154(2):220-224.

CHAPTER

27

Peripheral Vessels Mark E. Lockhart, Heidi R. Umphrey, Therese M. Weber, and Michelle L. Robbin

SUMMARY OF KEY POINTS • Key aspects of vascular Doppler imaging include knowledge of anatomy and waveform morphology, scanning technique, and attention to detail. • Spectral Doppler velocity criteria can characterize stenosis detected by gray-scale and color Doppler. • Doppler evaluation of peripheral artery disease can provide diagnostic information and enable surgical planning and evaluation of bypass grafts. • Extremity aneurysm and pseudoaneurysm have typical Doppler indings similar to other areas of the arterial system. • Evaluation of the upper and lower extremity venous system is primarily performed with sonography.

• Differentiation of acute from residual or chronic deep venous thrombosis (DVT) with imaging and clinical parameters is often dificult. • Controversial venous issues include clinical criteria for treatment of DVT, when to recommend a follow-up examination, calf vein evaluation, and two-point or focused examination approach. • Preoperative sonographic mapping of upper extremity and thigh vessels assists surgical planning for placement of hemodialysis arteriovenous istula (AVF) and grafts. • Postoperative evaluation of hemodialysis AVF and grafts with ultrasound aids the assessment of AVF maturation, as well as evaluation for access stenosis, steal, thrombus, and focal complications.

CHAPTER OUTLINE PERIPHERAL ARTERIES Sonographic Examination Technique Stenosis Evaluation Lower Extremity Arteries Normal Anatomy Ultrasound Examination and Imaging Protocol Peripheral Arterial Occlusion Peripheral Arterial Stenosis Aneurysm Pseudoaneurysm Arteriovenous Fistula Lower Extremity Vein Bypass Grafts Upper Extremity Arteries Normal Anatomy Ultrasound Examination and Imaging Protocol Arterial Occlusion, Aneurysm, and Pseudoaneurysm Arterial Stenosis Subclavian Stenosis Thoracic Outlet Syndrome Radial Artery Evaluation for Coronary Bypass Graft

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PERIPHERAL VEINS Sonographic Examination Technique Lower Extremity Veins Normal Anatomy Ultrasound Examination and Imaging Protocol Acute Deep Venous Thrombosis Residual (Chronic) Deep Venous Thrombosis Potential Pitfalls Complete Venous Doppler Versus More Limited Examinations Recommendations for Deep Venous Thrombosis Follow-Up Venous Insuficiency Venous Mapping Upper Extremity Veins Normal Anatomy Ultrasound Examination and Imaging Protocol Upper Extremity Acute Deep Venous Thrombosis Differentiation of Acute From Residual or Chronic Venous Thrombosis

Potential Pitfalls HEMODIALYSIS Sonographic Examination Technique Vascular Mapping Before Hemodialysis Access Upper Extremity Ultrasound Examination and Imaging Protocol Arteriovenous Fistula and Graft Arteriovenous Fistula Graft Palpable Focal Masses Near Arteriovenous Fistula and Graft Arteriovenous Fistula Maturation Evaluation Arteriovenous Fistula and Graft Stenosis Arterial Steal Arm and Leg Swelling With Arteriovenous Fistula or Graft Arteriovenous Fistula and Graft Occlusion CONCLUSION

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rior chapters have described details of physics of Doppler analysis and use of ultrasound in the assessment of the vasculature supplying the head and neck. In this chapter we describe assessment of the peripheral arteries and veins, as well as arteriovenous istula (AVF) and grats. In general, these areas are readily evaluated by Doppler ultrasound. Because they are usually located at depths of 6 cm or less, the extremity vessels are more consistently imaged than those in the abdomen or thorax. Availability of suicient imaging windows allows the transducer to be placed over the vascular area of interest with overlying tissue containing bone or gas. Transducers with frequencies greater than 5 MHz can typically be used. Gray-scale sonography is useful for evaluating the presence of atherosclerotic plaque or conirming extravascular masses. Color low Doppler imaging allows for a rapid survey of the area of interest, and then spectral Doppler can be used to characterize blood low patterns. Standardized protocols, such as those provided by the American College of Radiology (ACR), American Institute of Ultrasound in Medicine, and Society of Radiologists in Ultrasound should be followed.1,2 It is recommended that examinations be performed in an accredited laboratory with participation in one of the vascular accreditation programs, such as the ACR or the Intersocietal Commission for the Accreditation of Vascular Laboratories, in order to achieve a national standard of excellence and to improve the chance of success of peripheral arterial and venous ultrasound examinations.3 In the setting of a dedicated staf and with physician support, ultrasound can be used to diagnose many peripheral vascular abnormalities deinitively and avoid the need for ionizing radiation or intravenous contrasted cross-sectional studies.

PERIPHERAL ARTERIES A variety of symptoms and signs can be evaluated by arterial ultrasound. Sonographic examination is relatively rapid and has beneits over other modalities, such as real-time technique, lack of ionizing radiation, and relatively low expense. In the last two decades, the number of indications for peripheral artery ultrasound has expanded. he most recent ACR practice parameter on the topic lists indications for the examination, which include claudication and/or rest pain in the lower extremities to evaluate for arterial stenosis or occlusion.2 Patients with pain, discoloration, or ulcer formation in the extremities (most commonly lower) may have tissue ischemia or necrosis from arterial stenosis or occlusion. Additional symptoms of numbness or cold extremity may be noted. However, symptomatology may vary depending on the rapidity of onset and whether collaterals have developed to decrease the efects of stenosis on the tissues. In some patients, vascular abnormalities may be subclinical and found incidentally on imaging for other indications. Once an abnormality has been identiied, ultrasound can monitor progression of disease, determine success or failure ater intervention, and identify acceptable vessels for bypass grat creation. Other extremity abnormalities can be evaluated sonographically. Focal masses can be assessed to exclude vascular causes such as aneurysm or istula with venous enlargement. When

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chronic positional upper extremity symptoms are present, ultrasound can evaluate for thoracic outlet syndrome. More peripherally, Doppler can document patency of the palmar arch in surgical planning for bypass grat harvesting, and it can assess the radial artery before and ater vascular access. In the acute setting, traumatic injuries can be evaluated to determine adjacent arterial patency. Pseudoaneurysms and dissections are visible by ultrasound in these patients. Speciic levels of embolic disease can also be depicted.

Sonographic Examination Technique Gray-scale evaluation of the peripheral arteries is important to determine the amount of atherosclerotic disease or thrombus present. he highest frequency transducer that allows good penetration and visualization should be applied, typically a 5- to 12-MHz linear array transducer, with a higher frequency transducer used in areas where the arteries are more supericial. Occasionally, a 3- to 5-MHz sector or curved array probe may be necessary in large patients or those with large amounts of edema. Occasionally, atherosclerotic plaque or thrombus is hypoechoic, and color Doppler is extremely useful to evaluate residual lumen, with the gain adjusted so color does not overlap into adjacent tissues. he spectral Doppler gate is adjusted within the lumen of the artery to allow adequate signal. he scale and gain should be optimized to show strong low signals that use most of the scale to display the waveform. Normally, a medium or high wall ilter is used in arterial evaluation. If there is slow low, a low wall ilter may be used to improve detection. In general, for detection of small channels of slow low in areas of near-occlusion, power Doppler may be more sensitive than color Doppler.4 However, the advances in color Doppler may have reduced this diference in recent years. he components of the sonographic evaluation difer based on the indication. For example, imaging for suspected arterial stenosis or occlusion is very diferent from evaluation of a focal mass or aneurysm. he technical components of the examination have been recently described in the ACR practice parameters.2

Stenosis Evaluation Color and spectral Doppler imaging are key to stenosis evaluation, using a combination of waveform morphology and velocity characteristics. On gray-scale imaging, a focal stenosis or occlusion may be visible, but this should be conirmed by Doppler. Collaterals should also prompt additional attention with Doppler. Any areas of visible narrowing or turbulent color Doppler signal should be further characterized with spectral Doppler. A change in spectral waveform morphology from one arterial segment to the next should also be further evaluated with color and spectral Doppler to locate a point of transition (Fig. 27.1). Spectral Doppler should be performed in the longitudinal plane and should be angle corrected 60% or less from the center beam. If a jet at or downstream from a stenosis is seen, angle correction parallel to the orientation of the jet should be performed to more accurately measure peak systolic velocity (PSV). Using this technique, waveform morphology and peak velocity should be evaluated at any suspected area of stenosis, as well as the feeding vessel

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Triphasic Normal Biphasic, low velocity, high resistance Distal obstruction

Inflow obstruction

Monophasic, low velocity, lower resistance

Monophasic, high velocity, lower resistance Arteriovenous fistula

Biphasic, reciprocating Pseudoaneurysm FIG. 27.1 Diagrams of Doppler Flow Patterns in Normal and Abnormal Scenarios. The normal Doppler spectrum of lowing blood in the lower extremity arteries typically has a triphasic pattern: (1) forward low during systole, (2) a short period of low reversal in early diastole, and (3) low-velocity low during the remainder of diastole. Arterial Doppler signals are altered depending on the pathologic change. The four other patterns are examples of common arterial pathologies: distal obstruction, inlow obstruction, arteriovenous istula, and pseudoaneurysm.

within 4 cm upstream, and the draining artery within 4 cm downstream. he inlow velocity is used as a reference to assess for increased peak velocity at the stenosis, and the downstream location is evaluated for peak velocity drop, decreased resistance, and tardus parvus morphology. he same concepts apply to bypass grats, when looking for stenosis and occlusion, with additional evaluation at the anastomoses, which are common sites of abnormality. Ultrasound is the primary screening for bypass abnormalities but can be a time-consuming study if used to cover all areas of concern in a patient with difuse atherosclerotic disease. If difuse atherosclerotic disease is suspected, other imaging techniques such as computed tomography (CT) or magnetic resonance angiography may be able to survey large areas more efectively.

Lower Extremity Arteries Normal Anatomy Each lower extremity arterial system is primarily supplied from the common femoral artery, which originates from the external

iliac artery at the level of the inguinal ligament and extends caudally a few centimeters until it divides into the supericial femoral artery (SFA) and profunda femoris artery. he profunda femoris artery supplies the femoral head and the deep muscles of the thigh through perforators, as well as the medial circumlex artery and the lateral circumlex artery. he SFA continues along the medial thigh to the adductor canal in parallel with the femoral vein (FV). Below the adductor canal, it becomes the popliteal artery, coursing posterior to the knee and supplying branches of the calf. he popliteal artery branches into the anterior tibial artery and the tibioperoneal trunk. he anterior tibial artery courses laterally, perforating through the interosseous membrane between the tibia and ibula into the anterior compartment of the lower leg. he anterior tibial artery becomes the dorsalis pedis artery in the dorsum of the ankle and along the irst intertarsal space of the foot. he tibioperoneal trunk divides ater approximately 3 to 4 cm into the posterior tibial artery and the peroneal artery. he posterior tibial artery courses posterior to the medial malleolus of the ankle. he peroneal artery courses through the interosseous membrane above the ankle, and then supplies branches of the lateral ankle and foot.

Ultrasound Examination and Imaging Protocol Lower extremity arterial inlow from the external iliac artery is assessed by groin insonation in supine position, and then each major vessel in the leg is directly evaluated throughout its entire course. Normal arteries have thin smooth walls with anechoic lumens and lack of atherosclerotic plaques or stenosis on grayscale imaging (Fig. 27.2). Ater gray-scale evaluation, long arterial segments can be screened rapidly with color Doppler to ind areas of suspected stenosis. Color Doppler is set to barely ill the lumen in a normal area of the artery. Color aliasing can alert the sonographer to areas of luminal narrowing that need to be evaluated further with spectral Doppler to determine signiicance. For evaluation of focal abnormalities other than stenosis, the examination may be limited to the general region of concern. he ACR-AIUM-SRU practice parameter for the performance of peripheral arterial ultrasound suggests that lower extremity ultrasound should examine the common femoral artery; the proximal, mid, and distal SFA; and the popliteal artery above and below the knee.2 Other arteries are examined as deemed clinically appropriate. he practice parameter states that these may include “iliac, deep femoral, tibioperoneal trunk, anterior tibial, posterior tibial, peroneal, and dorsalis pedis arteries.” he guideline further suggests that angle-corrected longitudinal Doppler and/or gray-scale imaging should be documented in each normal and at any abnormal segment. Angle-corrected spectral Doppler is recommended proximal to, at, and beyond any suspected stenosis.2 Supine position of the patient is acceptable for the thigh vessels, but a decubitus position may aid evaluation of the popliteal artery. Depending on the symptoms and indings of these arteries, imaging of the iliac arterial system may look for inlow disease, or imaging of the calf arteries may be indicated. Normal outer diameters of the common femoral artery, SFA, popliteal artery, posterior tibial artery, and anterior tibial artery

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FIG. 27.2 Normal Common Femoral Artery Bifurcation. (A) Gray-scale imaging shows the normal appearance of arterial wall with lack of plaque. (B) Color and spectral Doppler normal triphasic spectral waveform in the profunda femoris artery.

are 8.1 mm, 6.1 mm, 6.0 mm, 2.1 mm, and 2.0 mm, respectively, and these vessels are slightly larger in males.5 he common femoral artery, SFA, and popliteal artery become slightly larger with age, whereas the calf arteries become smaller.5 Laminar low is present without turbulence or aliasing on color Doppler. A high-resistance triphasic waveform with sharp upstroke and transient low reversal is typically present in the normal lower extremity arteries on spectral Doppler. A monophasic waveform morphology that does not return to baseline can occur ater exercise in normal patients, but can be also seen in lower extremity atherosclerotic disease. For diferentiation, the PSV will decrease in the ischemic limb of a patient with peripheral artery disease ater exercise, whereas it will increase in a patient with a healthy arterial system. For calf assessment, a posterior medial approach is used for the posterior tibial artery in the midcalf with longitudinal Doppler, and then the artery can be followed proximally and distally. Alternatively, it can be found at the medial malleolus at the ankle and followed cranially. An anterior transducer placement is applied for the anterior tibial artery with the patient lying supine. he anterior tibial artery is well seen along the interosseous membrane near the ibula. he peroneal artery can also be seen from this anterior probe placement; it is more deeply located posterior to the interosseous membrane. A posterior lateral approach may also be used to locate the peroneal artery.

Peripheral Arterial Occlusion Acute arterial occlusion is an emergent situation that can generate severe symptomatology and requires immediate attention. It is usually present in the setting of atherosclerotic disease, although traumatic dissection or embolic disease can occur (Fig. 27.3, Video 27.1). Use of Doppler allows for sensitive and speciic demonstration of absent low, and can diferentiate occlusion from stenosis in the lower extremity with 98% accuracy.6 In another study, sensitivities for occlusion of the SFA and popliteal artery were 97% and 83%, respectively.7 In the lower leg, Doppler

FIG. 27.3 Acute Thrombus in the Supericial Femoral Artery. Note the echogenic material within the arterial lumen. See also Video 27.1, which shows the thrombus to be slightly mobile.

performs better in the anterior and posterior tibial arteries than in the peroneal. Doppler sensitivity for patency of the tibial artery was 93% in a recent study, but with many false positives related to angiography.8 On gray-scale imaging, the anechoic lumen is typically illed with medium-echogenicity thrombus. Using a similar technique as generally performed for detection of deep venous thrombus, the artery can be externally compressed by the transducer to show focal thrombus that is noncompressible. However, if the artery walls completely coapt, then the indings are likely artifactual. On color and spectral Doppler of an occluded artery,

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no low signal should be detectable (Fig. 27.4). Collaterals suggest chronic occlusion, but there may be a superimposed acute-onchronic thrombotic component (Fig. 27.5, Video 27.2).

Peripheral Arterial Stenosis Detection of stenosis in the setting of atherosclerotic disease is important owing to its role as a precursor to occlusion. Ultrasound is the primary screening tool for detection of stenosis, using a combination of gray-scale, color, and spectral Doppler. Duplex Doppler should be performed in these patients because of its superior performance relative to segmental Doppler pressures.9 In a study of 151 lower extremities, duplex Doppler demonstrated 78% to 95% sensitivity and 97% to 100% speciicity for high-grade lower extremity arterial stenosis. Spectral broadening can be seen in nonlow-limiting stenoses less than 50%, with

B

FIG. 27.4 Occluded Popliteal Artery. (A) Spectral Doppler shows high-resistance low pattern upstream to the occlusion. (B) Occluded portion of the popliteal artery without low on spectral Doppler. (C) Tardus parvus pattern in the dorsalis pedis distal to the occluded popliteal artery indicates reconstitution of the artery by collaterals.

an otherwise normal waveform (Fig. 27.6). As regional measurements are made in the arteries of the lower extremity, there may be a change noted from normal triphasic arterial morphology to a pulsatile but monophasic waveform that does not return to baseline or demonstrate transient reversal (Fig. 27.7). When this transition is encountered, the artery between these two measurements should be more closely evaluated by color and spectral Doppler to locate a focal velocity elevation associated with visible narrowing of the artery. Gray-scale can characterize overall plaque burden, but calciications may limit sonographic penetration into the artery lumen (Fig. 27.8, Video 27.3). In a patient with difuse atherosclerotic disease and generalized calciications, there may be numerous mild stenoses that have a combined efect to reduce low pressures to the lower leg without a dominant stenosis. Gray-scale imaging is limited in its ability

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to measure narrowing of the vessel, and velocity and waveform criteria are more widely applied. Color Doppler improves the examination by rapidly depicting areas of turbulent or highvelocity low that can be further sampled by spectral Doppler for velocity characterization. he main criteria for characterizing arterial stenosis involve waveform morphology, PSV, and end-diastolic velocity (EDV). For velocity criteria, the absolute values and the peak velocity ratio (deined as peak velocity at or in the downstream jet divided by peak velocity of the artery 2 cm upstream) have both been applied efectively. In a study of 338 arterial segments, focal increase in the PSV ratio at the stenosis relative to the

adjacent nonstenotic artery exceeding 2.0 is consistent with at least 50% diameter stenosis when combined with spectral broadening and loss of transient low reversal in the artery10 (Fig. 27.9). he distal artery waveform will be abnormal with tardus parvus waveforms in the setting of stenosis greater than 50% (Fig. 27.10) but is typically normal if a lesser degree of stenosis is present.10 Direct measurement of PSVs can also be performed. For the femoral-popliteal region of native vessels, a combination of thresholds of PSV greater than 200 cm/sec and ratio above 2 : 1 have been suggested as criteria for greater than 70% stenosis with sensitivity of 79% and speciicity of 99%11 (Fig. 27.11).

FIG. 27.5 Occlusion of the Supericial Femoral Artery With a Large Collateral Exiting Proximal to the Occlusion (Arrow). The presence of a collateral suggests chronic occlusion. See also Video 27.2.

FIG. 27.6 Common Femoral Artery Stenosis. Color and spectral Doppler shows normal biphasic waveform, with ill-in of the waveform spectral envelope, indicating some degree of stenosis but less than 50%.

A

B

FIG. 27.7 Focal High-Grade Stenosis in the Proximal Supericial Femoral Artery (SFA). (A) Elevated peak systolic velocity at a focal high-grade stenosis in the proximal SFA. (B) Tardus parvus pattern downstream.

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Velocity

FIG. 27.8 Calciication of the Supericial Femoral Artery (SFA). (A) Severe calciication of the SFA limits ability to see within the artery lumen with gray-scale imaging. Color Doppler is useful to locate a place where spectral Doppler can be sampled. (B) Spectral Doppler of the artery has mild spectral broadening but otherwise normal triphasic waveform, without signiicant stenosis in this location. See also Video 27.3.

Time

Velocity

2 to 4 cm proximal

Time At the stenosis FIG. 27.9 Blood Flow Velocity Alterations Occur With Stenosis of at Least 50%. Proximal to the lesion, the low pattern is normal. At the stenosis, the peak systolic velocity increases in proportion to the degree of stenosis. Alterations in the diastolic portion of the Doppler waveform sampled at the lesion depend on the state of the distal arteries and the severity and geometry of the lesion; diastolic low may increase dramatically or may be almost absent.

Ultrasound can direct intervention in these patients. Patients with nonacute conditions can beneit from ultrasound to characterize subacute occlusion or embolic disease versus chronic ischemic disease to help the surgeon decide among therapies such as thrombectomy or bypass procedure.12,13 Mapping with Doppler before bypass is very useful. Lesions are characterized by severity using the Trans-Atlantic Inter-Society Consensus (TASC) guidelines.14 Isolated and short category A and B lesions typically are directed to endovascular repair, whereas more

complex or longer lesions, C and D, in general require bypass. In one study of 622 TASC C or D lesions, Doppler mapping successfully identiied lesions for intervention with sensitivity of 97% and speciicity of 99%.15 Similar high accuracy has been shown in other studies as well.16,17 Doppler can also predict which lesions are suitable for percutaneous transluminal angioplasty with good success.18,19 However, duplex assessment may underestimate the length of stenosis. he lesions treated by angioplasty are generally short

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FIG. 27.10 Iliac Artery Stenosis With Tardus Parvus Waveform. (A) Tardus parvus waveform in the right common femoral artery indicates severe upstream stenosis or occlusion. (B) Normal velocity biphasic waveform of the contralateral left common femoral artery indicates atherosclerotic disease is in right common or external iliac artery, and not in the aorta (unilateral abnormal waveform).

A

B

FIG. 27.11 Supericial Femoral Artery (SFA) With >70% Stenosis. (A) Moderately severe stenosis in the SFA with a peak systolic velocity (PSV) of 269 cm/sec. (B) At 4 cm upstream from the stenosis the PSV is 85.0 cm/sec, for a ratio exceeding 3 : 1, indicative of greater than 70% stenosis.

and isolated and have a diameter reduction of greater than 50%. In patients with endovascular intervention and stenting, Doppler can monitor success of the procedure and survey for recurrent stenosis at follow-up. In patients treated for critical limb ischemia, Doppler follow-up should occur every 3 months for the irst year.20 Normal triphasic waveforms at the ankle help exclude stenosis, but spectral Doppler is still performed even in the absence of symptoms. For evaluation of stenosis within a stented artery, the best Doppler criteria to characterize SFA in-stent stenosis of 80% or greater include a combination of PSV above

275 cm/sec and PSV ratio (the ratio of the highest PSV within the stent to the PSV in a disease-free arterial segment 3 cm above the stented area) above 3.5.21 In patients with stent repair of SFA stenosis, Doppler and CT angiography have strong agreement.22

Aneurysm An aneurysm occurs when weakness of the arterial layers allows expansion of the arterial caliber beyond normal limits. Aneurysms of the peripheral arteries are uncommon, but most are found in

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FIG. 27.12 Popliteal Artery Aneurysms. (A) Popliteal artery aneurysm measures 1.2 cm diameter (arrows). (B) In a different patient, a 3.7-cm popliteal artery aneurysm contains low-level echoes and is partially thrombosed (cursors).

the popliteal regions.23 Less commonly, aneurysms are present in the SFA. In more than half of patients with popliteal artery aneurysm, they are bilateral. An association exists between popliteal artery aneurysms and abdominal aortic aneurysm, and thus if a popliteal artery aneurysm is found, the abdominal aorta should be evaluated. here is also an association among peripheral artery aneurysm, tobacco use, and hypertension. Peripheral artery aneurysms may contain clot, which may result in distal emboli with or without sot tissue ischemia and infarction. In these cases, intervention is necessary regardless of aneurysm size. he walls of an aneurysm may calcify, and the presence of calciications may have some protective efects against rupture. On gray-scale ultrasound, an aneurysm may appear as a fusiform anechoic or hypoechoic mass along the course of an artery. he Doppler signal depends on the amount of thrombus, the size of the neck of the aneurysm, and presence of calciication. Aneurysms may be saccular and commonly occur at branch points. he normal popliteal artery measures 4 to 6 mm in diameter.24 A bulge or focal enlargement of 20% of the vessel diameter constitutes a simple functional deinition of an aneurysm (Fig. 27.12). Empirically, a 2-cm cutof has been used to determine need for intervention.25 For popliteal artery aneurysm, surgical exclusion (ligation of the aneurysm) is the traditional treatment and has high rates of success.26 However, a recent meta-analysis showed that endovascular repair has similar success.27 Doppler ultrasound can be used to monitor the success of the intervention.28 Aneurysm exclusion with covered stents is an increasingly used therapy in place of surgical intervention. Doppler ultrasound can be used to monitor the patency of the stent and conirm the exclusion of the aneurysm from the circulation.29,30

Pseudoaneurysm Pseudoaneurysm describes disruption of an artery with low in a space beyond the vessel wall. It may arise from any arterial structure and may occur with direct trauma or tumor or inlammatory erosion. Pseudoaneurysms are found in less than 1% of diagnostic angiography examinations and more commonly in coronary angiography.31 Pathologically, the arterial wall has been

at least partially breached. Outer arterial layers, perivascular tissues, clot, or reactive ibrosis contain the pseudoaneurysm sac.32 he mechanism of pseudoaneurysm formation has been well characterized. A hematoma forms adjacent to the artery at the point of injury. Eventual lysis of the clot results in pseudoaneurysm. A pseudoaneurysm is diferent from an aneurysm in that at least one layer of wall is disrupted. It difers from active extravasation in that blood within the pseudoaneurysm lows back into the feeding artery through a narrowed opening rather than into adjacent tissues. Arteriovenous communication, when present, is used to guide appropriate therapy. In patients with arteriovenous communication, thrombin repair is contraindicated owing to the potential for embolization of the thrombin into the venous system with resultant unintended regions of thrombosis. Gray-scale ultrasound is typically performed irst to identify the abnormality. he pseudoaneurysm can appear as a round or oval anechoic structure with or without associated thrombus. When present, thrombus appears isoechoic or hypoechoic; it may be located along the edge of the pseudoaneurysm lumen. Attention should be directed to these areas of extraluminal hematoma or any anechoic collections to determine if there are areas of low with color Doppler. If low is detected, spectral Doppler is next performed to characterize arterial versus venous low and to exclude a superimposed AVF. In the patent portion of a pseudoaneurysm, there may be turbulent or disorganized intraaneurysmal low with a “yin-yang” appearance. Communication of the sac with the adjacent artery occurs through a neck with a typical “to-and-fro” biphasic low on spectral Doppler33 (Fig. 27.13, Video 27.4). Measurement of the neck length and diameter of the neck of the artery is performed as part of the assessment before thrombin injection. A neck with larger diameter has clinical implications because these are less successfully treated by thrombin injection. If the sac is thrombosed, the neck may represent the only patent portion of the pseudoaneurysm. At least one-third of pseudoaneurysm require repair, but spontaneous closure is common for pseudoaneurysm smaller than 1.8 cm in diameter.34 If the sac is patent, ultrasound-guided thrombin

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FIG. 27.13 Common Femoral Artery Pseudoaneurysm. (A) Common femoral artery pseudoaneurysm with “yin-yang” color low pattern in the pseudoaneurysm (arrows). (B) Spectral Doppler of the pseudoaneurysm neck shows a high-velocity “to-and-fro” pattern. (C) Measurement of the length of the neck from the common femoral artery to the pseudoaneurysm (calipers). (D) Measurement of the diameter of the neck (calipers) off of the common femoral artery indicates size of hole in artery; a “rent” in the artery is less amenable to thrombin injection. It is preferable to measure the diameter in gray-scale because color may overestimate the diameter, but sometimes the neck cannot be seen without color (as in this case). See also Video 27.4.

injection into the pseudoaneurysm to thrombose is commonly performed, with a success rate of 94% to 97% without surgical intervention.35-37 Treatment with sonographically guided direct compression has been used in the past but is less successful (up to 85% pseudoaneurysm thrombosis).38

Arteriovenous Fistula he term “istula” describes an abnormal communication between the arterial and venous circulations. here is disruption through all layers of the arterial wall as well as a focal disruption of a nearby venous structure, allowing communication from high– arterial pressure to low-pressure veins. his communication bypasses the capillary bed. It can be congenital, acquired, or

rarely spontaneous in nature. Fistulas may be seen ater autologous vein bypass grating39 and do not appear to afect patency of the grat.40 In the absence of bypass grat, most are acquired and usually associated with a history of trauma.41 A traumatic arteriovenous istula may course from normal artery to normal vein in the setting of trauma, but congenital arteriovenous malformations (AVMs) may occur with associated abnormal vascular structures. Many are asymptomatic. However, symptomatic AVFs do not typically spontaneously resolve and oten require surgery.42 Gray-scale imaging may show very little arterial abnormality in a traumatic istula, but the cluster of dilated structures of an AVM can be identiied. In either abnormality, there may be venous

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FIG. 27.14 Common Femoral Artery to Common Femoral Vein Arteriovenous Fistula (AVF). (A) Color Doppler shows common femoral artery to common femoral vein AVF. Note the adjacent tissue vibration artifact (arrowheads). (B) Arterialized turbulent low is seen within the vein just downstream to the AVF. See also Video 27.5.

dilation. Color Doppler ultrasound is the best noninvasive imaging modality to evaluate AVF or AVM and may show a large cluster of tortuous vessels with abnormal hyperemic low. Spectral Doppler waveforms of the inlow arteries feeding the AVF may show low-resistance low because they bypass the capillary bed. Doppler can show arterialized waveforms in the venous structures near the AVF. Tissue vibration artifact is commonly seen with AVFs, consisting of color pixels erroneously placed in the adjacent sot tissue by the ultrasound scanner because of the marked turbulence of the AVF. If the tissue vibration artifact is seen, a search should be made for an AVF. he arterialized waveform may be better seen during the Valsalva maneuver because with the increased thoracic pressure it causes, normal antegrade venous low is decreased (Fig. 27.14, Video 27.5).

Lower Extremity Vein Bypass Grafts Bypass grats may use arterial segments or veins for arterial revascularization. Like bypass conduits in other portions of the body, these have potential complications that can limit their functionality. Failures soon ater surgery may result from poor bypass conduit selection or surgical technical factors such as poor selection of the sites for anastomosis. In addition, the valves of an autologous vein may not be fully lysed during surgical preparation. Although completion imaging is commonly performed at the time of surgery, a recent study showed no improvement in grat survival in patients with intraoperative completion angiography or ultrasound.43,44 In the longer term, ibrosis may occur at the site of a vein valve, or there may be intimal hyperplasia at an anastomotic region. If the bypass survives long enough, the underlying atherosclerotic disease may afect the bypass and inlow vessels to limit function. For synthetic grats, the characterization of occlusion is similar to the native vessels, with

absence of low on color or spectral Doppler. Echogenic thrombus may be identiied within the grat on gray-scale technique. Ultrasound is a good technique to identify lesions that are likely to result in native vein bypass grat failure. Once the arterial bypass grat has been created, ultrasound is the primary screening modality; Doppler surveillance with revisions when needed is cost-efective.45 he diagnosis depends on visible identiication of stenosis on gray-scale imaging in combination with characterization by color and spectral Doppler. Normal triphasic or biphasic waveforms in the ankle arteries distal to the bypass suggest patency of the bypass. Generalized reduced or monophasic low velocities in a grat are concerning for disease, and further search for a focal abnormality should be performed. Color Doppler sonography can be used to search for areas of aliasing, and subsequent spectral Doppler evaluation for velocity changes is then performed. When a stenosis is detected in a nonbranching vessel, a velocity ratio can be applied to evaluate signiicance. he PSV ratio is calculated by dividing the PSV at the stenotic site by peak velocity in the grat 2 cm upstream. A PSV ratio of at least 2.0 corresponds to at least 50% diameter stenosis.46,47 Likewise, a PSV above 180 cm/sec has been associated with stenosis of greater than 50% diameter47 in lower extremity bypass vein grats (Fig. 27.15, Video 27.6). Several ultrasound parameters, including PSV ratio, are associated with future bypass grat dysfunction. Once the PSV ratio measures at least 3.5 to 4.0, showing severe stenosis, treatment should be considered if it has not been performed at less severe degrees of stenosis, even in less symptomatic patients.46,47 A recent study of Doppler and CT showed that patients with PSV ratio above 3.5 were at high risk for grat failure, whereas high-grade stenosis on CT did not correlate as well with grat failure.48 Velocity criteria for severe stenosis used by Wixon and

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colleagues suggest that PSV above 300 cm/sec and PSV ratio above 3.5 should direct the patient to intervention of a vein grat stenosis. In patients who meet these criteria, the intervention should be immediate if low velocity within the grat falls below 45 cm/sec.45 Decreased low relative to a prior study is also a worrisome inding on spectral Doppler. In surveillance of vein grats by Doppler with intervention on stenotic lesions, there is increased survival of the surveillance group. In patients with greater than 70% stenosis, 100% of grats failed without revision, but only 10% failed with ultrasound detection and a subsequent revision pathway.49 Patients with venous bypass grat may form pseudoaneurysms or true aneurysms, but these are rare. When present, they occur most frequently in the anastomotic regions. In a study of saphenous vein grats, only 10 of 260 (4%) developed true arterial aneurysm,50 with higher incidence in patients with preexisting aneurysm and in males. he average time to diagnosis was 7 years ater grat placement.51

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FIG. 27.15 Supericial Femoral Artery Bypass Graft. (A) Color and spectral Doppler show normal biphasic low in the proximal bypass graft, with a peak systolic velocity of 83.5 cm/sec. (B) Grayscale imaging in the midcalf shows a focal area of narrowing or thrombosis (arrow). (C) Spectral Doppler at the stenosis with aliasing and a peak velocity of 253 cm/sec, consistent with at least 50% stenosis. See also Video 27.6.

Upper Extremity Arteries Normal Anatomy Each upper extremity arterial system is supplied from either the brachiocephalic artery (right) or the subclavian artery (let) in patients without normal anatomic variations. he artery is anterior to the vein when insonated from the supraclavicular fossa. he subclavian artery courses laterally and becomes the axillary artery once it is beyond the lateral margin of the irst rib. he axillary artery courses medially over the proximal humeral head to the inferior margin of the pectoralis muscle, where it becomes the brachial artery. he brachial artery typically courses along the medial upper arm to the antecubital fossa and divides into the radial, ulnar, and smaller interosseous arteries. Occasionally, there is high brachial artery bifurcation above the antecubital fossa52 (Fig. 27.16). Regardless of the level of origin, the radial and ulnar branches extend to the wrist. On gray-scale imaging, normal upper extremity arteries have smooth

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FIG. 27.16 High Brachial Artery Bifurcation. High brachial artery bifurcation, with two arteries (A) (radial and ulnar) and their paired accompanying veins (V), above the antecubital fossa.

walls with anechoic lumens and lack of atherosclerotic plaques or stenosis, similar to lower extremity arteries. Laminar low is present without turbulence or aliasing on color Doppler. A similar high-resistance triphasic waveform with sharp upstroke and transient low reversal is typically present in the upper extremity arteries on spectral Doppler.

Ultrasound Examination and Imaging Protocol Higher frequency imaging is usually possible owing to decreased size of the arm with respect to the leg. he subclavian artery, axillary artery, and brachial artery are evaluated to the level of the elbow. Both upper extremities should usually be insonated so that the symptomatic side can be compared with the asymptomatic. he ipsilateral innominate artery should be evaluated to determine an abnormal inlow etiology of the problem when the subclavian artery waveform is abnormal. In the forearm, imaging of the radial and ulnar arteries is the key to most diagnoses. he ACR-AIUM-SRU practice parameter for the performance of peripheral arterial ultrasound suggests that upper extremity ultrasound should examine the subclavian artery, axillary artery, and brachial artery.2 Other arteries are examined as deemed clinically appropriate. It states that these may include “innominate, radial, and ulnar arteries, and the palmar arch.” he guideline further suggests that angle-corrected longitudinal Doppler and/ or gray-scale imaging should be documented in each normal and at any abnormal segment. Angle-corrected spectral Doppler is recommended proximal to, at, and beyond any suspected stenosis.2 Arterial Occlusion, Aneurysm, and Pseudoaneurysm Upper arm arterial occlusion is usually the result of trauma, oten iatrogenic. he rate of radial artery occlusion ater artery access for coronary angiography may be as high as 30.5%, although lower rates are also reported in the literature.53 For surgical bypass harvest planning, documentation of patency of the palmar arch is an additional component. For detection and characterization of arterial aneurysm, the maximal outer diameters of the aneurysm should be measured in transverse (short axis) with gray-scale

technique. Doppler can diferentiate the patent component from mural thrombus. In pseudoaneurysm characterization, the size and Doppler components are also measured, but the pseudoaneurysm neck is also evaluated with spectral Doppler as detailed earlier in the section on lower extremity arteries (Fig. 27.17, Video 27.7 and Video 27.8). If there is concern for AVF, both the arterial inlow portion and venous outlow should be characterized by duplex Doppler within several centimeters of the pseudoaneurysm, because the characteristic arterialization of the downstream venous waveform may be dampened farther away from the istula. Turbulent low through the istula may afect surrounding tissues causing a tissue reverberation artifact, which may be the irst clue that an AVF is present.

Arterial Stenosis Atherosclerotic disease can cause upper extremity stenosis but is a less common problem in the arm than encountered in the lower extremities. Gray-scale indings are similar to the lower extremities and include intimal plaques and/or visible irregularity of the vessel lumen. Color Doppler may show aliasing with turbulent low similar to those indings seen in lower extremity arterial stenosis. On spectral Doppler, velocity criteria are not well deined for the upper extremity arteries. However, for a stenosis in most nonbranching arteries, a greater than 2 : 1 PSV ratio of the stenosis relative to the upstream artery within 2 to 4 cm is consistent with at least 50% diameter stenosis. Depending on the timing and whether collaterals have formed, this degree of stenosis may or may not be symptomatic or clinically signiicant (Fig. 27.18). Subclavian Stenosis Subclavian stenosis most commonly occurs proximal to the origin of the let vertebral artery. In a subset of patients, low to the arm is provided by illing through the vertebral artery via retrograde low. If this reversed low is signiicant, there can be a steal phenomenon (“subclavian steal”) from the brain, leading to dizziness with certain arm movements as additional low is diverted to the arm. In these patients, the vertebral artery waveform should be insonated (Fig. 27.19, Video 27.9). Transient early systolic deceleration with resultant transient cessation of antegrade low or transient reversal of low (Fig. 27.20) correlated with subclavian artery mean diameter stenosis of 72% and 78%, respectively.54 Similar stenosis can occur in the right subclavian artery, but less frequently. If these abnormal vertebral artery waveforms are seen, an attempt should be made to directly visualize a stenosis by gray-scale and duplex Doppler in the subclavian artery itself. Thoracic Outlet Syndrome In distal upper extremity ischemic symptoms, embolic or traumatic injury (commonly iatrogenic) to the artery should also be considered. If embolic phenomena are seen, evaluation for thoracic outlet syndrome should be considered. In patients with symptoms elicited by speciic positioning of the arm, thoracic outlet syndrome is a form of arterial stenosis that should be considered. It occurs by external compression of the artery by adjacent muscles during abduction of the arm, and this narrowing

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can afect the waveform morphology of the downstream arteries.55 Bone and rib anomalies frequently contribute to the pathology.56 he velocities in the artery should be evaluated during adduction or neutral position then compared with velocities and waveforms in abduction. Over time, the artery may become injured, and this can lead to occlusion and formation of emboli, which may also be visible sonographically. hese emboli can then migrate distally within the upper extremity to cause pain in regions such as the hand. For sonographic evaluation of thoracic outlet syndrome in the proper clinical presentation, it is important to begin by insonating the arteries with the arm in neutral position for baseline waveform characterization. Waveforms are acquired from the forearm arteries with the patient sitting comfortably in an upright, seated position. Once the baseline morphology is clearly deined, the arm is moved into the inciting position, usually with abduction and elevation of the arm with external rotation. A combination of inspiration, breath holding, neck extension, and neck turn to the afected side, known as the Adson maneuver, may elicit a positive inding on Doppler.57 he

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FIG. 27.17 Radial Artery Pseudoaneurysm. (A) Large radial artery (*) pseudoaneurysm with rent in arterial wall (arrows). (B) Color Doppler shows typical “yin-yang” low in pseudoaneurysm. (C) “To-and-fro” low in pseudoaneurysm neck. See also Video 27.7 and Video 27.8.

waveform is monitored as the arm is moved into a variety of positions to elicit symptoms. If abnormal waveforms are not readily apparent, a variety of positions should be tested (Fig. 27.21). If positive, a diminished waveform should be apparent in the arteries of the forearm. Once this has been identiied, it may be helpful to repeat the baseline and positive results to show reproducibility of the indings. Further support of the diagnosis includes visible narrowing identiied in the subclavian artery, or the presence of an aneurysm in this region, if found.58 Pseudoaneurysms are frequently present in the setting of thoracic outlet syndrome and can lead to embolic events. Care must be taken in the diagnosis because hyperextension can produce arterial low abnormality in up to 20% of normal volunteers.59

Radial Artery Evaluation for Coronary Bypass Graft Another use of Doppler in bypass patients is to determine suitability of the radial artery for coronary artery grating. he ulnar artery typically provides the dominant source of blood

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low to the hand. he ulnar artery supplies the supericial palmar arch, which is oten incomplete. he radial artery supplies the deep palmar arch, which is more commonly complete, in communication with the ulnar artery. If the supericial palmar arch in the hand is patent, thus allowing low to the entire hand through the ulnar artery, then the radial artery is harvested. hus evaluation of palmar arch patency is necessary before harvest. Doppler evaluation of patency is more accurate than the modiied Allen test on physical examination, because only about 5 of 43 (12%) patients with an abnormal modiied Allen test result will have abnormal Doppler indings.60 A small linear array 12- to 15-MHz “hockey stick” transducer initially is used to determine antegrade low of the ulnar artery and radial artery at the wrist. With duplex Doppler, arterial low to the hand in the supericial palmar arch at the thenar eminence near the crease of the base of the thumb is characterized irst with normal distal radial artery inlow. Subsequently, the radial artery is transiently occluded by direct compression of the radial

B

FIG. 27.18 Subclavian Artery Stenosis Due to Atherosclerotic Disease. (A) Focal hypoechoic approximately 50% stenosis (arrow) in the proximal subclavian artery, outlined by color Doppler. (B) Peak systolic velocity (PSV) elevation at 208 cm/sec at stenosis. (C) PSV 2 cm upstream (proximal) to stenosis is 89.1 cm/sec for a PSV ratio of greater than 2 : 1.

artery at the wrist, and the resultant spectral Doppler waveform is evaluated. Care should be taken during examination not to hyperextend the hand with regard to the wrist, because a falsenegative examination inding may incorrectly suggest lack of patency of the arch. In patients with a patent supericial palmar arch, there should be reversed low of the radial artery in the hand, measured at the thenar eminence or in the region of the snuf box between the irst metacarpal and second carpal bone.61,62 If there is no low or absent reversed low, then the radial artery of that upper extremity is not suitable for harvest owing to an incomplete arch (Fig. 27.22). Increased low in the ulnar artery may also occur during radial artery compression if the arch is patent.63

PERIPHERAL VEINS Evaluation of the upper and lower extremity venous system is primarily performed with sonography. Useful applications

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FIG. 27.19 Subclavian Steal Phenomenon. (A) Reversed low in the right vertebral artery. Note that artery and vein are the same color, indicating abnormal low direction in one of the vessels. (B) Magnetic resonance imaging conirms signiicant stenosis in the subclavian artery just distal to the vertebral artery (arrow). See also Video 27.9.

FIG. 27.20 Subclavian Steal With Transient Flow Reversal in the Vertebral Artery.

include evaluation for thrombus, localization for venous access procedures, preoperative venous mapping for hemodialysis AVF and grat placement, and postoperative hemodialysis AVF and grat assessment. Key aspects of venous Doppler imaging include knowledge of anatomy, scanning technique, and attention to detail. he most common indication for venous Doppler ultrasound is to identify deep venous thrombosis (DVT). Undiagnosed and untreated DVT can result in fatal pulmonary embolism (PE). Sudden death is the irst symptom in about 25% of people who have PE64 (Fig. 27.23). Clinical evaluation of the peripheral venous system is frequently diicult, nonspeciic, and oten inaccurate. Clinical decision rules to improve pretest probability are recommended by the American College of Physicians and the American

Academy of Family Physicians.65-67 he Wells criteria generate a score for certain physical examination indings and pertinent clinical history.68 Clinical factors associated with increased probability of DVT include active cancer, immobilization, localized tenderness along the distribution of the deep venous system, swollen extremity, pitting edema localized to the symptomatic extremity, collateral supericial veins, and previously documented DVT. A modiication of the Wells score creates two groups: DVT unlikely or DVT likely.69 Current guidelines recommend a D-dimer test for those with low risk.70,71 he D-dimer test measures a degradation product of ibrin and has a high negative predictive value that is sensitive, but not speciic for DVT.72 If the D-dimer test result is positive, the patient should be evaluated with venous Doppler. As with patients without cancer, the combination of low probability and negative D-dimer result can exclude DVT in cancer patients.73,74 In practice, many patients do not undergo this workup.75 Going directly to sonography is frequently faster than waiting for workup results and may ofer an alternative musculoskeletal diagnosis such as popliteal fossa cyst. Also, in cases of technically limited sonographic evaluation of the more central deep venous system (iliac veins and inferior vena cava [IVC]), magnetic resonance venography or CT venography may be more sensitive.76

Sonographic Examination Technique he supericial location of the upper and lower venous system allows the use of linear, higher frequency transducers. he highest frequency linear transducer that still gives adequate penetration should be used to optimize spatial resolution. Typically the examination is best performed using a 5- to 10-MHz linear array transducer, with application of the higher frequency range in upper arm, forearm, calf, and more supericial veins. A curved array or sector probe in the 3- to 5-MHz range may be necessary

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FIG. 27.21 Thoracic Outlet Syndrome. (A) Normal baseline subclavian artery waveform. (B) Altered waveform during hyperextension, with compression against the clavicle causing stenosis.

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FIG. 27.22 Radial Artery Evaluation for Coronary Bypass Graft. (A) Patent palmar arch, with reversal of low in the supericial palmar arch on radial artery compression at the wrist. (B) Incomplete palmar arch, with lack of low in the supericial palmar arch on radial artery compression at the wrist.

in very large patients or those with substantial extremity edema. Gray-scale imaging should include compression and should be performed in the transverse plane. Color low and spectral analysis are the most common applications of Doppler sonography, with occasional use of power Doppler. Both techniques evaluate the disease process in the peripheral veins and give additional information regarding altered venous hemodynamics. Anatomic and functional detail makes sonography a valuable tool. Color Doppler sonography can be used to evaluate venous segments that cannot be directly assessed by compression, such as the subclavian veins. Power Doppler provides improved detection of very slow low, especially in small veins. All spectral Doppler waveforms should be obtained in the longitudinal plane.

Lower Extremity Veins Normal Anatomy Deep Venous System. he venous anatomy of the leg is illustrated in Fig. 27.24. he common femoral vein (CFV) begins at the level of the inguinal ligament as the continuation of the external iliac vein and extends caudally to the bifurcation into the femoral vein (FV) and the profunda femoris vein, which lie medial to the adjacent artery. he FV courses medially to the adjacent artery through the adductor canal in the caudal thigh. he term “femoral vein,” previously called the “supericial femoral vein,” should be used to avoid clinical confusion regarding the deep versus supericial venous system.77 he popliteal vein (PV) represents the continuation of the FV ater its exit from the adductor canal in the posterior caudal thigh. he PV is located supericial

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FIG. 27.23 Pulmonary Emboli. (A) Axial CT with contrast shows a large saddle pulmonary embolus extending into the left and right pulmonary arteries (arrows). (B) Maximum-intensity projection coronal CT with contrast in the same patient shows extent of bilateral pulmonary emboli (arrows).

Common femoral vein

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Great saphenous vein

A Profunda femoris vein Femoral vein Adductor magnus muscle

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B Adductor canal

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Popliteal vein

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Anterior tibial veins Small saphenous vein

D Peroneal veins Posterior tibial veins

E FIG. 27.24 Venous Anatomy of the Lower Extremity.

to the artery and courses through the popliteal space into the proximal calf. Duplication of the FV can be seen in about 30% of patients.78 Duplication of the FV can also be segmental. It has been shown that these anatomic variants are associated with increased incidence of DVT.79,80 About 40% of patients with multiple vessels within the popliteal fossa arise from a high conluence of the posterior tibial and peroneal veins, rather than true PV duplication.78 Description of these anatomic variants assists in avoiding a missed diagnosis on follow-up examinations. he paired anterior tibial veins arise from the PV and course laterally along the anterior calf to the dorsum of the foot. he tibioperoneal trunk originates from the PV slightly caudal to the anterior tibial veins and bifurcates into the paired posterior tibial veins and peroneal veins. he peroneal veins course medial to the posterior aspect of the ibula, whereas the posterior tibial veins course through the posterior calf muscles posterior to the tibia and along the medial malleolus. Deep veins in the gastrocnemius and soleus calf muscles do not have an adjacent artery and are a common site of acute calf vein thrombus in postoperative or high-risk patients.81 Supericial Venous System. Anatomic terminology for the lower extremity supericial venous system was standardized in 2002. he great and small saphenous veins and their branches comprise the supericial venous system of the lower extremities.82 he great saphenous vein (GSV) empties into the medial aspect of the CFV in the proximal thigh superior to the bifurcation of the CFV. he GSV courses along the medial thigh and calf. he normal GSV typically is 1 to 3 mm in diameter at the level of the ankle and 3 to 5 mm in diameter at the saphenofemoral junction. hese measurements are important when performing saphenous vein mapping for harvesting an autologous vein grat. he small saphenous vein has a variable insertion into the posterior aspect of the PV and courses along the dorsal calf to the ankle. Measurements for the small saphenous vein are typically

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1 to 2 mm in diameter inferiorly and 2 to 4 mm at the saphenopopliteal junction. In cases of supericial venous insuiciency, both the GSV and small saphenous vein can become abnormally enlarged and tortuous.

Ultrasound Examination and Imaging Protocol he choice of transducer depends on the patient’s body habitus and depth of the vessel to be studied. Typically a high-resolution 5- to 7.5-MHz linear array transducer will be used. For larger patients a lower-frequency (2.5- or 3.5-MHz) curvilinear transducer may be needed. Appropriate gain settings are needed to ensure that the vessels show no artifactual internal echoes and that thrombus is not mistaken for echoes caused by slow-lowing blood. Color Doppler imaging settings must be optimized for sensitivity to slow, low-volume low. he lower extremity deep venous system should be evaluated from just above the inguinal ligament to the bifurcation of the PV in the upper calf, including compression, color, and spectral Doppler sonography with assessment of respiratory phasicity. he cranial profunda femoris vein and cranial GSV should also be examined. Ultrasound evaluation of the external iliac veins and IVC is helpful to determine extent of documented CFV when the top of the thrombus is not seen in the CFV. he patient is examined in the supine position with the leg abducted and externally rotated with slight lexion of the knee. he most important portion of the examination is venous grayscale compression. he veins of the deep system are compressed in the transverse plane and evaluated in a stepwise fashion every 1 to 2 cm through the level of the adductor canal (Fig. 27.25, Video 27.10). Pressure on the skin with the transducer should be applied to collapse the vein. If the adjacent artery is deforming, pressure application is adequate. Color Doppler is then performed in selected segments to evaluate for patency and any nonocclusive

or hypoechoic thrombus not seen on the gray-scale images. he spectral Doppler waveform obtained is assessed for respiratory phasicity and cardiac pulsatility. he PV is best evaluated with the patient’s leg bent in a frog leg position. Applying hand pressure to the posterior surface of the leg when imaging the adductor canal or creating simulated augmentation by asking the patient to “step on the gas” may aid in visualizing the vein if the veins are diicult to see because of slow low, increased depth, or signiicant edema.83 Ultrasound evaluation of the calf veins remains controversial owing to uncertain clinical value and cost-efectiveness. he ACR practice guidelines do not require evaluation of the calf veins. At a minimum, all symptomatic areas should be evaluated, including the calf, to determine the source of symptoms such as supericial varicosities, and thrombophlebitis. Some institutions that routinely evaluate the calf veins start at the PV and track the paired anterior tibial veins, posterior tibial veins, and peroneal veins to the ankle. Calf imaging has become more common and is required for accreditation by the Intersocietal Accreditation Commission,84 but there is not a standard study protocol.85 he American College of Chest Physicians guideline for antithrombotic therapy does not favor routine venous Doppler of the calf veins.65 he more benign natural history of calf venous thrombosis favors management with serial sonographic examination with treatment only if proximal DVT is demonstrated. If calf venous thrombosis is detected, the interpreting physician may not know whether a patient with calf venous thrombosis will be treated. A suggested general statement may include, “If this calf venous thrombosis is not treated, a follow-up in 1 week is recommended to evaluate for progression.”85 Imaging Protocol. he lower extremity venous imaging protocol includes the following images for each deep venous segment:

FIG. 27.25 Normal Femoral Vein (FV) Compression. Dual transverse image showing noncompressed (left) and compressed FV. (FV is completely compressed in right panel and thus not seen; location marked by arrow.) Accompanying Video 27.10 shows the compression maneuver. A, Supericial femoral artery; V, femoral vein.

CHAPTER 27 1. Transverse gray-scale image at rest and with compression, or a cine clip of the compression maneuver, of the saphenofemoral junction, CFV, FV (at minimum proximal and distal), and PV. 2. Longitudinal color Doppler with spectral waveform analysis. a. CFV at the level of the saphenofemoral junction and distal portions. If only a unilateral examination is requested, the contralateral CFV is also evaluated. b. PV at a minimum. Consider recording FV as well. c. A separate compression image of the profunda femoris vein at the bifurcation with the FV is not typically obtained, but patency is evaluated on the longitudinal color and spectral Doppler waveform of the CFV bifurcation into the proximal FV and profunda femoris vein. d. If a thrombus is seen in the CFV, the most proximal extent of thrombus should be demonstrated with inclusion of the external iliac veins and IVC in the evaluation.

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e. Document additional musculoskeletal indings (such as popliteal cyst, knee joint efusion, or hematoma if present in the region being evaluated).

Acute Deep Venous Thrombosis here are four indings of acute venous thrombosis: (1) intraluminal material that is deformable during compression, (2) dilation of the vein, (3) smooth intraluminal material, and (4) free tail loating proximally from the attachment of the clot on the vein wall.85 he classic gray-scale indings of acute DVT are noncompressibility of the vessel with direct visualization of the thrombus. With complete acute vein thrombosis, the vein will typically enlarge. hrombi may completely or partially occlude the lumen, may be adherent to the wall, or may be free loating (Fig. 27.26, Video 27.11). Compression ultrasound for DVT has been shown to have 95% accuracy with 98% speciicity.86

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FIG. 27.26 Acute Deep Venous Thrombosis (DVT). (A) Acute common femoral vein (CFV) thrombus: Compression image in the transverse plane shows acute CFV thrombus. Note that the vein (arrows) is larger than the adjacent artery (A). (B) Longitudinal color Doppler image in the same patient shows acute nearly occlusive common femoral vein thrombus with little low. See also Video 27.11. (C) Longitudinal image of acute DVT in the profunda femoris vein (*), with nonocclusive extension into the CFV (arrow), and a small amount of thrombus in the femoral vein as well. (D) Transverse color image of acute popliteal vein DVT, with expansion of the vein (arrow) relative to the popliteal artery (A).

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hrombus within the proximal GSV may be treated as a DVT if within several centimeters of the insertion of the GSV, or more than 5 cm long, according to physician preference.65 If the thrombus within the GSV extends into the CFV, it should be treated as a DVT (Fig. 27.27, Video 27.12). If the top of the thrombus is not seen in the CFV or external iliac vein, an IVC and iliac vein examination should be considered to assess for more central thrombus (Fig. 27.28, Video 27.13).

Residual (Chronic) Deep Venous Thrombosis Diferentiation of acute from residual or chronic DVT with imaging and clinical parameters is oten diicult. With compression ultrasound, both acute and chronic DVT may show noncompressibility of the vessel. Wall thickening and smaller caliber vein suggest residual or chronic DVT (Fig. 27.29). Because vein noncompressibility can be seen in both acute and chronic DVT, an attempt to diferentiate the two is important for the appropriate therapeutic decision. As the thrombus evolves, it loses bulk and the vein may return to normal size or may become smaller in caliber owing to scarring (Fig. 27.30, Video 27.14).

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Residual thrombus will become broadly adherent to the vein wall. Additional chronic indings that may assist in differentiating chronic from acute DVT are echogenic weblike illing defects within the vein (Fig. 27.31), collateral vessels (Fig. 27.32, Video 27.15), and valvular damage with relux and subsequent chronic deep venous insuiciency.23 Diferentiation of acute versus residual or chronic thrombus cannot be performed on thrombus echogenicity alone, although if calciications are present, there is at least an element of chronic thrombus present87 (Fig. 27.33). If the thrombus is small (several centimeters or less), measurement may be helpful to aid the clinician in determining clinical importance, especially ater catheter removal.

Potential Pitfalls Lower extremity potential pitfalls to avoid include the following: 1. Very slowly lowing blood may mimic the appearance of clot (Fig. 27.34, Video 27.16 and Video 27.17); however, compression will be normal.

B

FIG. 27.27 Great Saphenous Vein (GSV) Thrombus. Longitudinal gray-scale (A) and color Doppler (B) images show thrombus within the GSV (arrowheads) without extension into the common femoral vein (CFV) (arrow). (C) In a different patient, longitudinal image shows nonocclusive slightly mobile thrombus within the GSV (*) with extension into the CFV (arrow). See also Video 27.12.

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FIG. 27.28 Acute Deep Venous Thrombosis (DVT). (A) Transverse duplex Doppler image shows external iliac vein without demonstrable venous low (*). The top of the thrombus is not seen, so sonographic evaluation continues to the common iliac vein and inferior vena cava (IVC). (B) Longitudinal image of occluded external iliac vein shows large amount of low-level echoes within the vein, without low on spectral or color Doppler imaging. (C) Longitudinal image of caudal IVC shows no deinite echoes on gray-scale imaging, conirmed with duplex Doppler imaging (not shown). (D) Duplex Doppler longitudinal image of the mid IVC shows no thrombus. (E) Longitudinal gray-scale image of the intrahepatic IVC shows no thrombus. (F) Duplex Doppler longitudinal image of the intrahepatic IVC without thrombus, with normal spectral Doppler waveform. Because the spectral waveform in the left common femoral vein was normal (not shown), thrombus in this patient extended into either the right external or common iliac vein, but not into the IVC. See also Video 27.13.

A

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FIG. 27.29 Chronic Deep Venous Thrombosis (DVT). (A) Duplex Doppler longitudinal image of chronic femoral vein DVT, with small vein and peripheral nonocclusive low. (B) Duplex Doppler longitudinal image of chronic DVT and scarring in a patent popliteal vein, with peripheral irregular residual thrombus.

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FIG. 27.30 Chronic Vein Occlusion With Collaterals. (A) Transverse image of the popliteal fossa shows multiple small collateral veins (*) in the region of the popliteal vein, adjacent to the popliteal artery (A) in the setting of chronic popliteal vein deep venous thrombosis (DVT) and scarring. (B) Longitudinal image of chronic DVT and scarring in the popliteal vein shows mildly compressible nonocclusive thrombus with some portions adhering to the wall, in a small vein. See also Video 27.14.

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FIG. 27.31 Chronic Deep Venous Thrombosis (DVT) With Vein Web. Longitudinal gray-scale (A) and color Doppler (B) images show linear weblike chronic DVT (cursors) with patent channels around the web.

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FIG. 27.32 Chronic Common Femoral Vein (CFV) Occlusion With Flow Reversal in the Profunda Femoris Vein (PFV). Longitudinal gray-scale (A) and color Doppler (B) images show chronic CFV occlusion (arrows) and low reversal in the PFV (*). The artery (A) is located anteriorly. See also Video 27.15.

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FIG. 27.33 Calciications Indicating Chronic Thrombus. (A) Longitudinal image of the femoral vein shows multiple shadowing calciications (arrows). (B) Transverse image in another patient shows calciication in the popliteal vein (arrow). (C) Same patient as in (B) has new hypoechoic thrombus enlarging the popliteal vein (arrows)— acute-on-chronic deep venous thrombosis (DVT).

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2. Small nonocclusive thrombi in the profunda femoris vein may be missed if not carefully assessed. It is important to remember that DVT may initially be demonstrated in the profunda femoris vein only. 3. hrombosis of a duplicated FV may be challenging to detect. It is useful to record the presence of this common anatomic variant in the report for comparison in a subsequent study, when only one of several FVs may be thrombosed (Fig. 27.35, Video 27.18).

4. Proximal iliac vein thrombosis may be diicult to demonstrate because of overlying bowel gas. Loss of respiratory phasicity should be recognized as a secondary sign suggesting more proximal thrombosis or obstructive compression by masses or luid collections (Fig. 27.36). False-negative examination results may occur when the Valsalva maneuver is used while the pelvic veins are evaluated in patients with nonocclusive thrombus in the iliac veins who have well-developed pelvic venous collaterals.

FIG. 27.34 Slow Flow in Patent, Compressible Vein Without Deep Venous Thrombosis (DVT). Accompanying Videos 27.16 and 27.17 show slow low in longitudinal plane, and no DVT with compression.

FIG. 27.35 Thrombus in One of Paired Femoral Veins. Transverse image of compressed paired femoral veins shows that one of the veins does not compress because of deep venous thrombosis (DVT). Arrow shows position of one femoral vein, which is completely compressed and thus not seen. See also Video 27.18. A, Supericial femoral artery; V, thrombus in other (paired) femoral vein.

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FIG. 27.36 (A) Patient with large pelvic mass compressing the left external iliac vein (not shown). Monophasic low in left common femoral vein (CFV). (B) Normal phasic low in right CFV.

CHAPTER 27 5. Occasionally only the actual coapting of the vein walls is seen during compression, the so-called vessel “wink.” he FV can sometimes be diicult to visualize throughout its entire extent. However, isolated FV thrombus is relatively uncommon, reported to occur in fewer than 1% to 4% of patients.83

Complete Venous Doppler Versus More Limited Examinations Complete compression venous Doppler from the inguinal area to the popliteal area is accurate, with less than 1% venous thromboembolic disease at 3-month follow-up in recent analyses.88,89 Limited, less detailed examinations have recently been proposed. A variety of specialties are performing this type of examination in oice settings, intensive care units, and emergency departments. he two-point ultrasonography examination of the CFV and the PV using the compression technique has shown that most, but not all, proximal DVTs are detected.90,91 However, this approach requires a serial examination 1 week later to detect propagation of calf thrombus into proximal DVT. Two negative study results, 1 week apart, have shown a low likelihood of DVT in the months following the tests.89 he two-point technique has a 2% to 5.7% chance of detecting DVT on a repeat examination at 2 weeks.89,90 A carefully performed complete thigh venous ultrasound as detailed earlier remains the standard of care. Recommendations for Deep Venous Thrombosis Follow-Up If the patient’s clinical condition worsens, follow-up venous Doppler is warranted. In patients with documented DVT on therapy, a repeat venous Doppler during treatment is rarely warranted. Repeat Doppler should not be requested unless there is a clinical change.85,92 DVT typically lyses or ibroses over 6 to 18 months. Reevaluation near the anticipated end of anticoagulation should be encouraged to establish a new baseline for patients who return with new symptoms suggesting recurrent thrombus, especially those at high risk for recurrent DVT.85 In patients with isolated calf DVT, a follow-up Doppler examination at 1 week is warranted if the patient is not treated. In patients with scarring, pregnant women, patients with technically limited examinations, or patients with calf pain wherein DVT is not identiied, it may be prudent to suggest follow-up in 1 week. It has been established that use of two limited examinations, 1 week apart, is a safe strategy.90 In an otherwise normal report, it may be prudent, as a helpful reminder, to state, “If there remains suspicion for DVT or the clinical condition worsens, a follow-up should be considered.”85 Venous Insuficiency he cause of deep venous insuiciency in many patients is venous valvular damage ater DVT, which occurs in about 50% of patients with acute DVT.93 he physiology of venous insuiciency entails direct transmission of the hydrostatic pressure of the standing column of luid in the venous system to the caudal lower extremity. Clinical manifestations include lower extremity swelling, chronic skin and pigmentation changes, woody induration, and eventually nonhealing venous stasis ulcers.

Peripheral Vessels

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Supericial venous insuiciency has a much better prognosis than deep venous insuiciency and is associated with extensive varicosities. Perforating veins communicate between the supericial and deep system and may also become incompetent owing to chronic deep venous insuiciency. For assessment of venous insuiciency, the patient is placed in an upright or semi-upright position, with the body’s weight supported by the contralateral lower extremity. his positioning produces the hydrostatic pressure needed to reproduce venous insuiciency. Spectral analysis is obtained at several levels of the deep and supericial venous system during Valsalva and other provocative maneuvers in the CFV, proximal aspect of the GSV, PV, and saphenopopliteal junction. Distal augmentation is more reproducible and easier when performed by a single examiner.94 Normal veins ater brisk distal augmentation will show antegrade low, with a very short period of low reversal as returning blood closes the irst competent venous valve (Fig. 27.37, Video 27.19). Distal augmentation can be performed manually and more reproducibly with automated devices that inlate every 5 to 10 seconds. Insuicient veins show greater degree of reversed low for a longer duration (Fig. 27.38). It is important that each vascular laboratory validate its protocol and quantiication schemes.

Venous Mapping Vein mapping of supericial leg or arm veins is performed to determine patency, size, condition, and course of supericial veins to be used for vein grats. Ultrasound mapping is also helpful when a vein is harvested as autologous grat material for a peripheral arterial bypass grat. Any supericial vein can be used, but the GSV is most oten suitable for grat purposes. he examination is performed with the patient in the supine or reverse Trendelenburg position. he GSV is identiied from the level of

FIG. 27.37 Normal Femoral Vein Valve. Accompanying Video 27.19 shows normal coapting of valve, which prevents retrograde low.

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Augmentation

Augmentation

A

B

FIG. 27.38 Venous Insuficiency. (A) Duplex spectral analysis of the popliteal vein shows a normal waveform with distal augmentation. Note no reversal of low following distal augmentation. (B) Duplex spectral analysis of the great saphenous vein shows prolonged relux after distal augmentation, consistent with severe supericial venous insuficiency.

Internal jugular vein Brachiocephalic vein Subclavian vein Pectoralis minor muscle Axillary vein Teres major muscle Cephalic vein Brachial veins Basilic vein

FIG. 27.39 Venous Anatomy of the Upper Extremity Veins.

the saphenofemoral junction to as far inferiorly as possible. A supericial vein typically needs to be larger than 3 mm in diameter, but not varicose, to be suitable grat material.95 he small saphenous vein and cephalic and basilic veins are secondary choices and can be used if the GSV has already been harvested or is inadequate.

Upper Extremity Veins Normal Anatomy he venous anatomy of the neck and arm is illustrated in (Fig. 27.39). he deep venous system includes the paired radial and ulnar veins in the forearm, which unite distal to the level of the

CHAPTER 27 elbow to form the brachial veins. he brachial veins in the upper arm join with the basilic vein at a variable location, typically at the level of the teres major muscle. he conluence of the brachial and basilic veins continues as the axillary vein, which passes through the axilla from the teres major muscle to the irst rib. As the axillary vein crosses the irst rib, it becomes the lateral portion of the subclavian vein. he medial portion of the subclavian vein receives the smaller external jugular vein and the larger internal jugular vein (IJV) to form the brachiocephalic (innominate) vein. Most ultrasound laboratories deine the central veins as the brachiocephalic veins and superior vena cava, which oten are diicult to visualize sonographically. Because some angiographers include the subclavian vein when they describe the central veins, it is important to be very speciic about the vein segment examined when describing sonographic indings. he presence or absence of clinically important central stenosis or thrombosis may be inferred by evaluating the transmitted cardiac pulsatility and respiratory phasicity in the medial subclavian vein and distal IJV.96 he cephalic and basilic veins comprise the most important supericial named veins of the upper extremity. he more laterally located cephalic vein traverses in the supericial sot tissues of the shoulder to drain into the axillary vein in the lateral chest. he basilic vein is located more medially, and typically joins the brachial veins to form the axillary vein.

Ultrasound Examination and Imaging Protocol Upper extremity Duplex evaluation consists of gray-scale compression and color and spectral Doppler assessment of all the visualized portions of the IJV and subclavian, axillary, and innominate veins, as well as compression gray-scale ultrasound of the brachial, basilic, and cephalic veins in the upper arm

A

Peripheral Vessels

991

to the elbow. A high-frequency, small-footprint transducer can be applied to the suprasternal notch to better demonstrate the brachiocephalic junction and IVC, oten diicult to see because of overlying sternum and lung. Venous compression is applied to accessible veins in the transverse plane with adequate pressure on the skin to completely obliterate the normal vein lumen. he patient is scanned in a supine position with the examined arm abducted from the chest, with the patient’s head turned slightly away from the examined arm. Typically a 5- to 10-MHz linear array transducer will be used, with a higher frequency transducer chosen for more supericial veins. A curved array transducer or sector transducer may be more efective in larger patients, especially in the axillary area, because of its increased depth of penetration and larger ield of view. All veins are examined with compression every 1 to 2 cm in the transverse plane. Gray-scale transverse images with and without compression or cine clips during compression are obtained from the cranial aspect of the IJV in the neck to the thoracic inlet caudally (Fig. 27.40, Video 27.20). Longitudinal color and spectral images are obtained. he subclavian vein is evaluated from its medial to lateral aspect with longitudinal color and spectral images, assessing for transmitted respiratory variability, cardiac pulsatility, and color ill-in. To demonstrate the superior brachiocephalic vein and the medial portion of the subclavian vein, an inferiorly angled, supraclavicular approach with color Doppler is necessary. A small-footprint sector probe in or near the suprasternal notch may improve visualization of the brachiocephalic veins and the cranial aspect of the superior vena cava (Fig. 27.41). he midportion of the subclavian vein, located deep to the clavicle, frequently is incompletely imaged. An infraclavicular, superiorly angled approach can be used to demonstrate the lateral aspect of the

B

FIG. 27.40 Normal Internal Jugular Vein (IJV) and Subclavian Vein (SCV) Spectral Doppler Waveforms. (A) Normal IJV spectral Doppler waveform, with transmitted cardiac pulsatility and respiratory phasicity, with spectral waveform going to the baseline. Accompanying Video 27.20 shows normal IJV compression. (B) Normal medial SCV spectral Doppler, with transmitted cardiac pulsatility and respiratory phasicity, and spectral waveform going to the baseline.

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A

B

FIG. 27.41 Normal Brachiocephalic Veins. Gray-scale (A), and color and spectral Doppler (B) of left and right brachiocephalic veins (arrows) and cranial superior vena cava (SVC; *).

subclavian vein. In many cases the subclavian vein can be compressed. Accurate spectral waveform evaluation is critical to this examination. Documentation of normal low in the medial subclavian vein conirms patency of the brachiocephalic vein and superior vena cava, which cannot be examined directly. Each spectral image obtained in the longitudinal plane of the vessel with angle of insonation maintained at less than 60 degrees is evaluated for spontaneous, phasic, and pulsatile low. Demonstration of transmitted cardiac pulsatility and respiratory phasicity is necessary in the spectral analysis of the caudal IJV and medial subclavian vein. A normal spectral tracing should return to baseline. Absence of pulsatility may be caused by a more central venous stenosis or obstruction (Fig. 27.42).97 Spectral tracings from the medial subclavian vein should be compared with tracings from the lateral subclavian vein. A change between these two tracings suggests midsubclavian vein stenosis. Response to a brisk inspiratory snif or Valsalva maneuver may assist evaluation of venous patency. During a snif, the normal IJV or subclavian vein normally decreases in diameter or collapses completely. he Valsalva maneuver will increase the vein diameter, demonstrating response to the increased thoracic pressure and documenting communication with the central vasculature. Patients with signiicant stenosis or obstruction of the central brachiocephalic vein of the superior vena cava will lose this response.97 he upper extremity venous imaging protocol includes the following images for each deep venous segment: 1. Transverse gray-scale image at rest and with compression, or a cine clip of the compression maneuver of the proximal and distal IJV, subclavian, axillary, and brachial veins. he basilic and cephalic veins are evaluated in the upper arm to the elbow. 2. Longitudinal color Doppler with spectral waveform analysis is performed of the IJV, both proximal and distal portions, as well as the subclavian vein, both medially and laterally,

and the axillary vein. If only a unilateral examination is requested, the contralateral subclavian vein is also evaluated. 3. Evaluation of focal symptomatic areas if present, including the forearm.

Upper Extremity Acute Deep Venous Thrombosis Current literature shows the sensitivity and speciicity of venous Doppler ultrasound for upper extremity DVT to range from 78% to 100% and 82% to 100%, respectively.96,98-102 he classic ultrasound inding in acute upper extremity DVT is an enlarged, tubular structure illed with thrombus showing variable echogenicity and absence of color Doppler low (Fig. 27.43, Video 27.21). Nonocclusive thrombus may show low outlining the thrombus, with a variable appearance depending on whether the nonocclusive thrombus is acute or chronic. Nonocclusive thrombus usually does not result in enlargement of the vein (Fig. 27.44). When the obstruction is incomplete, nonphasic low is demonstrated when the luminal narrowing is signiicant enough to afect the transmitted cardiac pulsatility and respiratory phasicity from the thorax. Attention to detail is important in the normally paired brachial veins to avoid overlooking thrombus in one of the veins (Fig. 27.45, Video 27.22). Evaluation of central thrombus relies on spectral analysis. he presence of a nonpulsatile waveform (similar to portal venous low) that does not cross the baseline strongly suggests central venous thrombosis, stenosis, or extrinsic compression from an adjacent mass.96 A suspicious waveform should always be compared with the contralateral side to assess a unilateral versus bilateral process. Patel and colleagues103 found that absent or reduced cardiac pulsatility was a more sensitive parameter in patients who had unilateral venous thrombosis, even though respiratory phasicity oten was asymmetric. In cases of bilateral subclavian vein or superior vena cava occlusion, a high level of suspicion must be maintained to detect central thrombus or stenosis. Of importance, because of high-volume low, there may

CHAPTER 27

A

B

C

D

E

Peripheral Vessels

993

FIG. 27.42 Superior Vena Cava (SVC) Stenosis With Right Peripherally Inserted Central Catheter (PICC) Line. Abnormal caudal right internal jugular (A), right medial SCV (B), left caudal internal jugular (C), and left medial SCV (D) low do not go to baseline. (E) Venogram performed during right PICC line replacement shows mild-moderate SVC stenosis (arrows), which was accentuated by indwelling catheter.

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FIG. 27.45 Nonocclusive Thrombus in Brachial Vein. Transverse noncompressed image of nonocclusive thrombus (*) in one brachial vein in the paired brachial veins. A, Brachial artery. See also Video 27.22. FIG. 27.43 Acute Internal Jugular Thrombus. Transverse image of a noncompressible internal jugular vein illed with thrombus (*). Arrowhead shows carotid artery. See also Video 27.21.

FIG. 27.44 Nonocclusive Chronic Internal Jugular Thrombus. Longitudinal color Doppler image of the small-caliber proximal internal jugular vein with irregular thrombus adjacent to wall, with thickened valves (arrows).

be absence of phasicity without stenosis in the central veins if a hemodialysis grat or AVF is present in the upper arm. Unlike the lower extremity, most cases of upper extremity DVT are related to the presence of a central venous catheter or electrode leads from an implanted cardiac device. Approximately 35% to 75% of patients who have upper extremity venous catheters develop thrombosis, and approximately 75% are asymptomatic104-106 (Fig. 27.46, Video 27.23 and Video 27.24). Frequently a ibrin sheath is found adjacent to the catheter and may be seen ater catheter removal. It is important to look carefully at the valves for adherent thrombus. Whether the catheter access site is the subclavian vein or the IJV afects the complication

rate. Trerotola and colleagues107 examined only patients who had symptomatic upper extremity DVT and found a greater incidence of DVT in patients who had subclavian venous access than in those who had internal jugular access. he placement of large-bore catheters into the subclavian vein should be avoided, especially in patients who have end-stage renal disease (ESRD) for whom dialysis access is being considered. Subsequent development of subclavian vein stenosis or thrombosis would limit dialysis access possibilities for that upper extremity. Only 12% to 16% of patients who have upper extremity DVT develop PE.108,109 In comparison, 44% of patients who developed proximal lower extremity DVT detected by sonography had a subsequent PE diagnosed clinically.110 Acute pulmonary emboli in patients who have upper extremity DVT tend to occur in untreated patients.111,112 As expected, there is greater risk of PE in catheter-related upper extremity DVT than in upper extremity DVT from other causes.113 Venous stasis and insuiciency caused by venous thrombosis, more commonly seen with LE DVT, are less common and less severe in the upper extremity. he deep venous system in the arm has less exposure to the physiologic hydrostatic high-pressure pump mechanism that is seen in the lower extremity.114,115 Development of extensive collateral venous pathways in the arm and chest ater venous thrombosis or obstruction contributes to these diferences and may cause greater technical challenge in performing the upper extremity venous Doppler examination, as compared with the lower extremity.

Differentiation of Acute From Residual or Chronic Venous Thrombosis Findings suggesting residual or chronic DVT in the upper extremity include ixed valve lealets, synechiae, ibrin sheaths, small-caliber veins with noncompressible, thickened walls, and multiple serpiginous veins not paralleling the artery (Fig. 27.47). In some cases of residual or chronic thrombosis, the vein may not be seen in the expected location owing to ibrosis or scarring.

CHAPTER 27

Peripheral Vessels

995

A

B

C

A

FIG. 27.46 Thrombus Associated With Central Lines. (A) Transverse image shows acute thrombus around peripherally inserted central catheter (PICC) line in the basilic vein. Thrombus completely occludes noncompressible vein. (B) Acute thrombus around PICC catheter in the basilic vein. No low seen on duplex Doppler in the longitudinal plane. (C) Longitudinal image of the internal jugular vein shows a moderate amount of thrombus around a central line in another patient. See also Video 27.23 and Video 27.24.

B

FIG. 27.47 Collateral Formation in the Upper Extremity After Deep Venous Thrombosis (DVT). (A) Transverse images of many serpiginous veins (*) in the region of the chronically occluded proximal internal jugular vein near the base of the neck. C, Carotid. (B) Longitudinal duplex Doppler image shows no spectral low in the small, occluded distal internal jugular vein.

An excellent example is demonstration of only one brachial vein because of chronic scarring from prior DVT of the paired brachial veins116 (Fig. 27.48).

Potential Pitfalls Upper extremity pitfalls to avoid include the following117-119: 1. Axillary versus cephalic vein: he axillary vein of the deep venous system empties into the subclavian vein. he cephalic

vein of the supericial venous system empties into the axillary vein and will not have an adjacent artery along its course. Access to the axilla is generally improved by bending the patient’s elbow and placing the hand near the patient’s head, with an outstretched arm. Excessive abduction may alter the venous waveform, falsely suggesting a more central venous stenosis or obstruction; however, this will resolve with change in position.

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FIG. 27.48 Chronic Clot in Brachial Vein. One of the paired brachial veins is small and chronically occluded (arrow). A, Brachial artery; V, other, normal brachial vein.

2. Distal occlusion of IJV: he distal aspect of the IJV must be demonstrated lowing into the junction with the medial subclavian vein in the area of the brachiocephalic vein. If the vein being traced is located more than a few millimeters away from the carotid artery, it probably represents a collateral vessel, rather than the IJV. Well-developed collaterals may demonstrate normal respiratory phasicity, an additional pitfall. Collateral vessels tend to be multiple and serpiginous and to follow the occluded vein.

HEMODIALYSIS here were 661,648 patients being treated for ESRD by the end of 2013 in the United States, with 117,162 new cases that year.1 Approximately 64% of these patients were undergoing hemodialysis.120 A major cause of morbidity among ESRD patients is related to vascular access procedures and associated complications that increase health care costs in patients undergoing hemodialysis.121 here are two options for permanent access placement for ESRD patients requiring hemodialysis—an arteriovenous istula (AVF) or a synthetic arteriovenous grat. Mature AVFs are the preferred access when appropriate, because of the lower rates of infection and thrombosis than with grat or catheter access.122-124 Several studies have shown that preoperative ultrasound evaluation of the upper extremity veins and arteries may increase the number of successful AVF placements through optimization of surgical planning125-127 as well as before grat placement in the thigh.128 Although sonographic postoperative hemodialysis access evaluation may be beneicial in assessing AVF maturation,129-131 the role of postoperative ultrasound evaluation for the detection of access pathology and early intervention to improve the longevity of a particular access is still being studied.132-139 Ultrasound is useful in evaluation of palpable masses adjacent to the vascular access to diferentiate hematoma from pseudoaneurysm. It is also used in the evaluation of the swollen upper extremity in a patient with an AVF or grat, or a swollen lower extremity in a patient with a thigh grat, assessing for outlow

vein stenosis and DVT. Ultrasound is also used in the evaluation of patients with arm and hand pain ater access placement to evaluate for symptomatic steal. he surgical creation of an AVF is preferred over a grat when surgically and clinically feasible. Placement of access in the nondominant upper extremity is preferred to allow continuance of daily activities of life while the access site heals; however, a dominant arm AVF is preferred to a grat in most patients. Possible sites of hemodialysis access in order of preference are as follows: (1) forearm AVF (radiocephalic AVF or transposed forearm basilic vein to radial artery AVF); (2) upper arm brachiocephalic AVF; (3) transposed brachiobasilic AVF; (4) forearm loop grat; (5) upper arm straight grat (brachial artery to upper basilic or axillary vein); (6) upper arm axillary artery to axillary vein loop grat; and (7) thigh grat (Fig. 27.49). he cephalic vein is preferred over a basilic vein transposition for istula formation because the cephalic vein procedure involves less dissection and venous manipulation. Additional, less common access conigurations may also be placed based on surgical experience.140

Sonographic Examination Technique Both gray-scale and color Doppler ultrasound techniques should be optimized for venous and arterial imaging as previously discussed in this chapter. A high-frequency linear array 12- to 15-MHz transducer provides optimal spatial resolution and adequate depth penetration to successfully evaluate supericial vascular structures. A lighter-weight transducer with a smaller footprint, such as a hockey stick coniguration, can increase the speed and ease of the examination. A lower-frequency linear array 9- to 12-MHz transducer may be needed for adequate penetration in larger patients. A small-footprint curved array transducer may be useful for evaluation of the brachiocephalic vein and distal SVC. It is important to apply light pressure and use plenty of gel so as not to deform the circular shape of the vessels during the mapping examination for accurate vessel diameters. All diameter measurements are of the inner lumen measured in the anteroposterior dimension in the transverse plane. Color and spectral Doppler evaluation are performed in the longitudinal plane with angle correction of 60 degrees or less. Blood low rate measurements are performed in the longitudinal plane in a straight area that is not curvy. In blood low rate measurement, the Doppler gate is increased in size to encompass the entire vessel diameter, and is angle corrected to 60 degrees or less, parallel to the posterior vessel wall. hree to ive spectral Doppler waveforms are analyzed, using the automatic blood low rate calculation in most ultrasound scanners, using the formula of time-averaged mean velocity multiplied by the inner vessel diameter. hree measurements at the same location are performed and averaged, to ensure measurement reliability.

Vascular Mapping Before Hemodialysis Access Upper Extremity Attention to technical detail is necessary for optimum ultrasound evaluation for hemodialysis access planning.126,130,141-143 In general,

CHAPTER 27

Median cubital branch of cephalic vein

Peripheral Vessels

Basilic vein Brachial artery AVF anastomosis

997

Brachial artery AVF anastomosis

Cephalic vein Radial artery

Radial artery

AVF anastomosis

A

B

C

Axillary artery

Graft

Graft Brachial artery

Axillary vein

Brachial artery

Graft

D

E

F

Great saphenous vein

Common femoral artery

Graft

G FIG. 27.49 Most Common Arteriovenous Fistula (AVF) and Graft Placements. (A) Forearm cephalic vein–radial artery AVF. (B) Upper arm cephalic vein–brachial artery AVF, using the median cubital branch of the cephalic vein for the anastomosis. (C) Upper arm basilic vein–brachial artery AVF. (D) Forearm loop graft. (E) Upper arm straight graft. (F) Upper arm loop graft. (G) Thigh loop graft. (Reproduced with permission from Robbin ML, Lockhart ME. Ultrasound evaluation before and after hemodialysis access. In: Zweibel WJ, Pellerito JS, editors. Introduction to vascular ultrasonography. 5th ed. Philadelphia: Elsevier; 2005. p. 325-340.158)

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FIG. 27.51 Heavily Calciied Radial Artery at the Wrist. Longitudinal image shows heavy arterial wall calciication (arrows).

FIG. 27.50 Sonographic Evaluation of the Forearm Veins With Patient’s Arm Comfortably Resting on a Surgical Stand.

it is easier to map all the upper extremity arteries and veins on the same side at one sitting so the surgeon has adequate information if vessel character at surgery is suboptimal and another access site needs to be chosen. If a suitable site for AVF creation is not found on the arm evaluated, the other arm is evaluated. he patient should be sitting upright for optimal evaluation of the upper extremity arteries and veins, with the forearm resting comfortably on a table or armrest. A tourniquet should be placed ater arterial assessment, to assess vein caliber and distention144 (Fig. 27.50). Central venous evaluation to include the IJV and subclavian vein should then be performed with the patient supine, for easier and potentially more accurate waveform assessment. Sonographic assessment of the arterial wall should evaluate the amount of calciication and degree of stenosis or occlusion, if present. Vein walls should be described with as much detail as possible to assess for wall thickening and thrombus, which may limit future venous distention. he literature suggests that preoperative criteria include a minimum intraluminal arterial diameter of 2.0 mm and a minimal intraluminal venous diameter of 2.5 mm to allow successful AVF creation, and a minimum intraluminal venous diameter of 4.0 mm and a minimum arterial diameter threshold of 2.0 mm for grats.145,146 At least the caudal third of the brachial artery and the entire radial artery are evaluated for intimal thickening, calciication, stenosis, or occlusion, with more extensive evaluation of the brachial and ulnar arteries as warranted, as well as the axillary artery. he severity of arterial calciication may be categorized, depending on surgeon preference, because it may be diicult to

suture into a heavily calciied artery, and the risk of emboli at surgery may be higher123 (Fig. 27.51). he arterial waveform is evaluated for a normal triphasic or biphasic high-resistance low pattern, and PSV is measured in these regions (Fig. 27.52). A high brachial artery bifurcation is a common anatomic variant and should be suspected when two arteries with accompanying paired veins are seen in the upper arm52 (Fig. 27.53). he two arteries should be followed into the forearm to the wrist to conirm the presence of a high brachial artery bifurcation and to exclude a prominent arterial branch supplying the elbow, less commonly seen. For assessment of veins, the upright-seated position ensures venous distention owing to hydrostatic pressure. For optimal venous distention, the tourniquet should be placed on the arm cranial to the area of interrogation so that the veins are distended. Each vein should be inspected, with compression performed along the entire venous length to exclude thrombus (Fig. 27.54). he tourniquet is irst placed in the midforearm. he region of the cephalic vein at the wrist is percussed for about 2 minutes for maximal venous distention, and the cephalic vein inner diameter is measured at multiple points in the forearm (Fig. 27.55, Video 27.25). hereater, the tourniquet is placed at the antecubital fossa, and then the proximal upper arm, ater segmental vein diameter measurement. Cephalic vein anterior wall distance from the skin can be measured because if the cephalic vein is too deep for easy cannulation, it may need to be supericialized in a subsequent surgery (Fig. 27.56). It is not necessary to measure the distance of the basilic vein from the skin; the vein needs to be transposed for easier access. he median antecubital vein typically connects the cephalic vein to the basilic vein and is oten part of the AVF draining vein. he median antecubital vein also can be used in creating an upper arm basilic or cephalic vein AVF and so is commonly evaluated at the mapping ultrasound procedure. he axillary vein, subclavian vein, and IJV should be assessed for compressibility (when possible) and normal waveforms (see Fig. 27.40).

CHAPTER 27

A

C

FIG. 27.53 High Brachial Artery Bifurcation. Radial and ulnar arteries (A) and accompanying paired veins (V).

Peripheral Vessels

999

B

FIG. 27.52 Preoperative Mapping Ultrasound Meeting Criteria for Arteriovenous Fistula (AVF) Placement. (A) Arterial evaluation: radial artery diameter of 0.28 cm (cursors). (B) Mild medial calciication in arterial wall (arrows) does not preclude AVF placement. (C) Normal triphasic radial artery spectral waveform.

FIG. 27.54 Preoperative Mapping Ultrasound Meeting Criteria for Arteriovenous Fistula (AVF) Placement. Venous evaluation: cephalic vein in the midforearm is 0.27 cm (+ cursors). Anterior vein wall depth is 0.18 cm from skin (X cursor).

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FIG. 27.55 Thick-Walled Cephalic Vein With Chronic Thrombus. This vein may not dilate normally after arteriovenous istula (AVF) placement and should not be chosen for a potential AVF draining vein. See accompanying Video 27.25.

FIG. 27.56 Cephalic vein is quite deep from the skin surface (0.9 cm; X cursor), and may need to be supericialized after arteriovenous istula creation.

Ultrasound Examination and Imaging Protocol Upper Extremity. Ater assessment of the brachial and radial arteries, the inner luminal diameter of the brachial artery 2 cm proximal to the antecubital fossa, and the radial artery at the wrist are measured, along with the axillary artery diameter. Using sequential tourniquet placement and ater wrist percussion of the cephalic vein region, the cephalic vein inner diameter is measured at the wrist, midforearm, and proximal forearm (approximately 4 cm from the antecubital fossa). he proximal forearm measurement is used to evaluate the length of vein available to surgically move the vein from the forearm to the brachial artery in upper arm AVF creation. he cephalic and basilic vein diameters are measured at the antecubital fossa and mid and cranial upper arm. Distance of the anterior wall of the cephalic vein to the skin surface is measured. he axillary vein diameter is measured. he subclavian vein and IJV are assessed in the longitudinal plane with color and spectral Doppler assessment, and IJV compression is performed to assess for thrombus, stenosis, and occlusion.

Subclavian and internal jugular spectral Doppler waveforms are assessed for respiratory phasicity and transmitted cardiac pulsatility. Thigh. Once options to place AVF and grats in the upper extremity are exhausted, the thigh grat becomes a viable option. high grats are similar to upper extremity grats in length of time to permanent failure, with a trend toward increased loss because of infection.147 high grats are superior to dialysis via a catheter.148 If heavy arterial common femoral or supericial femoral arterial calciication is found at ultrasound, pelvic CT may be useful to determine the degree of atherosclerotic disease present. Careful sonographic assessment of atherosclerotic calciication and stenosis may limit immediate grat failure at surgical placement.128 high grat creation has typically been at the common femoral artery and vein (Fig. 27.57). An alternate place to anastomose the venous end of the grat is the GSV, to preserve the CFV when grat revision is necessary. However, to preserve proximal vasculature for grat revision, and potentially because of fewer infectious complications, midthigh grats are now being increasingly placed in the mid SFA and supericial femoral vein.149 Technical considerations for mapping the arteries and veins of the thigh for hemodialysis grat placement are similar to mapping the upper extremity as described earlier, although a lower-frequency linear transducer may be necessary because of greater thigh size. Evaluation of the degree of arterial calciication and the presence of thrombus is carefully performed in the thigh. More central stenosis or obstruction is assessed by spectral Doppler evaluation of the CFV and common femoral artery. Distance of the vein to the skin is not measured, because typically only thigh grats are surgically created. A tourniquet is not used in sonographic thigh grat mapping. he common femoral artery and vein inner luminal diameters are measured, and evaluated for the degree of atherosclerotic calciication. Spectral and color Doppler evaluation of the common femoral artery and vein are performed to evaluate for more proximal stenosis or occlusion. SFA waveforms are also assessed for normalcy. he length of the GSV, which is at least 0.4 cm inner diameter, is measured from its insertion into the CFV extending distally. Inner diameter measurements of the proximal and mid supericial femoral artery and FV are obtained. Compressibility of the veins assessing for thrombus and wall thickening is performed.128

Arteriovenous Fistula and Graft A surgically created hemodialysis access can have a variety of complications, and most of these can be successfully evaluated by ultrasound. Operative notes and pertinent patient history should be reviewed before sonographic evaluation of hemodialysis access. An overall ultrasound scan is performed initially to obtain an overview of the access anatomy and anastomoses. When the general layout is known, sonographic assessment is performed with duplex Doppler sonography, typically in a seated patient with his or her arm resting comfortably on a table. he caudal third of the feeding artery is assessed for stenosis, and the intraluminal diameter is measured in the transverse plane using gray-scale techniques. he feeding artery is further assessed with

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color and spectral Doppler in the longitudinal plane to document normal low-resistance low (Fig. 27.58). Measurements of PSV and EDV can be obtained in the feeding artery, and at least at the anastomosis(es). here may be multiple anastomoses in the case of a grat. he draining vein of the AVF or grat is inspected for wall thickening, stenosis, and thrombosis along its entire length.143 If a stenosis is seen, the highest PSV either within the stenosis or in the jet downstream from the stenosis is measured, using angle correction parallel to the jet if diferent from the angle with the posterior vascular wall, keeping the angle to 60 degrees or less. he PSV 2 cm upstream to the stenosis is measured, and a PSV ratio of the PSV at the stenosis divided by the upstream PSV is calculated. A longitudinal gray-scale image is obtained to document any intraluminal thrombus identiied within a draining vein or grat. Duplex Doppler should be performed to conirm absence of low, with use of the more sensitive power Doppler as needed. Description of artery and vein location with regard to the AVF and grat can be diicult. Terminology including cranial and caudal location with regard to a particular anastomosis, and upstream or downstream position,

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FIG. 27.57 Thigh Graft Preoperative Mapping. (A) Heavy arterial calciication is seen in the common femoral artery (CFA; *) with normal common femoral vein compression (compression not shown). (B) Longitudinal view of the mid supericial femoral artery (SFA) also shows heavy arterial calciication. (C) Spectral Doppler waveform of the mid SFA does not have a normal triphasic or biphasic waveform. These arteries may be too heavily calciied to sew into, and would likely prompt further evaluation of the patient’s arterial inlow to assess whether thigh graft placement is possible in this patient.

may be more useful than the conventional proximal and distal terminology.

Arteriovenous Fistula he feeding artery luminal diameter is measured. Spectral and color Doppler evaluations of the feeding artery are performed to evaluate for arterial stenosis or occlusion. he anastomosis is assessed for visible narrowing with subsequent spectral and color Doppler evaluation. he AVF draining vein diameter is evaluated at several levels from the anastomosis to 15 cm cranial to the anastomosis. he intraluminal draining vein diameter and the depth of the vein from the skin surface are measured at several points cranial to the arteriovenous anastomosis. Access challenges may result with a depth greater than 5 to 6 mm and require supericialization.131,150 he draining vein is interrogated for accessory branches (Fig. 27.59). Intraluminal diameter and distance from the anastomosis are recorded for each identiied accessory vein within 10 to 15 cm of the anastomotic site. he low volume rate measurements are obtained within the midportion of the draining vein of an AVF, typically at 10 cm cranial to the anastomosis. Optimal low volume measurement is obtained

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in an area with parallel vessel walls, minimal vessel tortuosity, and no stenosis (Fig. 27.60).

Graft Sonographic evaluation of the forearm or thigh grat is similar to that of the AVF. A normal grat is seen as two echogenic lines that represent strong specular relection from polytetraluoroethylene material. A low-resistance low (arterialized low) should be seen within a grat. Duplex Doppler evaluation of the feeding artery (including luminal diameter), arterial-grat anastomosis, grat (arterial side and venous side if loop grat), and venous

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FIG. 27.58 Normal Mature Forearm Arteriovenous Fistula (AVF) Ultrasound Evaluation (Radial Artery at the Wrist to Cephalic Vein). (A) Normal feeding artery internal diameter (cursors). (B) Color and spectral Doppler 2 cm upstream to the anastomosis measures 2.62 m/sec. (C) peak systolic velocity (PSV) measures 3.97 m/sec for a PSV ratio at anastomosis of less than 3 : 1, normal. Visual assessment of anastomosis is also normal, without stenosis. (D) Normal cephalic vein cranial to the anastomosis (cursors show internal diameter measurement). (E) Mid AVF draining vein volume low rate measurement (in midforearm) is 1000 mL/min.

anastomosis is performed, as well as draining vein and central vein evaluation. Flow volume is assessed within the midgrat (Fig. 27.61), and both arterial and venous limbs if a loop grat. Any points of visible narrowing are further assessed with spectral and color Doppler.

Palpable Focal Masses Near Arteriovenous Fistula and Graft Hematoma. Avascular, hypoechoic lesions adjacent to the AVF or grat oten represent postaccess or postprocedure hematomas (Fig. 27.62, Video 27.26). hese collections should

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FIG. 27.59 Accessory Arteriovenous Fistula (AVF) Branch Measurement. (A) Transverse image of the AVF draining vein (*) shows a branch of 0.24 cm (cursors). (B) Larger accessory AVF branch (cursors) of 0.44 cm may be large enough to sump blood away from the AVF draining vein (*).

FIG. 27.60 Volume Flow in a Fairly Straight Area of an Arteriovenous Fistula (AVF) Draining Vein.

be inspected for echogenic foci or gas. Fluid collections with echogenic foci associated with shadowing suspicious for gas may represent abscess in certain clinical settings. Aneurysm and Pseudoaneurysm. Focal or difuse aneurysmal dilation of the AVF draining vein may occur as a result of repeated puncture (Fig. 27.63). Pseudoaneurysms may develop within a istula or grat and oten are related to suboptimal compression ater cannulation. Color Doppler of a pseudoaneurysm reveals a circular low pattern termed “yin-yang” (Fig. 27.64, Video 27.27). here may be “to-and-fro” low identiied in the pseudoaneurysm neck. Evaluation of the depth of the anterior wall of the pseudoaneurysm from the skin surface is important to evaluate those pseudoaneurysms in danger of imminent rupture. A unique complication of grats is the degeneration of grat synthetic material. Irregularity of the grat wall is present, which may be associated with difuse or focal pseudoaneurysms along the length of the grat wall (Fig. 27.65, Video 27.28).

Arteriovenous Fistula Maturation Evaluation A 6-week postoperative AVF ultrasound is used in some clinical centers for routine evaluation of the AVF to determine its

development toward usability.130 A functioning AVF has a volume low of at least 300 to 800 mL/min.129,151 Robbin and colleagues showed that when an AVF had a minimum draining vein of 4 mm or larger or a blood low rate of 500 mL/min or higher, approximately 70% of AVFs were able to be used for hemodialysis. he likelihood of istula maturation was 95% if both criteria were met. If neither of these criteria was met, only 33% of istulas were used for hemodialysis.129 Sonographic criteria published by the National Kidney Foundation Kidney Disease Outcomes Quality Initiative suggestive of maturation include a draining vein greater than 6 mm diameter, blood low rate greater than 600 mL/min, and less than 6 mm skin depth. hese criteria may exclude many istulas that could subsequently provide hemodialysis access. Active investigation is underway with larger, multicenter trials to test these criteria. Etiology of failure to mature such as anastomotic or AVF draining vein stenosis, large accessory veins, or arterial inlow stenosis can be identiied and ultrasound used to triage the AVF for intervention.131

Arteriovenous Fistula and Graft Stenosis AVF. Stenoses associated with AVFs are most frequently juxta-anastomotic, followed in frequency by AVF draining vein, with central venous and feeding artery stenosis less common but not infrequent. Stenoses may be clinically relevant owing to resultant low decrease and can be associated with subsequent thrombosis. Potential sites for AVF stenosis include the feeding artery, juxta-anastomotic region, draining vein, and central veins. Early ater placement, juxta-anastomotic stenoses are the most common. Later, AVF draining vein and central vein stenoses are more common, including a “cephalic arch” stenosis in which the cephalic vein enters the subclavian vein in the cephalic vein AVF. A careful directed search to common areas of stenosis is important during the sonographic examination, because stenoses may be short and therefore overlooked. Fistula stenosis is characterized by two criteria: (1) visual narrowing of greater than 50% as assessed on gray-scale imaging, and (2) an elevated PSV ratio of the PSV at or just distal to the stenosis as compared with the PSV measured 2 cm upstream from the site of stenosis. A juxta-anastomotic stenosis is deined by a location within 2 cm of the anastomosis, encompassing both the feeding artery and the draining

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FIG. 27.61 Assessment of Upper Arm Graft (Brachial Artery to Axillary Vein Graft) With Peak Systolic Velocity (PSV) Measurement. (A) Normal color and spectral Doppler images show artery feeding the graft 2 cm cranial to the arterial anastomosis; PSV measures 3.7 m/sec. (B) Arterial anastomosis: PSV is 5.98 m/sec. PSV ratio is 3 : 1, concordant with visual assessment of a high-grade stenosis.

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FIG. 27.67 Graft or Arteriovenous Fistula (AVF) Draining Vein Stenosis Assessment Using Color and Spectral Doppler With Peak Systolic Velocity (PSV) Measurement. (A) Visual narrowing in draining vein greater than 2 cm downstream from anastomotic stenosis (therefore draining vein stenosis, not juxta-anastomotic stenosis). (B) PSV measurement of area of greatest narrowing is 8.5 m/sec. (C) PSV 2 cm upstream from draining vein stenosis is 3.4 m/sec for a PSV gradient of >2 : 1, with visual narrowing, consistent with at least 50% stenosis.

B

FIG. 27.68 Graft Venous Anastomotic Stenosis. (A) Gray-scale image shows signiicant narrowing at thigh graft– common femoral vein anastomosis. (B) Venous anastomosis peak systolic velocity (PSV) measures 6.1 m/sec in greatest jet. (C) PSV measurement within the graft 2 cm upstream from the venous anastomosis is 2.53 m/sec, for a PSV ratio >2 : 1, and concordant with visual narrowing, consistent with at least 50% stenosis. See also Video 27.29.

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FIG. 27.69 Arterial Steal in a Radial Artery to Cephalic Vein Arteriovenous Fistula (AVF) in the Proximal Forearm. (A) Grayscale image of anastomosis shows no stenosis. A, Feeding artery; V, draining AVF vein. (B) Reversal of low direction is seen in the radial artery just caudal (distal to the AVF anastomosis) in the radial artery—arterial steal. (C) Reversal of low in the distal radial artery at the wrist conirms arterial steal.

B

FIG. 27.70 Severe Subclavian Vein Stenosis. (A) Monophasic low in the medial subclavian vein does not return to baseline. (B) Monophasic low in the caudal internal jugular vein does not return to baseline. (C) Severe stenosis in proximal subclavian vein conirmed at venography before angioplasty.

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FIG. 27.71 Thrombosed Hemodialysis Graft. (A) No low seen on spectral Doppler (no low on color Doppler; not shown). (B) Color and spectral Doppler of artery upstream (cranial) from graft takeoff shows high-resistance waveform expected in graft thrombosis.

mapping, and surveillance of the upper and lower extremity venous system. Preoperative ultrasound evaluation of the veins and arteries before both upper extremity and thigh hemodialysis access placement may decrease complications related to access procedures and improve overall access utility. Ater access placement, ultrasound is useful in the assessment of complications including stenosis, pseudoaneurysm, steal, and AVF nonmaturation. REFERENCES 1. American College of Radiology (ACR), American Institute of Ultrasound in Medicine (AIUM), Society of Pediatric Radiology (SPR), Society of Radiologists in Ultrasound (SRU). ACR-AIUM-SPR-SRU Practice parameter for the performance of peripheral venous ultrasound examinations 2015. Available from: http://www.acr.org/~/media/ACR/Documents/PGTS/ guidelines/US_Peripheral_Venous.pdf. 2. American College of Radiology (ACR), American Institute of Ultrasound in Medicine (AIUM), Society of Radiologists in Ultrasound (SRU). Practice parameter for the performance of peripheral arterial ultrasound using color and spectral Doppler. Peripheral arterial US. 2014. Available from: https:// www.acr.org/~/media/ACR/Documents/PGTS/guidelines/US_Peripheral _Arterial.pdf. 3. Sanyal R, Krat B, Alexander LF, et al. Scanner-based protocol-driven ultrasound: an efective method to improve eiciency in an ultrasound department. AJR Am J Roentgenol. 2016;1-5. 4. AbuRahma AF, Jarrett K, Hayes DJ. Clinical implications of power Doppler three-dimensional ultrasonography. Vascular. 2004;12(5): 293-300. 5. Czyzewska D, Ustymowicz A, Krysiuk K, et al. Ultrasound assessment of the caliber of the arteries in the lower extremities in healthy persons—the dependency on age, sex and morphological parameters of the subjects. J Ultrason. 2012;12(51):420-427. 6. Moneta GL, Yeager RA, Antonovic R, et al. Accuracy of lower extremity arterial duplex mapping. J Vasc Surg. 1992;15(2):275-283. 7. Hatsukami TS, Primozich JF, Zierler RE, et al. Color Doppler imaging of infrainguinal arterial occlusive disease. J Vasc Surg. 1992;16(4):527531. 8. Mustapha JA, Saab F, Diaz-Sandoval L, et al. Comparison between angiographic and arterial duplex ultrasound assessment of tibial arteries in patients with peripheral arterial disease: on behalf of the Joint Endovascular and

Non-Invasive Assessment of LImb Perfusion (JENALI) Group. J Invasive Cardiol. 2013;25(11):606-611. 9. Moneta GL, Yeager RA, Lee RW, Porter JM. Noninvasive localization of arterial occlusive disease: a comparison of segmental Doppler pressures and arterial duplex mapping. J Vasc Surg. 1993;17(3):578-582. 10. Jager KA, Phillips DJ, Martin RL, et al. Noninvasive mapping of lower limb arterial lesions. Ultrasound Med Biol. 1985;11(3):515-521. 11. Khan SZ, Khan MA, Bradley B, et al. Utility of duplex ultrasound in detecting and grading de novo femoropopliteal lesions. J Vasc Surg. 2011;54(4): 1067-1073. 12. Elbadawy A, Aly H, Ibrahim M, Bakr H. Impact of duplex arterial mapping on decision making in non-acute ischemic limb patients. Int Angiol. 2015;34(6):538-544. 13. Fontcuberta J, Flores A, Orgaz A, et al. Reliability of preoperative duplex scanning in designing a therapeutic strategy for chronic lower limb ischemia. Ann Vasc Surg. 2009;23(5):577-582. 14. Norgren L, Hiatt WR, Dormandy JA, et al. Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II). J Vasc Surg. 2007;45(Suppl.S):S5-S67. 15. Sultan S, Tawick W, Hynes N. Ten-year technical and clinical outcomes in Trans-Atlantic Inter-Society Consensus II infrainguinal C/D lesions using duplex ultrasound arterial mapping as the sole imaging modality for critical lower limb ischemia. J Vasc Surg. 2013;57(4):1038-1045. 16. Davies AH, Willcox JH, Magee TR, et al. Colour duplex in assessing the infrainguinal arteries in patients with claudication. Cardiovasc Surg. 1995;3(2):211-212. 17. Legemate DA, Teeuwen C, Hoeneveld H, et al. he potential of duplex scanning to replace aorto-iliac and femoro-popliteal angiography. Eur J Vasc Surg. 1989;3(1):49-54. 18. Edwards JM, Coldwell DM, Goldman ML, Strandness Jr DE. he role of duplex scanning in the selection of patients for transluminal angioplasty. J Vasc Surg. 1991;13(1):69-74. 19. Lai DT, Huber D, Glasson R, et al. Colour-coded duplex ultrasonography in selection of patients for transluminal angioplasty. Australas Radiol. 1995;39(3):243-245. 20. Hodgkiss-Harlow KD, Bandyk DF. Interpretation of arterial duplex testing of lower-extremity arteries and interventions. Semin Vasc Surg. 2013;26(2-3):95-104. 21. Baril DT, Rhee RY, Kim J, et al. Duplex criteria for determination of in-stent stenosis ater angioplasty and stenting of the supericial femoral artery. J Vasc Surg. 2009;49(1):133-138. 22. Langenberger H, Schillinger M, Plank C, et al. Agreement of duplex ultrasonography vs. computed tomography angiography for evaluation of

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47. Gonsalves C, Bandyk DF, Avino AJ, Johnson BL. Duplex features of vein grat stenosis and the success of percutaneous transluminal angioplasty. J Endovasc Surg. 1999;6(1):66-72. 48. Rehfuss J, Scali S, He Y, et al. he correlation between computed tomography and duplex evaluation of autogenous vein bypass grats and their relationship to failure. J Vasc Surg. 2015;62(6):1546-1554 e1. 49. Idu MM, Blankenstein JD, de Gier P, et al. Impact of a color-low duplex surveillance program on infrainguinal vein grat patency: a ive-year experience. J Vasc Surg. 1993;17(1):42-52. 50. Szilagyi DE, Elliott JP, Hageman JH, et al. Biologic fate of autogenous vein implants as arterial substitutes: clinical, angiographic and histopathologic observations in femoro-popliteal operations for atherosclerosis. Ann Surg. 1973;178(3):232-246. 51. Cassina PC, Hailemariam S, Schmid RA, Hauser M. Infrainguinal aneurysm formation in arterialized autologous saphenous vein grats. J Vasc Surg. 1998;28(5):944-948. 52. McCormack LJ, Cauldwell EW, Anson BJ. Brachial and antebrachial arterial patterns; a study of 750 extremities. Surg Gynecol Obstet. 1953;96(1): 43-54. 53. Uhlemann M, Mobius-Winkler S, Mende M, et al. he Leipzig prospective vascular ultrasound registry in radial artery catheterization: impact of sheath size on vascular complications. JACC Cardiovasc Interv. 2012;5(1):3643. 54. Kliewer MA, Hertzberg BS, Kim DH, et al. Vertebral artery Doppler waveform changes indicating subclavian steal physiology. AJR Am J Roentgenol. 2000;174(3):815-819. 55. Longley DG, Yedlicka JW, Molina EJ, et al. horacic outlet syndrome: evaluation of the subclavian vessels by color duplex sonography. AJR Am J Roentgenol. 1992;158(3):623-630. 56. Wadhwani R, Chaubal N, Sukthankar R, et al. Color Doppler and duplex sonography in 5 patients with thoracic outlet syndrome. J Ultrasound Med. 2001;20(7):795-801. 57. Lee AD, Agarwal S, Sadhu D. Doppler Adson’s test: predictor of outcome of surgery in non-speciic thoracic outlet syndrome. World J Surg. 2006;30(3):291-292. 58. Criado E, Berguer R, Greenield L. he spectrum of arterial compression at the thoracic outlet. J Vasc Surg. 2010;52(2):406-411. 59. Chen H, Doornbos N, Williams K, Criado E. Physiologic variations in venous and arterial hemodynamics in response to postural changes at the thoracic outlet in normal volunteers. Ann Vasc Surg. 2014;28(7):15831588. 60. Abu-Omar Y, Mussa S, Anastasiadis K, et al. Duplex ultrasonography predicts safety of radial artery harvest in the presence of an abnormal Allen test. Ann horac Surg. 2004;77(1):116-119. 61. Habib J, Baetz L, Satiani B. Assessment of collateral circulation to the hand prior to radial artery harvest. Vasc Med. 2012;17(5):352-361. 62. Kochi K, Sueda T, Orihashi K, Matsuura Y. New noninvasive test alternative to Allen’s test: snuf-box technique. J horac Cardiovasc Surg. 1999;118(4): 756-758. 63. Pola P, Serricchio M, Flore R, et al. Safe removal of the radial artery for myocardial revascularization: a Doppler study to prevent ischemic complications to the hand. J horac Cardiovasc Surg. 1996;112(3): 737-744. 64. Lucena J, Rico A, Vazquez R, et al. Pulmonary embolism and suddenunexpected death: prospective study on 2477 forensic autopsies performed at the Institute of Legal Medicine in Seville. J Forensic Leg Med. 2009;16(4):196-201. 65. Bates SM, Jaeschke R, Stevens SM, et al. Diagnosis of DVT: antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest. 2012;141(2 Suppl.):e351S-e418S. 66. Ageno W, Squizzato A, Wells PS, et al. he diagnosis of symptomatic recurrent pulmonary embolism and deep vein thrombosis: guidance from the SSC of the ISTH. J hromb Haemost. 2013;11(8):1597-1602. 67. Wilbur J, Shian B. Diagnosis of deep venous thrombosis and pulmonary embolism. Am Fam Physician. 2012;86(10):913-919. 68. Wells PS. Integrated strategies for the diagnosis of venous thromboembolism. J hromb Haemost. 2007;5(Suppl. 1):41-50.

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Small Parts, Carotid Artery, and Peripheral Vessel Sonography

69. Le Gal G, Carrier M, Rodger M. Clinical decision rules in venous thromboembolism. Best Pract Res Clin Haematol. 2012;25(3):303317. 70. Qaseem A, Snow V, Barry P, et al. Current diagnosis of venous thromboembolism in primary care: a clinical practice guideline from the American Academy of Family Physicians and the American College of Physicians. Ann Fam Med. 2007;5(1):57-62. 71. Segal JB, Eng J, Tamariz LJ, Bass EB. Review of the evidence on diagnosis of deep venous thrombosis and pulmonary embolism. Ann Fam Med. 2007;5(1):63-73. 72. Wells PS, Anderson DR, Rodger M, et al. Evaluation of D-dimer in the diagnosis of suspected deep-vein thrombosis. N Engl J Med. 2003;349(13): 1227-1235. 73. Carrier M, Lee AY, Bates SM, et al. Accuracy and usefulness of a clinical prediction rule and D-dimer testing in excluding deep vein thrombosis in cancer patients. hromb Res. 2008;123(1):177-183. 74. Geersing GJ, Zuithof NP, Kearon C, et al. Exclusion of deep vein thrombosis using the Wells rule in clinically important subgroups: individual patient data meta-analysis. BMJ. 2014;348:g1340. 75. Squizzato A, Micieli E, Galli M, et al. Diagnosis and management of venous thromboembolism: results of a survey on current clinical practice. hromb Res. 2010;125(2):134-136. 76. Spritzer CE. Progress in MR imaging of the venous system. Perspect Vasc Surg Endovasc her. 2009;21(2):105-116. 77. Bundens WP, Bergan JJ, Halasz NA, et al. he supericial femoral vein. A potentially lethal misnomer. JAMA. 1995;274(16):12961298. 78. Quinlan DJ, Alikhan R, Gishen P, Sidhu PS. Variations in lower limb venous anatomy: implications for US diagnosis of deep vein thrombosis. Radiology. 2003;228(2):443-448. 79. Simpson WL, Krakowsi DM. Prevalence of lower extremity venous duplication. Indian J Radiol Imaging. 2010;20(3):230-234. 80. Dona E, Fletcher JP, Hughes TM, et al. Duplicated popliteal and supericial femoral veins: incidence and potential signiicance. Aust N Z J Surg. 2000;70(6):438-440. 81. Lautz TB, Abbas F, Walsh SJ, et al. Isolated gastrocnemius and soleal vein thrombosis: should these patients receive therapeutic anticoagulation? Ann Surg. 2010;251(4):735-742. 82. Caggiati A, Bergan JJ, Gloviczki P, et al. Nomenclature of the veins of the lower limbs: an international interdisciplinary consensus statement. J Vasc Surg. 2002;36(2):416-422. 83. Lockhart ME, Sheldon HI, Robbin ML. Augmentation in lower extremity sonography for the detection of deep venous thrombosis. AJR Am J Roentgenol. 2005;184(2):419-422. 84. Intersocietal Accreditation Commission (IAC). IAC standards and guidelines for vascular testing accreditation. IAC. Available from: http:// www.intersocietal.org/vascular/standards/IACVascularTestingStandards2016 .pdf. 85. Needleman L. Update on the lower extremity venous ultrasonography examination. Radiol Clin North Am. 2014;52(6):1359-1374. 86. Cronan JJ. Venous thromboembolic disease: the role of US. Radiology. 1993;186(3):619-630. 87. Rubin JM, Xie H, Kim K, et al. Sonographic elasticity imaging of acute and chronic deep venous thrombosis in humans. J Ultrasound Med. 2006;25(9): 1179-1186. 88. Johnson SA, Stevens SM, Woller SC, et al. Risk of deep vein thrombosis following a single negative whole-leg compression ultrasound: a systematic review and meta-analysis. JAMA. 2010;303(5):438-445. 89. Guanella R, Righini M. Serial limited versus single complete compression ultrasonography for the diagnosis of lower extremity deep vein thrombosis. Semin Respir Crit Care Med. 2012;33(2):144-150. 90. Birdwell BG, Raskob GE, Whitsett TL, et al. he clinical validity of normal compression ultrasonography in outpatients suspected of having deep venous thrombosis. Ann Intern Med. 1998;128(1):1-7. 91. Bernardi E, Camporese G, Buller HR, et al. Serial 2-point ultrasonography plus D-dimer vs whole-leg color-coded Doppler ultrasonography for diagnosing suspected symptomatic deep vein thrombosis: a randomized controlled trial. JAMA. 2008;300(14):1653-1659.

92. Society for Vascular Medicine. Five things physicians and patients should question. Choosing Wisely. 2014:1-2. Available from: http://www .choosingwisely.org/doctor-patient-lists/society-for-vascularmedicine/. 93. van Haarst EP, Liasis N, van Ramshorst B, Moll FL. he development of valvular incompetence ater deep vein thrombosis: a 7 year follow-up study with duplex scanning. Eur J Vasc Endovasc Surg. 1996;12(3):295-299. 94. horisson HM, Pollak JS, Scoutt L. he role of ultrasound in the diagnosis and treatment of chronic venous insuiciency. Ultrasound Q. 2007;23(2): 137-150. 95. Human P, Franz T, Scherman J, et al. Dimensional analysis of human saphenous vein grats: implications for external mesh support. J horac Cardiovasc Surg. 2009;137(5):1101-1108. 96. Chin EE, Zimmerman PT, Grant EG. Sonographic evaluation of upper extremity deep venous thrombosis. J Ultrasound Med. 2005;24(6): 829-838. 97. Gooding GA, Hightower DR, Moore EH, et al. Obstruction of the superior vena cava or subclavian veins: sonographic diagnosis. Radiology. 1986;159(3): 663-665. 98. Baarslag HJ, van Beek EJ, Koopman MM, Reekers JA. Prospective study of color duplex ultrasonography compared with contrast venography in patients suspected of having deep venous thrombosis of the upper extremities. Ann Intern Med. 2002;136(12):865-872. 99. Knudson GJ, Wiedmeyer DA, Erickson SJ, et al. Color Doppler sonographic imaging in the assessment of upper-extremity deep venous thrombosis. AJR Am J Roentgenol. 1990;154(2):399-403. 100. Baxter GM, Kincaid W, Jefrey RF, et al. Comparison of colour Doppler ultrasound with venography in the diagnosis of axillary and subclavian vein thrombosis. Br J Radiol. 1991;64(765):777-781. 101. Bernardi E, Piccioli A, Marchiori A, et al. Upper extremity deep vein thrombosis: risk factors, diagnosis, and management. Semin Vasc Med. 2001;1(1):105-110. 102. Fraser JD, Anderson DR. Venous protocols, techniques, and interpretations of the upper and lower extremities. Radiol Clin North Am. 2004;42(2): 279-296. 103. Patel MC, Berman LH, Moss HA, McPherson SJ. Subclavian and internal jugular veins at Doppler US: abnormal cardiac pulsatility and respiratory phasicity as a predictor of complete central occlusion. Radiology. 1999;211(2): 579-583. 104. Bonnet F, Loriferne JF, Texier JP, et al. Evaluation of Doppler examination for diagnosis of catheter-related deep vein thrombosis. Intensive Care Med. 1989;15(4):238-240. 105. McDonough JJ, Altemeier WA. Subclavian venous thrombosis secondary to indwelling cathers. Surg Gynecol Obstet. 1971;133(3):397-400. 106. Luciani A, Clement O, Halimi P, et al. Catheter-related upper extremity deep venous thrombosis in cancer patients: a prospective study based on Doppler US. Radiology. 2001;220(3):655-660. 107. Trerotola SO, Kuhn-Fulton J, Johnson MS, et al. Tunneled infusion catheters: increased incidence of symptomatic venous thrombosis ater subclavian versus internal jugular venous access. Radiology. 2000;217(1): 89-93. 108. Monreal M, Lafoz E, Ruiz J, et al. Upper-extremity deep venous thrombosis and pulmonary embolism. A prospective study. Chest. 1991;99(2):280283. 109. Becker DM, Philbrick JT, Walker FB. Axillary and subclavian venous thrombosis. Prognosis and treatment. Arch Intern Med. 1991;151(10): 1934-1943. 110. Kearon C. Natural history of venous thromboembolism. Circulation. 2003;107(23 Suppl. 1):I22-I30. 111. Horattas MC, Wright DJ, Fenton AH, et al. Changing concepts of deep venous thrombosis of the upper extremity—report of a series and review of the literature. Surgery. 1988;104(3):561-567. 112. Mustafa S, Stein PD, Patel KC, et al. Upper extremity deep venous thrombosis. Chest. 2003;123(6):1953-1956. 113. Kooij JD, van der Zant FM, van Beek EJ, Reekers JA. Pulmonary embolism in deep venous thrombosis of the upper extremity: more oten in catheterrelated thrombosis. Neth J Med. 1997;50(6):238-242. 114. Meissner MH, Moneta G, Burnand K, et al. he hemodynamics and diagnosis of venous disease. J Vasc Surg. 2007;46(Suppl.S):4S-24S.

CHAPTER 27 115. Recek C. Calf pump activity inluencing venous hemodynamics in the lower extremity. Int J Angiol. 2013;22(1):23-30. 116. Weber TM, Lockhart ME, Robbin ML. Upper extremity venous Doppler ultrasound. Radiol Clin North Am. 2007;45(3):513-524, viii-ix. 117. Kremkau FW, Taylor KJ. Artifacts in ultrasound imaging. J Ultrasound Med. 1986;5(4):227-237. 118. Reading CC, Charboneau JW, Allison JW, Cooperberg PL. Color and spectral Doppler mirror-image artifact of the subclavian artery. Radiology. 1990;174(1):41-42. 119. Pozniak MA, Zagzebski JA, Scanlan KA. Spectral and color Doppler artifacts. Radiographics. 1992;12(1):35-44. 120. U.S. Renal Data System (USRDS). 2015 USRDS annual data report: epidemiology of kidney disease in the United States. Bethesda, MD: National Institutes of Health; 2015. 121. Feldman HI, Kobrin S, Wasserstein A. Hemodialysis vascular access morbidity. J Am Soc Nephrol. 1996;7(4):523-535. 122. Vascular Access Work Group. Clinical practice guidelines for vascular access, pt 1. Am J Kidney Dis. 2006;48(Suppl. 1):S176-S247. 123. Hodges TC, Fillinger MF, Zwolak RM, et al. Longitudinal comparison of dialysis access methods: risk factors for failure. J Vasc Surg. 1997;26(6): 1009-1019. 124. Allon M, Robbin ML. Increasing arteriovenous istulas in hemodialysis patients: problems and solutions. Kidney Int. 2002;62(4):1109-1124. 125. Allon M, Lockhart ME, Lilly RZ, et al. Efect of preoperative sonographic mapping on vascular access outcomes in hemodialysis patients. Kidney Int. 2001;60(5):2013-2020. 126. Robbin ML, Gallichio MH, Deierhoi MH, et al. US vascular mapping before hemodialysis access placement. Radiology. 2000;217(1):83-88. 127. Gibson KD, Caps MT, Kohler TR, et al. Assessment of a policy to reduce placement of prosthetic hemodialysis access. Kidney Int. 2001;59(6): 2335-2345. 128. Little MD, Allon M, McNamara MM, et al. Risk evaluation of immediate surgical failure during thigh hemodialysis grat placement by sonographic screening. J Ultrasound Med. 2015;34(9):1613-1619. 129. Robbin ML, Chamberlain NE, Lockhart ME, et al. Hemodialysis arteriovenous istula maturity: US evaluation. Radiology. 2002;225(1):59-64. 130. Robbin ML, Greene T, Cheung AK, et al. Arteriovenous istula development in the irst 6 weeks ater creation. Radiology. 2015;150385. 131. Singh P, Robbin ML, Lockhart ME, Allon M. Clinically immature arteriovenous hemodialysis istulas: efect of US on salvage. Radiology. 2008; 246(1):299-305. 132. Allon M, Bailey R, Ballard R, et al. A multidisciplinary approach to hemodialysis access: prospective evaluation. Kidney Int. 1998;53(2): 473-479. 133. Robbin ML, Oser RF, Lee JY, et al. Randomized comparison of ultrasound surveillance and clinical monitoring on arteriovenous grat outcomes. Kidney Int. 2006;69(4):730-735. 134. Lumsden AB, MacDonald MJ, Kikeri D, et al. Prophylactic balloon angioplasty fails to prolong the patency of expanded polytetraluoroethylene arteriovenous grats: results of a prospective randomized study. J Vasc Surg. 1997;26(3): 382-390. 135. Ram SJ, Work J, Caldito GC, et al. A randomized controlled trial of blood low and stenosis surveillance of hemodialysis grats. Kidney Int. 2003;64(1):272-280. 136. Malik J, Slavikova M, Svobodova J, Tuka V. Regular ultrasonographic screening signiicantly prolongs patency of PTFE grats. Kidney Int. 2005;67(4): 1554-1558. 137. Dember LM, Holmberg EF, Kaufman JS. Randomized controlled trial of prophylactic repair of hemodialysis arteriovenous grat stenosis. Kidney Int. 2004;66(1):390-398.

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138. Tonelli M, James M, Wiebe N, et al. Ultrasound monitoring to detect access stenosis in hemodialysis patients: a systematic review. Am J Kidney Dis. 2008;51(4):630-640. 139. Allon M, Robbin ML. Hemodialysis vascular access monitoring: current concepts. Hemodial Int. 2009;13(2):153-162. 140. Jennings WC, Sideman MJ, Taubman KE, Broughan TA. Brachial vein transposition arteriovenous istulas for hemodialysis access. J Vasc Surg. 2009;50(5):1121-1126. 141. Robbin ML, Oser RF, Allon M, et al. Hemodialysis access grat stenosis: US detection. Radiology. 1998;208(3):655-661. 142. Lockhart ME, Robbin ML. Hemodialysis access ultrasound. Ultrasound Q. 2001;17(3):157-167. 143. Umphrey HR, Abts CA, Robbin ML. Dialysis grats and istulae: planning and assessment. Ultrasound Clin. 2011;6(4):477-490. 144. Lockhart ME, Robbin ML, Fineberg NS, et al. Cephalic vein measurement before forearm istula creation: does use of a tourniquet to meet the venous diameter threshold increase the number of usable istulas? J Ultrasound Med. 2006;25(12):1541-1545. 145. Glass CJM, DiGragio W, Illig KA. A meta-analysis of preoperative duplex ultrasound vessel diameters for successful radiocephalic istula placement. J Vasc Ultrasound. 2009;65-68(4). 146. Sidawy AN, Spergel LM, Besarab A, et al. he Society for Vascular Surgery: clinical practice guidelines for the surgical placement and maintenance of arteriovenous hemodialysis access. J Vasc Surg. 2008;48(5 Suppl.):2S-25S. 147. Miller CD, Robbin ML, Barker J, Allon M. Comparison of arteriovenous grats in the thigh and upper extremities in hemodialysis patients. J Am Soc Nephrol. 2003;14(11):2942-2947. 148. Ong S, Barker-Finkel J, Allon M. Long-term outcomes of arteriovenous thigh grats in hemodialysis patients: a comparison with tunneled dialysis catheters. Clin J Am Soc Nephrol. 2013;8(5):804-809. 149. Scott JD, Cull DL, Kalbaugh CA, et al. he mid-thigh loop arteriovenous grat: patient selection, technique, and results. Am Surg. 2006; 72(9):825-828. 150. National Kidney Foundation. KDOQI clinical practice guidelines and clinical practice recommendations for vascular access 2006. Am J Kidney Dis. 2006;48(Suppl. 1):S176-S322. 151. Falk A. Maintenance and salvage of arteriovenous istulas. J Vasc Interv Radiol. 2006;17(5):807-813. 152. Clark TW, Hirsch DA, Jindal KJ, et al. Outcome and prognostic factors of restenosis ater percutaneous treatment of native hemodialysis istulas. J Vasc Interv Radiol. 2002;13(1):51-59. 153. Beathard GA, Arnold P, Jackson J, et al. Aggressive treatment of early istula failure. Kidney Int. 2003;64(4):1487-1494. 154. May RE, Himmelfarb J, Yenicesu M, et al. Predictive measures of vascular access thrombosis: a prospective study. Kidney Int. 1997;52(6): 1656-1662. 155. Shackleton CR, Taylor DC, Buckley AR, et al. Predicting failure in polytetraluoroethylene vascular access grats for hemodialysis: a pilot study. Can J Surg. 1987;30(6):442-444. 156. Leake AE, Winger DG, Leers SA, et al. Management and outcomes of dialysis access-associated steal syndrome. J Vasc Surg. 2015;61(3):754-760. 157. Valji K, Hye RJ, Roberts AC, et al. Hand ischemia in patients with hemodialysis access grats: angiographic diagnosis and treatment. Radiology. 1995;196(3):697-701. 158. Robbin ML, Lockhart ME. Ultrasound evaluation before and ater hemodialysis access. In: Zweibel WJ, Pellerito JS, editors. Introduction to vascular ultrasonography. 5th ed. Philadelphia: Elsevier; 2005. p. 325-340.

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APPENDIX

Ultrasound Artifacts: A Virtual Chapter Korosh Khalili, Hojun Yu, Alexander Jesurum, and Deborah Levine

SUMMARY OF KEY POINTS • Artifacts are common in ultrasound imaging. • Knowledge of artifacts can aid in diagnosis.

• Understanding ultrasound physics allows for correction of artifacts that distort the visualized anatomy.

CHAPTER OUTLINE ASSUMPTIONS IN GRAY-SCALE IMAGING Velocity of Sound Attenuation of Sound Path of Sound Beam Proile PROPAGATION VELOCITY ARTIFACT ATTENUATION ERRORS Shadowing Increased Through Transmission PATH OF SOUND-RELATED ARTIFACTS Mirror Image Artifact Comet-Tail Artifact

Refraction Anisotropy Reverberation Artifact GAS-RELATED ARTIFACTS Reverberation Artifact Ring-Down Artifact Dirty Shadowing Artifact BEAM PROFILE–RELATED ARTIFACTS Side Lobe and Grating Lobe Artifacts Partial Volume Averaging DOPPLER IMAGING ARTIFACTS Loss or Distortion of Doppler Information

A

lmost all ultrasound images contain artifacts. Many of these artifacts go unrecognized because they are contained within (and contribute to) the background noise. However, when artifacts substantially alter the signal, they become recognizable on images. Certain artifacts distort the images and must be recognized in order to improve image quality or prevent a false diagnosis. Other artifacts add useful data and thus are important for understanding the composition, anatomy, and pathology of the image being visualized. We hope you enjoy this virtual chapter, which encompasses animated illustrations of how artifacts are produced as well as multiple examples of images and videos from the text.

ASSUMPTIONS IN GRAY-SCALE IMAGING Several assumptions about the propagation of sound waves are made when ultrasound equipment maps echoes onto the image.1 When one or more of these assumptions prove invalid, artifacts result.

Artifactual Vascular Flow Tissue Vibration Artifact Aliasing and Velocity Scale Errors Spectral Broadening Blooming Artifact Twinkle Artifact Acknowledgment

Velocity of Sound he speed of sound throughout the tissues is assumed to be uniform at 1540 m/sec. When the waves travel through tissues that substantially alter sound velocity, propagation velocity artifacts occur.

Attenuation of Sound Sound waves normally become fainter—that is, their intensity decreases—as they travel through tissues. he equipment assumes that this attenuation of intensity occurs at a constant rate. If the waves travel through tissues that either do not attenuate as much or attenuate more than the adjacent tissues, attenuation errors such as increased through transmission or shadowing arise.

Path of Sound In creating the image, the equipment assumes that the generated sound wave travels from the surface of the probe in a straight line, is relected of a relector only once, and returns directly back to the probe at the same angle exactly to the point from which it let the probe. If the sound waves undergo more than one relection, then artifacts such as mirror image, reverberation,

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or comet-tail occur. And if the direction of the beam or its echo is altered, refraction or anisotropy artifact may be produced.

Beam Proile An assumption is made that the sound beam generated by the transducer is a narrow line. When the beam is not suiciency narrow in the imaging plane or in the elevation plane (i.e., along the short axis of the transducer), side lobe or grating lobe or partial volume averaging artifacts may occur.

large structure composed of tissue that propagates speed at a diferent velocity is encountered, then propagation velocity artifact can occur.1 In the case of a fatty lesion, the slower speed of propagation (approximately 1450 m/sec) means that the echo will take longer to return to the transducer; thus the lesion is displayed deeper in the image than its true location. Some newer ultrasound machines with multibeam (spatial compounding) features and improved signal processing can minimize this artifact. Click here to see an explanatory video of propagation velocity artifact (Video A.1).

PROPAGATION VELOCITY ARTIFACT Ultrasound image processing assumes that the speed of sound in tissue is a constant 1540 m/sec. However, when a suiciently Air

330

Fat

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1500

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Propagation velocity (meters/second) FIG. A.1 Propagation Velocity. Propagation velocity of different body tissues.2 (See Chapter 1, Fig. 1.2.)

FIG. A.2 Propagation Velocity. When sound passes through a fatty mass, in this case a myelolipoma, its speed slows down to 1450 m/sec. Because the ultrasound scanner assumes that sound is being propagated at the average velocity of 1540 m/sec, the delay in echo return is interpreted as indicating a deeper target. Therefore the inal image shows a misregistration artifact in which the diaphragm (arrow) is shown in a deeper position than expected in this patient with a right adrenal myelolipoma. The computed tomography image depicts the myelolipoma, conirming its fatty nature.

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Shadowing

ATTENUATION ERRORS When the ultrasound beam encounters a focal lesion that attenuates the sound to a greater or lesser extent than the surrounding tissues, the intensity of the beam deep to the lesion will be either weaker (shadowing) or stronger (increased through transmission) than in the surrounding tissues. Click here to see an explanatory video of attenuation-related artifacts (Video A.2).

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Ultrasound Artifacts: A Virtual Chapter

Shadowing results when there is a marked reduction in the intensity of the ultrasound deep to a strong relector, attenuator, or refractor. Clean dark shadows will be seen behind calciied objects when the focal zone is at or just below the structure. Click here to see an explanatory video of shadowing (Video A.3).

0.00 0.18

Blood Fat

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Attenuation (dB/cm/MHz) FIG. A.3 As sound passes through tissue, it loses energy through the transfer of energy to tissue by heating, relection, and scattering. Attenuation is determined by the insonating frequency and the nature of the attenuating medium. Attenuation values for normal tissues show considerable variation. Attenuation also increases in proportion to insonating frequency, resulting in less penetration at higher frequencies.2 (See Chapter 1, Fig. 1.9.)

FIG. A.4 Gallstone With Shadowing. Note the dark, well-deined shadow.3 (See Chapter 6, Fig. 6.39C.)

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FIG. A.5 Shadowing From Hernia Repair Mesh.

FIG. A.6 Shadowing From Ovarian Fibroma. This is a slightly less “clean” shadow since the ibroma is not as dense as a calciied stone.

FIG. A.7 Shadowing From an Intrauterine Device.4 (See Chapter 15, Fig. 15.25A.)

FIG. A.8 Shadowing. Coned down view of distal neonatal spine shows shadowing from vertebral bodies that interrupt the linear appearance of the nerve roots.5 (See Chapter 49, Fig. 49.3.)

APPENDIX Click here to see real-time cine clip of showing in region of cauda equina (Video A.4).5

Ultrasound Artifacts: A Virtual Chapter

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Edge shadowing is caused by excessive refraction and commonly occurs from the edges vessels, cystic structures, and bones.

FIG. A.10 Edge Shadowing. Note the edge shadowing artifact behind the posterior aspect of the fetal skull. The beam bends at curved surface and loses intensity, producing a shadow (arrow).7 (See Chapter 34, Fig. 34.3.)

FIG. A.9 Shadowing. Shadowing from dense plaque prevents assessment of color low in that region. Note that there must be low present because similar color is visualized before and after the shadow.6 (See Chapter 26, Fig. 26.8.)

FIG. A.11 Edge Shadowing 2. Endometrial polyp shows both through transmission behind the cystic spaces and edge shadowing at the margins of the cysts.4 (See Chapter 15, Fig. 15.14B.)

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Increased Through Transmission Increased through transmission occurs when an object (such as a cyst) attenuates the sound waves less than the surrounding tissues. Click here to an explanatory video of increased through transmission (Video A.5).

FIG. A.13 Increased Through Transmission. The hepatic parenchyma distal to the cysts is falsely displayed as increased in echogenicity (arrows) secondary to increased through-transmission artifact.

–0 dB

Gain compensated

–10 + 10 dB

+10–3 = +7 dB

–20 + 20 dB

+20–13 = +7 dB

FIG. A.12 Increased Through Transmission. The cyst attenuates 7 dB less than the normal tissue, and time gain curve correction for normal tissue results in overampliication of the signals deep to the cyst, producing increased through transmission of these tissues.2 (See Chapter 1, Fig. 1.31C.)

FIG. A.14 Increased Through Transmission. Nabothian cysts show both increased through transmission behind the cysts and edge shadowing at the margins of the cysts.4 (See Chapter 15, Fig. 15.7C.)

APPENDIX

PATH OF SOUND-RELATED ARTIFACTS In mapping a returning echo onto the generated image, an assumption is made that it originated from the same part of the transducer from which it was produced. Also, an assumption is made that the echo is the result of a single relection. he depth of the relector is calculated based on the time it took for the sound wave to travel from the transducer to the relector and back, assuming a single relection. When these assumptions do not hold, various types of artifacts occur. Click here to see an explanatory video of path of sound assumption (Video A.6).

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Mirror Image Artifact A mirror image artifact is created when the primary beam encounters a highly relective surface that acts like a mirror. he relected echoes then encounter other relectors and bounce back onto the mirror before being directed to the transducer. he result is artifactually inverted projection of the relectors deeper to the surface of the mirror. he image is displayed deeper because of the longer path of the relected sound. If the mirror image artifact causes confusion, it can be decreased or eliminated by moving the transducer to center it on the region of interest and/ or placing the focal zone at the level of interest in the real structure. Click here to see an explanatory video of mirror image artifact (Video A.7).

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FIG. A.15 Mirror Image. Picture of relection in water—similar to mirror image artifact.

FIG. A.16 Mirror Image Artifact. Soft tissue–gas interfaces, such as the diaphragm, are excellent relectors of the sound beam owing to the large difference in the acoustic impedance between the two materials. Therefore hepatic structures are frequently seen mirrored beyond the diaphragm onto the lungs. These two igures show liver parenchyma, hepatic veins in part A, and a hepatic hemangioma in part B all inversely projected onto lung.

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Comet-Tail Artifact Comet-tail artifact is a type of reverberation artifact.8 he repetitive relections occur within very small structures, such as tiny cysts in the case of von Meyenburg complexes and tiny crypts in the wall of the gallbladder in the case of adenomyomatosis. Accordingly, the reverberated echoes may not be individually visible. he tapered, comet-tail appearance is due to the decreasing amplitude of each reverberation as a result of beam attenuation. Click here to see the explanatory video of comet-tail artifact in adenomyomatosis (Video A.8).

FIG. A.17 Comet-Tail Artifact in Association With Adenomyomatosis. This is felt to be due to cholesterol crystals within the prominent Rokitansky-Aschoff sinuses.3 (See Chapter 6, Fig. 6.45.)

FIG. A.18 Comet-Tail Artifact. On color and spectral Doppler this can look like a twinkle artifact, but it is a color representation of the comet-tail. (See section on color Doppler artifacts for description of the twinkling.3) (See Chapter 6, Fig. 6.46.)

FIG. A.19 Adenomyomatosis and Comet-Tail Artifact.

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Click here to see real time scanning of comet-tail artifact in adenomyomatosis (Video A.9).

FIG. A.20 Comet-Tail Artifact Behind von Meyenburg Complex in Two Patients.9 (See Chapter 4, Fig. 4.16.)

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FIG. A.21 Colloid Cyst in Thyroid Gland With Characteristic Comet-Tail Artifact (Arrow).10 (See Chapter 19, Fig. 19.10A.)

FIG. A.22 Strong Comet-Tail Artifact Due to Fiducial Marker in Patient With Prostate Cancer.11 (See Chapter 10, Fig. 10.13.)

APPENDIX

Refraction As sound moves between tissues with diferent propagation velocities, such as from muscle to fat, it changes its direction at their interface as a result of refraction. he physical properties of refraction are explained by Snell’s law, as demonstrated in Figs. A.2312 and A.24. he change in the direction of the sound waves results in violation of the assumption made by the ultrasound equipment that the incident and relected waves travel in a

Ultrasound Artifacts: A Virtual Chapter

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straight line. herefore, with refraction, structures insonated by the bent path of sound waves are artifactually translated to appear as if the sound waves had traveled along a straight path. If refraction is suspected, it can be minimized by increasing the scan angle so that sound waves travel perpendicular to the interface. Click here to see an explanatory video of refraction from the anterior abdominal wall (Video A.10).

FIG. A.23 Refraction. Refraction can be due to tissues with different propagation velocities. When sound passes from soft tissue with propagation velocity (C1) of 1540 m/sec to fat with a propagation velocity (C2) of 1450 m/sec, there is a change in the direction of the sound wave because of refraction. The degree of change is related to the ratio of the propagating velocities of the media forming the interface (sinθ1/sinθ2 = C1/C2)2. Note that when the incident angle is changed to zero degrees— that is, the incident beam is perpendicular to the interface (θ1 = 0°)—the artifact disappears.

FIG. A.24 Refraction. Image of a straw in water. Refraction has occurred owing to the difference between air and water, causing an offset in the appearance of the straw. Note also how the straw appears larger in the water because of distortion of the image.

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FIG. A.25 Refraction. This igure shows what appears to be a second gestational sac due to refraction artifact. This is sometimes called “ghosting.”2 (See Chapter 1, Fig. 1.8.)

FIG. A.26 Refraction. A panoramic view of the Achilles tendon demonstrates a rupture within the midportion of the tendon. The proximal aspect of the tendon is chronically thickened and hypoechoic (arrows). Refraction artifact (arrowheads) is caused by the interfaces between the ruptured tendon edges and hemorrhage. C, Calcaneus.13 (See Chapter 23, Fig. 23.11.)

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Anisotropy Anisotropy is an artifact caused by structures that are composed of bundles of highly relective ibers running parallel to each other, such as tendons and ligaments. If the sound beam hits the tendon or ligament ibers perpendicular to their length, it is relected directly back, resulting in an echogenic appearance. But if the angle of insonation is not perpendicular to the tendon ibers, the beam is relected away from the transducer, leading to the generation of an image with artifactual hypoechogenicity within the tendon. Click here to see an explanatory video of anisotropy (Video A.11).

FIG. A.27 Anisotropy. The insertion of supraspinatus tendon artifactually appears hypoechoic due to anisotropy.

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Click here for video of real-time scanning of anisotropy at supraspinatus insertion (Video A.12).

FIG. A.28 Anisotropy. The peritrigonal region of the white matter (ellipse) appears relatively echogenic, also called “peritrigonal blush.” This anisotropic effect artifact occurs because in the trigone region, the parallel white matter ibers run perpendicular to the incident sound beam, causing increased relection.14 The artifact is visible only in the region of the trigone when the anterior fontanelle is used as a scanning window.

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A

B

FIG. A.29 Anisotropy. (A) In this long-axis scan of the Achilles insertion on the calcaneus, the proximal portion of the imaged tendon demonstrates a normal ibrillar appearance (arrow), whereas the distal tendon insertion is hypoechoic (arrowhead). (B) When the transducer is angled 90 degrees to the distal tendon insertion, the tendon then becomes ibrillar and is normal in appearance (arrowhead). C, Calcaneus.13 (See Chapter 23, Fig. 23.8.)

A

B

FIG. A.30 Anisotropy. Short-axis images of the supraspinatus tendon. (A) Artifactual hypoechogenicity of the supraspinatus tendon (arrows) may simulate tendinosis or tear. (B) Correction of angle of insonation to be perpendicular to the tendon permits visualization of the normal intact tendon.15 (See Chapter 24, Fig. 24.30.)

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Reverberation Artifact Reverberation artifact occurs when a strong relector runs perpendicular to the direction of the beam (i.e., parallel to the probe surface), usually close to the skin surface.1 he sound waves may then get partially “trapped” between the relector and skin, reverberating back and forth and causing the appearance of multiple regular lines when some of the waves eventually

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reach the probe. Oten the relectors are the skin and subcutaneous fascia (see Fig. A.31). Reverberation artifact is angle dependent, so moving the transducer slightly will cause a decrease in or elimination of the artifact. Reverberation can be helpful during biopsies, to see a needle. If it is distracting, try changing the angle of insonation, using a diferent window, or decreasing the gain.

FIG. A.31 Reverberation Artifact. Reverberation artifacts arise when the ultrasound signal relects repeatedly between highly relective interfaces near the transducer, resulting in delayed echo return to the transducer. This appears in the image as a series of regularly spaced echoes at increasing depth.2 (See Chapter 1, Fig. 1.27.)

FIG. A.32 Mirror Image and Reverberation Artifacts Behind a Pacemaker. The highly relective and mirrorlike surface of the pacemaker (arrow) results in repeated bouncing of sound wave among the probe surface, pacemaker, and skin.

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For reverberation due to gas, see next section.

GAS-RELATED ARTIFACTS Several physical properties of gases lead to unique artifacts in ultrasound that help identify gas but also may hinder visualization of other organs. hese properties include the very dissimilar acoustic impedance of gas compared with sot tissues, making them highly relective surfaces. he varied and ever-changing shape of gas in the body, including foam, leads to variability of its appearance even in the same ield. he very low density of gases makes them quite compressible, and they can undergo resonant oscillation in response to sound waves, leading to ampliication of echoes. hese properties result in three distinct artifacts, which can be present at the same time: reverberation, ring-down, and dirty shadowing.16

Reverberation Artifact he physical pressure of the probe on the sot tissues, such as the abdominal wall, lattens their shape in the near ield, making them perpendicular to the surface of the probe and the incident sound beam. Because gases conform to the shape of their containers, they too will form a linear and perpendicular interface to the incident sound beam, especially when in the form of a large bubble. he highly relective gas interface will act like a mirror, resulting in reverberation artifacts. Click here to see an explanatory video of reverberation artifact due to gas (Video A.13).

FIG. A.33 Reverberation Artifact. Small amount of gas within the bladder is recognizable by the reverberation artifact (arrow).

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Ring-Down Artifact Ring-down artifact occurs when the ultrasound waves cause oscillation within luid trapped by a tetrahedron of gas bubbles.17 hese oscillations create a continuous sound wave that is transmitted back to the transducer. What will be seen is a line or series of parallel bands extending posterior to a gas collection. Although this has the appearance of reverberation artifact, it actually has a diferent mechanism. Click here to see an explanatory video of ring-down artifact (Video A.14).

A

B

FIG. A.34 Ring-Down Artifact. Pneumobilia causing ring-down artifact in the biliary tree (A) and gallbladder (B).3 (See Chapter 6, Fig. 6.13.)

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Click here to see a video clip of ring-down artifact in peripheral ducts of the liver (Video A.15).

FIG. A.35 Ring-Down Artifact. Iatrogenic air in the bladder introduced at cystoscopy appears as a nondependent bright region with ring-down artifact.18 (See Chapter 9, Fig. 9.36.)

Dirty Shadowing Artifact Dirty shadowing results from a combination of relection, reverberation, and ring-down artifacts arising from multiple variably sized bubbles in foam.16 Click here to see an explanatory video of dirty shadowing artifact (Video A.16).

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FIG. A.36 Dirty Shadowing. Sonographic image of the liver shows gas in liver mass with reverberation artifact illing the cavity. See comparison computed tomography scan.9 (See Fig. 4.19.)

FIG. A.37 Dirty Shadowing Posterior to Emphysematous Cholecystitis.3 (See Chapter 6, Fig. 6.40.)

FIG. A.38 Dirty Shadowing in the Kidney Due to Emphysematous Pyelonephritis.18 (See Chapter 9, Fig. 9.22.)

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BEAM PROFILE–RELATED ARTIFACTS Frequently echoes are seen within what should be an anechoic structure. his can occur as a result of side lobe or grating lobe artifacts in which information from the side of the image projects centrally, or because of partial volume averaging (owing to the thickness of the ultrasound beam (resolution in the Z plane).

FIG. A.39 The ultrasound beam is not a narrow straight line but has a complex proile that varies depending on the type and shape of the transducer. Although most of the energy generated by a transducer is emitted in a beam along the central axis of the transducer (A), some energy is also emitted at the periphery of the primary beam (B and C). These are called “side lobes” (B) or “grating lobes” (C) and are lower in intensity than the primary beam. Side lobes or grating lobes may interact with strong relectors that lie outside of the scan plane and produce artifacts that are displayed in the ultrasound image.2 They are more evident when the misplaced echoes overlap an expected anechoic structure. (See Chapter 1, Fig. 1.28.)

Side Lobe and Grating Lobe Artifacts Click here to see an explanatory video of side lobe artifact (Video A.17).

FIG. A.40 Side or Grating Lobe 1. Transverse image of the gallbladder reveals a bright internal echo (A) that suggests a band or septum within the gallbladder. This is a side lobe artifact related to the presence of a strong out-of-plane relector (B) medial to the gallbladder. The low-level echoes in the dependent portion of the gallbladder (C) are also artifactual and are caused by the same phenomenon. Side lobe and slice thickness artifacts are of clinical importance because they may create the impression of debris in luid-illed structures.2 (See Chapter 1, Fig. 1.29.)

APPENDIX

FIG. A.41 Side or Grating Lobe. In this patient with a ureterovesical junction stone there are echoes seen in the nondependent portion of the bladder. These are due to grating lobe artifact, wherein off-axis signal projects into the ield of view.18 Note also the shadowing behind the bladder stone.18 (See Chapter 9, Fig. 9.43.)

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FIG. A.42 Partial Volume Averaging. The bladder wall is indistinct in region of this image. It is unclear if there are masses or if this is due to grating lobe artifact or partial volume artifact or both. Moving the patient or transducer to avoid bowel gas and putting the focal zone in the region in question should aid in evaluation. For the area closer to the patient’s anterior abdominal wall, a higher-frequency transducer might be helpful.18 (See Chapter 9, Fig. 9.57.)

Partial Volume Averaging he ultrasound beam not only has a complex shape in the imaging plane but also has a real proile in the third dimension, called the “elevation plane” or “Z plane.” he ultrasound image appears as a lat two-dimensional image, but the brightness of each pixel is representative of the average sum of all the echoes received within the thickness of the beam in the elevation plane. his results in echoes being projected in structures that should be anechoic. Click here to see an explanatory video of partial volume averaging (Video A.18).

FIG. A.43 Partial Volume Averaging. A radiofrequency ablation zone present in the liver just outside the scanning plane is depicted onto the lungs through both partial volume averaging and mirror image artifacts.

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DOPPLER IMAGING ARTIFACTS he appearance of color Doppler signal is afected by several variables including color-write priority, gray-scale gain, and pulse repetition frequency. If the color gain is too low, low might not be visualized. If the gain is too high, artifactual low may be seen in adjacent sot tissues, and thrombus within the vessel might be missed.

Loss or Distortion of Doppler Information Incorrect gain, wall-ilter, and velocity scale can all lead to loss or distortion of Doppler signal. A rule of thumb for gain adjustment in Doppler imaging is to turn up the color gain until noise is encountered and then back of just until the noise clears from the image. In estimating frequency, the rule of thumb is to use a Doppler angle less than 60 degrees (but not 0). Wall ilters eliminate low-frequency noise, but a high setting can lead to loss of signal. In general, wall ilters should be kept at the lowest practical level, typically in the range of 50 to 100 Hz.

A (PRF = 700 Hz)

θ = 60° cos θ = 0.5 ∆F = 0.5

θ = 90° cos θ = 0.0 ∆F = 0.0

θ = 0° cos θ = 1.0 ∆F = 1.0

FIG. A.44 Effect of Doppler Angle on Frequency Shift. At an angle of 60 degrees, the detected frequency shift detected by the transducer is only 50% of the shift detected at an angle of 0 degrees. At 90 degrees, there is no relative movement of the target toward or away from the transducer, and no frequency shift is detected. The detected Doppler frequency shift is reduced in proportion to the cosine of the Doppler angle. Because the cosine of the angle changes rapidly at angles above 60 degrees, the use of Doppler angles of less than 60 degrees is recommended in making velocity estimates.2 (See Chapter 1, Fig. 1.35.)

B (PRF = 4500 Hz)

FIG. A.45 Artifactual Lack of Flow. Color Doppler image of a carotid artery and jugular vein. In (A), the pulse repetition frequency (PRF) is 700 Hz and there is aliasing in the carotid artery, but slow low in the jugular vein is seen. In (B), the PRF is 4500 Hz, eliminating aliasing in the artery but also suppressing the display of the low Doppler frequencies in the internal jugular vein.2 (See Chapter 1, Fig. 1.43.)

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A

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B

FIG. A.46 Artifactual Lack of Flow. (A) Color Doppler image shows low in the portal vein. (B) When a color image is taken to assess the common duct, no low is visible in the portal vein. Note the difference in overall gain in image B.

FIG. A.47 Color Direction. Shown in color is a portion of the portal venous system. Note how the low direction appears to change in the region of branching, but this is merely a result of the orientation of low with respect to the mid transducer. Note the aliasing in the posterior branch of the right portal vein. This is due to the curve of the vein and change in Doppler angle.19 (See Chapter 51, Fig. 51.22.)

FIG. A.48 Color Direction as Shown in Recanalized Umbilical Vein. Flow on color Doppler will sometimes appear to change direction, but the low needs to be assessed with respect to the transducer in order to determine if it is in the appropriate direction or not. In this example, transverse paramedian gray-scale and color Doppler sonograms show left lobe of liver in a child with cirrhosis and portal hypertension.19 The recanalized umbilical vein is always lowing in relatively the same direction out of the liver, but at times, due to tortuosity, appears to change low direction. Note that the low changes from red (toward the transducer) to blue (away from the midpoint of the transducer), but at each interface there is a black region where the Doppler angle is 90. (See Chapter 51, Fig. 51.28.)

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Artifactual Vascular Flow he Doppler efect (shit) is not speciic to vascular low and occurs with movement of any relector toward or away from the ultrasound beam. Fluid or solid tissue motion can mimic vascular low. Transmitted pulsations, especially close to the heart or major arteries, can therefore result in artifactual appearance of low within thrombosed veins or avascular areas. Artifactual vascular low can also be visualized if the color gain is too high or the color-write priority is too high.

FIG. A.49 Artifactual Vascular Flow. Color Doppler jets in the bladder use color motion to indicate that there is low from each ureteral oriice.18 (See Chapter 9, Fig. 9.42A.)

A

B

FIG. A.50 Artifactual Vascular Flow. Color low Doppler signal in pleural luid with debris. (A) Gray-scale sonogram shows left pleural luid with much debris. (B) Color low Doppler signal.20 (See Chapter 50, Fig. 50.14.)

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#

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*

* #

FIG. A.51 Artifactual Vascular Flow. Power Doppler ultrasound vocal fremitus can be used to distinguish a mural nodule from a fat-luid level. The lipid layer is not attached to the cyst wall, so the fremitus artifact will not pass through it. On the other hand, true papillary lesions that are attached to the cyst wall will vibrate and transmit the fremitus artifact on power Doppler; having the patient hum in a deep voice creates a color artifact on power Doppler ultrasound.21 (See Chapter 21, Fig. 21.26.)

A

B

FIG. A.52 Color Streaking Artifact. (A) This complicated cyst contains loating punctate echoes that move posteriorly while being scanned, creating a scintillating appearance on gray-scale sonography. (B) Power Doppler ultrasound pushes the echoes posteriorly faster and with more energy than does the gray-scale beam. The echoes move fast enough that color persistence creates the appearance of “color streaking” artifact.21 (See Chapter 21, Fig. 21.21.)

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FIG. A.53 Flash Artifact From Pulsation. In this image of the left portal vein, note how transmitted pulsation from the heart causes artifactual low in the adjacent liver owing to motion.

Tissue Vibration Artifact Tissue vibration artifact consists of color pixels erroneously placed in the adjacent sot tissue by the ultrasound scanner because of the transmitted vibration from a region of marked turbulence. It is commonly seen with shunts, tight stenoses of large arteries, and especially arteriovenous istulas. If tissue vibration artifact is seen, a search should be made for an arteriovenous istula.

A FIG. A.54 Tissue Vibration Artifact From Common Femoral Artery to Common Femoral Vein Arteriovenous Fistula. Turbulent low through the istula may affect surrounding tissues, causing a tissue vibration artifact, which may be the irst clue that an arteriovenous istula (AVF) is present. Common femoral artery to common femoral vein AVF. (A) Color Doppler shows common femoral artery to common femoral vein AVF. Note the adjacent tissue vibration artifact (arrowheads). (See Chapter 27, Fig. 27.14.)

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Click here to see the video of tissue vibration (Video A.19).

FIG. A.55 Tissue Vibration Artifact. Postbiopsy arteriovenous istula. Color Doppler image shows markedly increased lower-pole blood low (arrows) with adjacent soft tissue color artifact related to tissue vibration (arrowheads).22 (See Chapter 52, Fig. 52.49.)

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Aliasing and Velocity Scale Errors Aliasing is an artifact due to undersampling of Doppler signal, resulting in incorrect estimation of low velocity. To measure the Doppler frequency shit appropriately by pulsed Doppler, at least two samples from the cycle are required (Nyquist limit). If the pulse repetition frequency is less than twice the maximum frequency shit produced by movement of the target, aliasing results. he Doppler signal wraps around either the spectrum (spectral Doppler) or the color scale (color Doppler). he most common methods for correcting for aliasing are to shit the baseline down or up, or increase the pulse repetition frequency (or velocity scale). A lower-frequency transducer can also be used to help in correcting for aliasing. As angulation approaches 90 degrees, directional ambiguity can occur, suggesting bidirectional low. Errors in Doppler angle correction can also lead to misleading assessments of low velocity. FIG. A.56 Tissue Vibration Artifact. Spectral waveform at site of superior mesenteric artery stenosis shows very high systolic velocity, and diastolic velocities of greater than 500 cm/sec. Color portion of the image shows color bruit consisting of color outside the vessel near the stenosis site. Color bruit is believed to be caused by tissue vibration.23 (See Chapter 12, Fig. 12.27A.)

Click for video showing tissue vibration artifact in patient with stenotic superior mesenteric artery with color bruit (Video A.20). (See also Video 12.11.)

APPENDIX

A

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B

D

FIG. A.57 Aliasing. Pulse repetition frequency (PRF) determines the sampling rate of a given Doppler frequency. (A) If PRF (arrows) is suficient, the sampled waveform (orange curve) will accurately estimate the frequency being sampled (yellow curve). (B) If PRF is less than half the frequency being measured, undersampling will result in a lower-frequency shift being displayed (orange curve). (C) Aliasing appears in the spectral display as a “wraparound” of the higher frequencies to display below the baseline. (D) In color Doppler display, aliasing results in a wraparound of the frequency color map from one low direction to the opposite direction.2 Unlike a true direction of low change, with aliasing there will be no transition of unsaturated color. (See Chapter 1, Fig. 1.46.)

FIG. A.58 Aliasing. Note that aliasing prevents precise calculation of the maximum systolic velocity. However, because it is greater than 500 cm/sec, the precise number is not needed. The aliasing in the image allows for easier identiication of the region of highest velocity for placement of the spectral Doppler gate.6 (See Chapter 26, Fig. 26.20.)

FIG. A.59 Aliasing in Superior Mesenteric Artery (SMA) Due to High-Velocity Flow.23 (See Chapter 12, Fig. 12.28.)

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A

B

FIG. A.60 Aliasing Due to Doppler Angle Theta Changes. (A) Velocity obtained in the distal internal carotid artery with angle theta of 60 degrees is higher than that obtained at 44 degrees (arrow). (B) However, the sample angle does not parallel the vessel wall at 60 degrees. Note central color aliasing in the region of highest velocity (curved arrow).6 (See Chapter 26, Fig. 26.16.)

FIG. A.61 Aliasing in Pseudoaneurysm. Note the swirling low in a pseudoaneurysm, resulting in a yin-yang appearance.24 At the midline border of red and blue, there is a black line where the Doppler angle is 90 degrees. Here the low is perpendicular to the sound beam, and so it is not detected. At 3 and 9 o’clock positions, there is aliasing within the blue and red areas. Here the Doppler angle is zero degrees with the low directly toward and away from the transducer, thus appearing with maximal velocity. As the velocity exceeds the selected 35-cm/sec Doppler velocity range, aliasing results with artifactual opposite direction color signal. (See Chapter 27, Fig. 27.63.)

Click here to see the pseudoaneurysm video clip showing even more dramatic aliasing in the femoral artery (Video A.21).24 (See also Chapter 27, Video 27.5.)

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Spectral Broadening Spectral broadening occurs when there are multiple diferent velocities of low within a vessel. his can be a sign of stenosis. However, artifactual spectral broadening can occur owing to improper positioning of the sample volume near the vessel wall, use of an excessively large sample volume, or excessive system gain.

FIG. A.63 Spectral Broadening. True spectral broadening due to ECA stenosis.6 (See Chapter 26, Fig. 26.18.)

FIG. A.62 Spectral Broadening. The range of velocities detected at a given time in the pulse cycle is relected in the Doppler spectrum as spectral broadening. (A) Normal spectrum. Spectral broadening may arise from turbulent low in association with vessel stenosis. (B and C) Artifactual spectral broadening may be produced by improper positioning of the sample volume near the vessel wall, use of an excessively large sample volume (B), or excessive system gain (C).2 (See Chapter 1, Fig. 1.45.)

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Blooming Artifact Blooming artifact occurs when color reaches beyond the vessel wall, making the vessels look larger than expected. It is gain dependent in that lowering the gain will decrease blooming. It is also wall ilter and color-overwrite dependent, in that increasing the wall ilter will decrease the artifact.

A

B

FIG. A.64 Blooming Artifact. Two images of the same carotid artery. In (A) the gain and wall ilter are appropriate to show the low centrally in the vessel. In (B) the gain and wall ilter have been changed (in a manner beyond what would be used in clinical imaging) to demonstrate how these can make the vessel “bloom” and appear larger.

A

B

FIG. A.65 Blooming artifact due to use of contrast and tissue motion. (A) Use of contrast material creates color Doppler artifacts owing to blooming and tissue motion. (B) Contrast-speciic imaging shows blood vessels not seen with Doppler.25 (See Chapter 3, Fig. 3.7.)

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Twinkle Artifact Twinkle artifact is the artifactual depiction of color signal on crystalline materials in the body. It appears as discrete foci of alternating colors with or without an associated color comet-tail artifact. he appearance of twinkle artifact is highly dependent on machine settings and is likely generated by a narrow-band, intrinsic machine noise called “phase (or clock) jitter.” his, along with a strongly relecting, rough surface such as a renal stone, results in a high-amplitude, broadband signal appearing as random motion on color Doppler sonography. he twinkle artifact is quite useful clinically because it can aid in the detection of small stones, calciications, and other crystalline material within the body. View the PowerPoint illustration of twinkle artifact here (Video A.22).

FIG. A.67 Calciications in Chronic Pancreatitis With Twinkle Artifact.26 (See Chapter 7, Fig. 7.49B.)

FIG. A.66 Twinkle Artifact Posterior to Pancreatic Duct Stone.26 (See Chapter 7, Fig. 7.48D.)

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Click here for associated cine clip (Video A.23).26 (See also Chapter 7, Video 7.5.)

FIG. A.68 Twinkle Behind Distal Ureterovesical Junction Stone.27 (See Chapter 54, Fig. 54.61.)

FIG. A.69 Twinkle Behind a Kidney Stone.18 (See Chapter 9, Fig. 9.38.)

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FIG. A.70 Twinkle Behind Multiple Kidney Stones.22 (See Chapter 52, Fig. 52.37.)

FIG. A.71 Appearances of Twinkle Artifact on Color, Power, and Pulsed Wave Doppler. Note how the spectral Doppler tracing of a twinkle artifact shows lines going through the tracing, which allow distinction from true blood low.28 (See Chapter 18, Fig. 18.52.)

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FIG. A.72 Power Doppler Image of Twinkle Behind Prostatic Calciications.11 (See Chapter 10, Fig. 10.7.)

Acknowledgment Most of the images in this virtual chapter were obtained from chapters in the ith edition of Diagnostic Ultrasound. We thank the authors for the use of their work. REFERENCES 1. Hoskins P, Martin K, hrush A. Diagnostic ultrasound: physics and equipment. 2nd ed. Cambridge, UK: Cambridge University Press; 2010. 2. Merritt C. Physics of ultrasound. In: Levine D, Rumack C, editors. Diagnostic ultrasound. 5th ed. Philadelphia: Elsevier; 2017. 3. Khalili K, Wilson S. he biliary tree and gallbladder. In: Levine D, Rumack C, editors. Diagnostic ultrasound. 5th ed. Philadelphia: Elsevier; 2017. 4. Brown D, Levine D. he uterus. In: Levine D, Rumack C, editors. Diagnostic ultrasound. 5th ed. Philadelphia: Elsevier; 2017. 5. Castro I, Levine D, Rumack C. he pediatric spinal canal. In: Levine D, Rumack C, editors. Diagnostic ultrasound. 5th ed. Philadelphia: Elsevier; 2017. 6. Bluth E, Troxclair L, Johnson S. he extracranial cerebral vessels. In: Levine D, Rumack C, editors. Diagnostic ultrasound. 5th ed. Philadelphia: Elsevier; 2017. 7. Toi A, Levine D. he fetal brain. In: Levine D, Rumack C, editors. Diagnostic ultrasound. 5th ed. Philadelphia: Elsevier; 2017. 8. Feldman MK, Katyal S, Blackwood MS. US artifacts. Radiographics. 2009;29(4):1179-1789. 9. Wilson S, Withers C. he liver. In: Levine D, Rumack C, editors. Diagnostic ultrasound. 5th ed. Philadelphia: Elsevier; 2017. 10. Solbiati L, Charboneau J, Reading C, et al. he thyroid gland. In: Levine D, Rumack C, editors. Diagnostic ultrasound. 5th ed. Philadelphia: Elsevier; 2017. 11. Toi A. he prostate and transrectal ultrasound. In: Levine D, Rumack C, editors. Diagnostic ultrasound. 5th ed. Philadelphia: Elsevier; 2017. 12. Vandeman FN, Meilstrup JW, Nealey PA. Acoustic prism causing sonographic duplication artifact in the upper abdomen. Invest Radiol. 1990;25(6): 658-663. 13. McMahon C, Yablon C. Overview of musculoskeletal ultrasound techniques and applications. In: Levine D, Rumack C, editors. Diagnostic ultrasound. 5th ed. Philadelphia: Elsevier; 2017.

14. DiPietro MA, Brody BA, Teele RL. Peritrigonal echogenic “blush” on cranial sonography: pathologic correlates. AJR Am J Roentgenol. 1986;146(5): 1067-1072. 15. McMahon C, Yablon C. he shoulder. In: Levine D, Rumack C, editors. Diagnostic ultrasound. 5th ed. Philadelphia: Elsevier; 2017. 16. Wilson SR, Burns PN, Wilkinson LM, et al. Gas at abdominal US: appearance, relevance, and analysis of artifacts. Radiology. 1999;210(1):113-123. 17. Avruch L, Cooperberg PL. he ring-down artifact. J Ultrasound Med. 1985;4(1):21-28. 18. Tublin M, Levine D, hurston W, Wilson S. he kidney and urinary tract. In: Levine D, Rumack C, editors. Diagnostic ultrasound. 5th ed. Philadelphia: Elsevier; 2017. 19. O’Hara S. he pediatric liver and spleen. In: Levine D, Rumack C, editors. Diagnostic ultrasound. 5th ed. Philadelphia: Elsevier; 2017. 20. Shah C, Greenberg S. he pediatric chest. In: Levine D, Rumack C, editors. Diagnostic ultrasound. 5th ed. Philadelphia: Elsevier; 2017. 21. Phillips J, Mehta R. he breast. In: Levine D, Rumack C, editors. Diagnostic ultrasound. 5th ed. Philadelphia: Elsevier; 2017. 22. Paltiel H, Babcock D. he pediatric kidney and adrenal glands. In: Levine D, Rumack C, editors. Diagnostic ultrasound. 5th ed. Philadelphia: Elsevier; 2017. 23. Bertino R, Mustafaraj E. he retroperitoneum. In: Levine D, Rumack C, editors. Diagnostic ultrasound. 5th ed. Philadelphia: Elsevier; 2017. 24. Lockhart M, Umphrey H, Weber T, Robbin M. Peripheral vessels. In: Levine D, Rumack C, editors. Diagnostic ultrasound. 5th ed. Philadelphia: Elsevier; 2017. 25. Burns P. Contrast agents for ultrasound imaging and Doppler. In: Levine D, Rumack C, editors. Diagnostic ultrasound. 5th ed. Philadelphia: Elsevier; 2017. 26. Winter T, Sun M. he pancreas. In: Levine D, Rumack C, editors. Diagnostic ultrasound. 5th ed. Philadelphia: Elsevier; 2017. 27. Kotlus Rosenberg H, Simpson Jr W, Chaudhry H. Pediatric pelvic sonography. In: Levine D, Rumack C, editors. Diagnostic ultrasound. 5th ed. Philadelphia: Elsevier; 2017. 28. Muradali D, Chawla T. Organ transplantation. In: Levine D, Rumack C, editors. Diagnostic ultrasound. 5th ed. Philadelphia: Elsevier; 2017.

Index A AA anastomoses. See Arterial/arterial anastomoses AAA. See Abdominal aortic aneurysm Aase syndrome, 1401 Abciximab, 598 Abdomen. See also Acute abdomen abscess of, drainage of, 612, 613f blunt trauma to, small bowel obstruction from, 1843 calciications of, meconium peritonitis and, 1313, 1314f ectopic pregnancy implantation in, 1074, 1075f fetal circumference of, in gestational age determination, 1448, 1450f circumference of, in second-trimester, 1023f musculature of, absent, in prune belly syndrome, 1361–1362 routine sonographic views of, 1021, 1026f lymphangiomas of, pediatric, 1862, 1864f pediatric, systemic veins of, low patterns in, 1750 Abdominal aorta. See also Iliac veins; Inferior vena cava; Mesenteric artery(ies); Renal artery(ies) anatomy of, 433, 433f dilation of, 439–441 aneurysm causing, 433–439 aortic ectasia causing, 440 arteriomegaly causing, 440 inlammatory AAAs causing, 439–440, 443f penetrating ulcer causing, 441, 444f pseudoaneurysm causing, 441 diseases of, 445–464 dissection complications with, renal artery stenosis and, 447, 448f endovascular aortic repair for ruptured, 438 stenotic disease of, 441–445, 445f Abdominal aortic aneurysm (AAA), 433–439 deinition of, 433–434, 434f endoleaks ater repair of, 438–439, 440f–442f inlammatory, 439–440, 443f medical therapy for, 434 mortality from, 433 natural history of, 434 pathophysiology of, 434 postoperative ultrasound assessment for, 438–439, 440f–442f rupture of, evaluation of, ultrasound compared to CT for, 438, 439f screening for, 434–435 CT in, 437 false-positive/false-negative results in, 437f–438f, 438 recent studies in, 434–435 ultrasound approach to, 435

Page numbers followed by f indicate igures; t, tables; b, boxes.

Abdominal aortic aneurysm (AAA) (Continued) surveillance of, 435–437 CT in, 437 sonographic technique for, 436–437, 436f–437f treatment planning for, 438 Abdominal cervical cerclage, 1506, 1506f Abdominal ectopia cordis, 1295 Abdominal ectopic pregnancy, 1074, 1075f Abdominal wall defects in, thickened NT in, 1095–1096 hernias of anterior, dynamic ultrasound of contents of, 472–473 entities stimulating, 500–501, 502f maneuvers for, 473–474, 474f–475f technical requirements for, 471 types of, 471, 471f ventral, 488–494 Abdominal wall, fetal, 1322–1330 amniotic band syndrome and, 1330, 1330f bladder exstrophy and, 1326, 1328f body stalk anomaly and, 1329 cloacal exstrophy and, 1328–1329, 1329f ectopia cordis and, 1329, 1329f embryology of, 1322, 1323f gastroschisis and, 1322–1325 associated conditions of, 1324–1325 epidemiology of, 1322–1323 management of, 1325 pathogenesis of, 1323 prenatal diagnosis of, 1323–1324, 1324f maternal serum alpha-fetoprotein and defects of, 1322 omphalocele and, 1325–1326, 1326f associated conditions with, 1325, 1327f epidemiology of, 1325 management of, 1325–1326 prenatal diagnosis of, 1325, 1327f pentalogy of Cantrell and, 1329 Abductor tendon, injection for, 905–907, 907f Ablation. See also Ethanol ablation adrenal, 428 endometrial, 551–552, 552f Abscess(es) abdominal, drainage of, 612 adrenal, bacterial, 423 amebic liver, 613 appendiceal, pediatric, 1871f hemorrhagic ovarian cyst diferentiated from, 1877 branchial sinus, type IV, 1643–1645, 1645f, 1651, 1653f breast, 803–804, 803f–804f cellulitis leading to, 874, 874f complicated lymphadenitis with, in children, 1634, 1658–1660 costochondral junction, pediatric, aspiration and drainage of, 1963f in Crohn disease, 275–276, 278f–279f empyemas diferentiated from, pediatric, 1725, 1726f enteric, 612

Abscess(es) (Continued) gastrointestinal, 592 hydatid, 613 of kidneys acute pyelonephritis and, 325, 325f drainage of, 617, 618f pediatric, complicating acute pyelonephritis, 1792–1793 transplantation complications with, 651, 656f liver drainage of pyogenic, 612–613, 614f–615f ater liver transplantation, 638–639, 646f pyogenic, 85–86, 87f liver, pediatric, 1746–1748 parasitic, 1747–1748 pyogenic, 1746–1747, 1751f lung, pediatric, 1711, 1713f pancreatic, acute pancreatitis complications with, 230 parenchymal, pediatric renal transplantation and, 1812 parotid, pediatric, 1632–1633, 1633f pediatric drainage of, interventional sonography for, 1953 transrectal, 1953–1954, 1954f pelvic, 283, 591 drainage of, 612, 613f percutaneous needle biopsy complications with, 609, 610f perforated appendicitis and, pediatric, 1857, 1861f perianal, perianal inlammatory disease and, 305–306 perinephric acute pyelonephritis and, 325 pediatric renal transplantation and, 1812 ater renal transplantation, 664–665 perinephric luid collections and, 1809 peritonitis and, 517, 520f prostate, 389, 390f, 392 splenic, 148, 151f drainage of, 617 pediatric, 1769 stitch, ater herniorrhaphy, 494–496, 495f subphrenic, 1716 testicular, 831–832, 831f tubo-ovarian, in pelvic inlammatory disease, 588–589, 588f ABUS. See Automated whole-breast ultrasound ACA. See Anterior cerebral artery Acalculous cholecystitis, 200 Acardiac twins, hydrops and, 1429 ACAS. See Asymptomatic Carotid Atherosclerosis Study Accessory and cavitated uterine mass (ACUM), 541 Accessory arteries, 445–446 Accessory lobes, of placenta, 1480–1481, 1481f Accessory spleen, 158–159, 160f, 1771f Acetabular dysplasia, familial, 1921 Volume I pp 1–1014 • Volume II pp 1015–1968

I-1

I-2

Index

Acetabulum description of, in evaluation of infant at risk, 1927–1929 development of, 1923 Acetylcholinesterase (AChE), in neural tube defect screening, 1228 Achilles tendon rheumatoid nodules in, 867, 868f tendinosis in, 861, 861f Achillodynia, peritendinous injections of foot and ankle for, 902, 903f Achondrogenesis, 1383f, 1391 diagnosis of, 1376–1377 type 1, 1391 type 2, 1391, 1391f Achondroplasia heterozygous, 1396–1398, 1398f detection of, gestational age for, 1381 inheritance pattern for, 1379–1380 homozygous, thanatophoric dysplasia diferentiated from, 1389, 1389f “trident hand” coniguration in, 1407, 1408f Achondroplasia, megalencephaly associated with, 1194–1195 Acinic cell carcinoma, parotid gland, pediatric, 1638, 1639f Acinus, 78 ACN. See Acute cortical necrosis ACOG. See American College of Obstetricians and Gynecologists Acorn cysts, in breast, 778f Acoustic attenuation, in uterine ibroids, 539f, 540, 540b Acoustic cavitation, 35 bubbles generated from, 41–42, 42f considerations for acoustic output increases and, 44 contrast agents and, 43, 44b efects of, 40–46 inertial, 40 lithotripters as evidence of, 42–43, 42f in lung and intestine, 43 mechanical index for, 44–45, 45f potential sources of, 40–42, 42f sonochemistry and, 42, 42f Acoustic enhancement, pleural luid producing, 1709–1710 Acoustic frequency, 2 Acoustic impedance, 3–4 Acoustic power, 5 Acoustic radiation force imaging (ARFI), 1764, 1765f Acoustic shadowing, 786 breast sonography and, 791–792, 793f carcinoma causing, 791–792, 793f decreased/absent, in skeletal dysplasias, 1381–1382 malignant masses causes, diferential diagnosis for, 792 by rib, in pediatric chest sonography, 1710 Acoustic standof, in breast tumor imaging, 767, 767f Acoustics attenuation of sound energy in, 5–7, 7f basics of, 2–7 distance measurement in, 3, 4f frequency and wavelength in, 2, 2f impedance of, 3–4 microbubble behavior and, 57t, 58–59, 59f relection in, 4, 5f refraction in, 5, 6f sound propagation in, 2–3, 3f Acquired cystic kidney disease, 364, 364f renal cell carcinoma and, 340

Acquired immunodeiciency syndrome (AIDS) acute typhlitis and, 287–288, 289f gastrointestinal tract infections and, 296 genitourinary infections in, 331–333, 332f–333f lymphoma related to, 266, 266f Pneumocystis carinii opportunistic infection of liver and, 91, 91f Acrania, 1179 Acromelia, 1381, 1381b, 1382f Acromioclavicular joint, 878–879, 878f injection of, 902, 902f osteoarthritis of, 893, 894f Acromion, 878–879, 878f Active surveillance, for prostate cancer, 401 ACUM. See Accessory and cavitated uterine mass Acute abdomen. See also Diverticulitis, acute luid collections in, 281 free intraperitoneal gas in, 277–281, 282f gastrointestinal tract and, 277–290 let lower quadrant pain in, 288–290 from acute diverticulitis, 288–290 mesenteric adenopathy in, 282 perienteric sot tissues in, 281–282 pneumatosis intestinalis in, 277–281 right lower quadrant pain in, 282–288 from acute appendicitis, 282–285 from acute typhlitis, 287–288, 289f from Crohn appendicitis, 285, 287f from mesenteric adenitis, 288 from right-sided diverticulitis, 285–287, 288f from right-sided segmental omental infarction, 288, 289f sonographic evaluation of, 277–282, 281b, 282f Acute cortical necrosis (ACN), 370, 372f, 1795–1796 Acute interstitial nephritis, 370 Acute kidney injury (AKI), 1795–1796, 1796b, 1797f Acute pancreatitis, microlithiasis and, 221 Acute suppurative thyroiditis, 723–724 Acute tubular necrosis (ATN), 370 acute kidney injury and, 1795–1796, 1797f renal transplantation complication with, 649–651, 653f, 1809 Addisonian crisis, 426–427 Adduction, Barlow test with, in dynamic examination in coronal/lexion view, 1927 in transverse/lexion view, 1927 Adenitis, mesenteric pediatric, 1858–1860, 1862f right lower quadrant pain in acute abdomen from, 288 Adenocarcinoma(s). See also Pancreas, carcinoma of of bladder, 348 colorectal, 261–264, 263f–264f gastrointestinal, 261–264, 263f–264f genitourinary, 348 pancreatic, 172f pancreatic ductal, 236–238 prostate, 395 of renal pelvis, 348 urachal, 355 of ureter, 348 Adenoid cystic carcinoma, salivary gland, pediatric, 1638 Adenolymphomas, pediatric, parotid gland, 1638 Adenoma(s) adrenal, 418–420, 418b in Conn syndrome, 419 in Cushing disease and Cushing syndrome, 419 functioning, 419 imaging considerations for, 418–420, 419f

Adenoma(s) (Continued) nonfunctioning, 419 percutaneous needle biopsy of, 607 benign follicular, 697 bleeding and, 117, 118f CEUS for diagnosis of, 116–117, 117f FNH diferentiated from, 116–117 of gallbladder, 203–204, 205f in GSD, 1740f of liver, 115–117, 116f–118f inborn errors of metabolism and, pediatric, 1738 pediatric, 1746 malignum, 544 parathyroid carcinomas diferentiated from, 735–736, 738f carotid sheath/undescended, 740, 742f combined modalities for accuracy with, 748 compression for detection of, 739 CT accuracy for, 748, 748f echogenicity of, 735, 736f ectopic locations of, 739–741 false-negative examination for, 745b, 746 false-positive examination for, 745–746, 745b ine-needle aspiration biopsy accuracy for, 746 hypoechoic, 735 imaging accuracy with, 746–749 inferior, 738–739, 739f internal architecture of, 735, 736f intrathyroid, 740, 742f localization of, 736–741 mediastinal, 740, 741f, 748 MRI accuracy in, 748, 749f multiple gland disease in, 735, 738f pediatric, 1650, 1650f percutaneous needle biopsy of, 750–751, 753f pitfalls in examination of, 745–746, 745b retrotracheal/retroesophageal, 739–740, 740f scintigraphy accuracy for, 747, 747f shape of, 735, 735f size of, 735, 737f sonographic appearance of, 735–736 sonographic examination and typical locations in, 736–739, 739f superior, 738–739, 739f surgical removal of, 749, 750f ultrasound accuracy for, 746–747, 748f vascularity of, 735, 737f pleomorphic, salivary gland, pediatric, 1636–1638, 1638f primary hyperparathyroidism caused by, 734, 734b thyroid follicular, pediatric, 1646–1648, 1647f nodular disease and, 697, 700f Adenomatoid tumor(s) paratesticular, 1904 scrotal, 840, 840f Adenomyomas, of gallbladder, 202–204, 204f–205f Adenomyomatosis, gallbladder, 202, 203f–205f Adenomyosis, 540–541, 540b, 542f Adenovirus infection, fetal, hydrops from, 1431–1432 Adhesions, endometrial, 551, 552f ADI. See Agent detection imaging Adnexa. See also Fallopian tube(s); Ovary(ies); Round ligament(s) anatomy of, 564–570, 565f cysts of, in pregnancy, 1020 mass of, ectopic pregnancy and, 1072, 1073f mass of, pediatric, in ectopic pregnancy, 1884–1885, 1898f pediatric, torsion of, 1875–1876 sonography for, 564 technique for, 566 torsion of, 576–578, 577f

Index Adnexa (Continued) transvaginal ultrasound for assessment of, 566 vascular abnormalities in, 589–590 ovarian vein thrombosis and thrombophlebitis as, 589–590, 589f pelvic congestion syndrome as, 590, 590f vascularity of, 565–566, 565f ADPKD. See Autosomal dominant polycystic kidney disease Adrenal ablation, 428 Adrenal cortex carcinoma of, 424–425, 426f functions of, 417 Adrenal gland(s) anatomy of, 416–417, 417f benign neoplasms of, 418–424 adenomas as, 418–420, 418b, 419f, 607 cysts as, 421–422, 422b, 423f hemorrhage as, 422–424, 424f management of, 428 myelolipomas as, 420–421, 420b, 420f pheochromocytomas as, 421, 422f rare, 427–428 calciication of, 423, 425f causes of, 424b cysts of, 421–422, 422b, 423f fetal congenital hyperplasia of, genitalia in, 1367–1368 masses in, 1353–1354, 1353f, 1353t normal, 1353, 1353f hemorrhage in, 422–424, 424f ater liver transplantation, 638, 645f histoplasmosis of, 423 hypertrophy of, 416–417 immunosuppression and, 423 infectious diseases of, 423–424, 425f interventions for neoplasms of, 428–429 endoscopic ultrasound for, 428–429, 429f intraoperative ultrasound for, 429 ultrasound-guided biopsy for, 428, 429f let, 416–417, 417f multiplanar scanning of, 418 malignant neoplasms of, 424–427 adrenocortical carcinomas as, 424–425, 426f lymphomas as, 426–427, 427f management of, 428 metastases as, 425–426, 426f–427f rare, 427–428 pediatric adrenocortical neoplasms of, 1827, 1827f carcinoma of, 1827, 1827f congenital hyperplasia of, 1822–1824, 1824f, 1900–1901 hemorrhage into, neonatal, 1824–1825, 1825f measurements of, in neonates, 1820–1821, 1823t neuroblastoma and, 1825–1826, 1826f normal anatomy of, 1820–1822, 1824f pheochromocytoma and, 1826–1827, 1827f sonography of, 1820–1827 percutaneous needle biopsy of, 606–607, 608f physiology of, 416–417, 417f right, 416–417, 417f multiplanar scanning of, 417–418, 418f sonographic imaging and technique for, 417–418, 418f tuberculosis of, 423 Adrenal insuiciency, 426–427 Adrenal medulla, functions of, 417 Adrenal rests, testicular, 832–833, 833f, 1824 pediatric, 1900–1901 Adrenarche, pseudoprecocious puberty and, 1888 Adrenocortical neoplasms, pediatric, 1827, 1827f

Adson maneuver, 976–977 Aferent loop obstruction, mechanical bowel and, 293 AFI. See Amniotic luid index Age. See Gestational age; Maternal age Age, pediatric kidney length and comparison of, 1776–1778, 1777f reference values for, 1776–1778, 1778t with single functioning kidney, 1779t kidney volume according to reference values for, 1776–1778, 1778t with single functioning kidney, 1779t Agent detection imaging (ADI), 66 Agnathia, 1154, 1159f Agyria, in lissencephaly, 1195 Aicardi syndrome choroid plexus papillomas in, 1209 corpus callosum agenesis and, 1526–1528 AIDS. See Acquired immunodeiciency syndrome AIDS cholangitis, 181 Air bronchograms, sonographic in atelectatic lung, 1714, 1716f in consolidated lung, 1711, 1714f–1715f pneumonia and, 1702, 1703f, 1708f round, 1712, 1715f Air bubbles, encapsulated, as blood pool contrast agents, 55–56, 55t AIUM. See American Institute of Ultrasound in Medicine AKI. See Acute kidney injury Alagille syndrome, pediatric, 1737 ALARA, 31, 1041–1042 Albunex, 55–56 Aldosterone, secretion of, 417 Aliasing in color Doppler ultrasound, 28, 29f, 966 high-velocity jets and, 933 in Doppler ultrasound, 29b, 32f in pediatric abdominal vessel imaging, 1749 in pulsed Doppler ultrasound, 939, 939f in renal artery duplex Doppler sonography, 449 Alkaline-encrusted pyelitis, 324–325 Allantois, 1059, 1337f, 1338 Allergy, milk, gastric mucosa thickening and, 1839–1840 Allograt nephropathy, chronic, 1810, 1812f Alloimmune arteritis, ater pancreas transplantation, 677 Alloimmune thrombocytopenia, intracranial hemorrhage and, 1206 Alpha angle, in hip joint classiication, 1924, 1924f–1925f Alpha-fetoprotein, maternal serum, 1117 elevated, causes of, 1226, 1226b, 1228 fetal abdominal wall defects and, 1322 gestational age compared to levels of, 1227f spina biida screening and, 1221, 1226–1228, 1226b, 1227f 17-alpha hydroxy-progesterone caproate (17αOHPC), vaginal progesterone compared to, 1507 Alport syndrome, CKD and, 1796–1798 Alternating current, 8 Ambient cistern, fetal, normal sonographic appearance of, 1168 Amebiasis, hepatic, 87–88, 89f in children, 1747–1748 Amebic liver abscesses, 613 Amelia, deinition of, 1399 Amenorrhea, primary, causes of, 1887 American College of Obstetricians and Gynecologists (ACOG), 1107

I-3

American Institute of Ultrasound in Medicine (AIUM), 1041 on bioefects of diagnostic ultrasound with gas body contrast agents, 43, 44b in gas bodies, 45–46, 46b safety statements of, general, 47, 47b thermal, 40, 40b–41b hermal Index Working Group of, 38–40 Amniocentesis diagnostic, in NTD screening, 1228 genetic, 1108–1109, 1108f in multifetal pregnancy, 1125–1126 therapeutic, in fetal hydrops, 1436 Amnion chorion separation from, 1469, 1469f early pregnancy failure and size of, 1066, 1067f–1068f normal sonographic appearance of, 1057, 1059f–1060f unfused, 1057 Amnion inclusion cyst, 1061 Amnionicity, in multifetal pregnancy, 1057, 1058f, 1115–1116, 1116f sonographic determination of, 1117, 1119t triplets and, 1122f Amniotic band sequence amputations caused by, 1401, 1403f anencephaly diferentiated from, 1179 fetal brain and, 1180f, 1182–1183 terminal transverse limb defects and, 1400 Amniotic band syndrome, 1057 facial clets in, 1152–1153 fetal abdominal wall and, 1330, 1330f Amniotic bands circumvallate placenta confused with, 1479–1480 constrictive, 1182–1183 Amniotic cavity, formation of, 1051, 1052f Amniotic luid assessment of, 1339b volume of, 1339–1340 Amniotic luid index (AFI), 1339 method for obtaining, 1340 values for, in normal pregnancy, 1341t A-mode ultrasound, 9 Amplitude evaluation of, power Doppler in, 935 modulation imaging, 64, 65f Ampulla, 565 Amputations, from amniotic band sequence, 1401, 1403f Amyand hernias, 472–473, 473f Amyloidosis, renal failure in, 372 Anabolic steroid therapy, hepatic adenomas and, 1746 Anal atresia, 1311 Anal canal, endosonography of, 302–307, 304f–307f, 306b Anal dimple, 1311–1312, 1311f fetal cloacal exstrophy and, 1328 Analgesia, TRUS-guided biopsy and, 407 Anaplastic carcinoma, of thyroid gland, 707–708, 708b, 709f Anasarca, fetal, in hydrops, 1417, 1420f Anastomotic pseudoaneurysms, 438 Anastomotic strictures, bladder augmentation and, 1912–1913 Anderson-Carr-Randall theory of stone progression, 339, 1798–1799 Androblastoma, 585 Androgens, secretion of, 417 Anechoic cysts, 331 Volume I pp 1–1014 • Volume II pp 1015–1968

I-4

Index

Anemia fetal, hydrops from, 1431 pediatric, Fanconi, 1746 Anencephaly, 1218 CDH and, 1263 detection of, early, 1018–1019, 1019f embryonic, 1077 in fetal brain, 1179, 1180f temperature increase in utero and, 1037 thickened NT and, 1096f Anesthetics local, for pediatric interventional sonography, 1951, 1952f for musculoskeletal injections, 901 Aneuploidy. See also Trisomy 21 background risk for, 1088, 1089f deinition of, 1088 fetal echogenic bowel and, 1315–1316, 1315f fetal gastroschisis and, 1324–1325 fetal liver calciications and, 1316–1318 hand and foot abnormalities in, 1404, 1406f identiication of, luorescent in situ hybridization in, 1433–1434 pyelectasis as marker for, 1355 risk of, NT in assessing for, 1018–1019, 1019f, 1049 screening for, irst-trimester, 1089–1097 with cell-free DNA, 1107 combined, 1090–1091 contingent, 1091 cystic hygroma in, 1093, 1093f integrated, 1091 in multifetal pregnancy, 1091 nasal bone in, 1093–1095, 1094b, 1094f NT in trisomy 13 and 18, 1093 NT in trisomy 21 and, 1089, 1090f NT measurement technique and, 1091–1093, 1092b reversed low in ductus venosus in, 1095, 1095f sequential, 1091 serum biochemical markers in, 1089–1090 thickened NT in congenital heart defects and, 1095–1097, 1096f tricuspid regurgitation in, 1095 skeletal indings with, 1407–1409 Aneurysm(s). See also Abdominal aortic aneurysm abdominal aortic, 433–439 atrial septal, 1295 in AVF for hemodialysis, 1003, 1005f carotid low disturbances in, 928 common carotid artery, 947–948 hepatic artery, ater liver transplantation, 1768, 1769f–1770f of peripheral arteries lower extremity, 971–972, 972f upper extremity, 976 portal vein, 103–104 ater liver transplantation, 1768, 1769f–1770f renal artery, 369, 369f, 451 in synthetic arteriovenous grat for hemodialysis, 1003 umbilical artery, 1483 vein of Galen, 1204, 1206f arachnoid cysts diferentiated from, 1192–1193 cavum veli interpositi cysts diferentiated from, 1170 in neonatal/infant brain, duplex Doppler sonography of, 1583–1584, 1585f–1586f ventricular, congenital, 1294 Angiogenesis, in yolk sac wall, 1057 Angiography, in carotid stenosis diagnosis, 916

Angiomas, littoral cell, splenic, 153–156, 156f Angiomyolipomas of liver, 117–118, 119f renal, 351–352, 351f–352f pediatric, 1820, 1822f Angiosarcoma hepatic, 123 splenic lesions in, 153, 155f Angle of incidence, 5 Angle of insonation, 4 Angle of refraction, 5 Angle theta consistent, in carotid spectral analysis, 926–927 Doppler deinition of, 926 measurement of, 926–927, 926f increasing, to overcome aliasing, 939 Angular margins, in breast sonography, 788–789, 790f Aniridia, sporadic, Wilms tumor screening with, 1818 Anisospondyly, in dyssegmental dysplasia, 1399 Anisotropic efect, in HPS sonography, 1838, 1838b, 1839f Anisotropic efect artifact, 1517 Anisotropy shoulder ultrasound and, 895, 895f tendon, 859, 860f, 899 Ankle, injection of, 901 supericial peritendinous and periarticular, 902–904, 903f–904f Annular constricting lesions, 261–264, 263f Annular pancreas, fetal, 1320, 1321f Anomalous pulmonary venous return (APVR), 1280, 1282f, 1290, 1291f total compared to partial, 1290 Anophthalmia, 1140, 1145f Anorchidism, 1890 Anorectal malformations, fetal, 1310–1312, 1311f Anterior cerebral artery (ACA) of infant, RI in, 1576, 1577t of infant, RI in, fontanelle compression in hydrocephalus and, 1582, 1584f stenosis of, SCD and, 1607f TCD sonography for collateral low in, 1610, 1611f as transtemporal approach landmark, 1592, 1593f–1594f Antibiotic prophylaxis, TRUS-guided biopsy and, 407, 408f Antibiotics, for pediatric interventional sonography, 1951 Anticoagulants, deiciency of physiologic, dural sinus thrombosis from, 1205–1206 Antley-Bixler syndrome, craniosynostosis in, 1136–1138 Antral dyskinesia, 1836–1838 Antral foveolar hyperplasia, prostaglandininduced, 1839–1840 Antral web, pediatric, 1839, 1840f Anus ectopic, pediatric, 1847–1848, 1850f imperforate, 1310–1311 block vertebrae with, 1689, 1692f high, pediatric, risk of spinal dysraphism with, 1689 pediatric, 1847–1848, 1850f Aorta coarctation of, 1291, 1292f fetal, hydrops from, 1423–1424 hypoplastic let heart syndrome with, 1287 fetal, continuity of, 1278f small, in Turner syndrome, 1106f, 1107 Aortic arch fetal, 1275, 1279f pediatric, cervical, 1658

Aortic balloon pump, carotid low waveforms and, 936–937, 936f Aortic coarctation, renal artery stenosis and, 447, 449f Aortic root, fetal, diameter of, 1277f Aortic stenosis, 1292 carotid low waveforms and, 936–937 fetal, hydrops from, 1423–1424 Aortic valve, lesions of, carotid low waveforms and, 936–937 Aortoenteric istulas, 438 Apert syndrome craniosynostosis in, 1136–1138 midface hypoplasia in, 1148 Aplasia pulmonary, 1245–1246 of thyroid gland, 694, 694f Apnea, sleep, pediatric TCD sonography for, 1611 Aponeurosis, torn, in spigelian hernia, 483–484, 487f Appendices epiploicae, torsion of, 290 Appendicitis acute clinical misdiagnosis of, 283–285 pathophysiology of, 283 right lower quadrant pain from, 282–285 sonographic diagnosis of, 283, 283b symptoms of, 283 transvaginal ultrasound for diagnosis of, 283, 285f Crohn, 285, 287f focally inlamed fat in, 521 pediatric, 1855–1860 acute, 1857, 1859f Meckel diverticulum resembling, 1858–1860, 1862f normal appearance of, 1857, 1858f perforated, 1857, 1857b, 1861f sonographic signs of, 1857b Appendicolith, 283 Appendix. See also Appendicitis inlammation of, 282–285 mucocele of, 299, 299f pediatric abscess of, 1871f, 1877 abscess of, drainage of, 1956, 1960f gangrenous, 1857, 1861f normal, 1857, 1858f perforations of, 283–285, 285b, 286f Appendix epididymis, pediatric, 1897, 1897f Appendix testis, 820–821, 820f pediatric, 1897 “Apple peel” jejunal atresia, 1310 Aprosencephaly, 1186 APVR. See Anomalous pulmonary venous return Aqueduct of Sylvius in rhombencephalosynapsis, 1192 stenosis of obstructive hydrocephalus from, 1538, 1540f VM and, 1177, 1177f Arachnoid cyst(s) cavum veli interpositi cysts diferentiated from, 1170 corpus callosum agenesis and, 1526–1528 fetal brain and, 1192–1193, 1193f of neonatal/infant brain, 1563–1565, 1565b spinal canal and, pediatric, 1695–1697, 1696f Arachnoid granulations, 1177 Arcuate arteries, calciications of, 531–532, 533f Arcuate uterus, 534, 536–538, 536f–537f Area cerebrovasculosa, in anencephaly, 1179 Area membranacea, 1189 Arelexia, detrusor, 372–374, 373f ARFI. See Acoustic radiation force imaging ARPKD. See Autosomal recessive polycystic kidney disease

Index Arrays, transducer, 11–12 Arrhenoblastoma, 585 pediatric, 1880 Arrhythmia(s) early pregnancy loss and, 1069 Ebstein anomaly with, 1286 fetal heart, 1295–1297 bradycardia as, 1297, 1297f CHD and, 1270–1273 congenital heart block as, 1297, 1297f hydrops from, 1424, 1425f PACs and PVCs as, 1295–1296 tachycardia as, 1296–1297, 1296f Arsenic, 123 Arterial venous (AV) anastomoses, 1125, 1125f Arterial/arterial (AA) anastomoses, 1125, 1125f Arteriomegaly, 440 Arteriovenous istulas (AVFs) arteries supplying, spectral broadening in, 927–928 of common femoral artery, 974f dural, TCD sonography assessing, 1614 hemodialysis and aneurysms near, 1003, 1005f arm and leg swelling with, 1006, 1009f hematomas near, 1002–1003, 1005f maturation of, evaluating, 1003 occlusion of, 1006 palpable focal masses near, 1002–1003 placement of, 996, 997f pseudoaneurysms near, 1003, 1005f stenoses associated with, 1003–1006, 1007f–1008f ultrasound evaluation of, 1000–1006, 1002f–1003f of lower extremity peripheral arteries, 973–974, 974f ater pancreas transplantation, 678, 680f pediatric, of neck, 1658 renal, 366–367 percutaneous needle biopsy of, 606, 607f renal biopsies and, Doppler assessment of, 1809, 1810f traumatic, 973 Arteriovenous grat, synthetic, hemodialysis and arm and leg swelling with, 1006, 1009f hematomas near, 1002–1003 occlusion of, 1006, 1010f palpable focal masses near, 1002–1003 placement of, 996, 997f ultrasound evaluation of, 1002, 1004f Arteriovenous malformations (AVMs) arteries supplying, spectral broadening in, 927–928 cerebral, pediatric, TCD sonography detecting, 1614, 1615f fetal hydrops from, 1430–1431 of lower extremity peripheral arteries, 973 pediatric, of neck, 1657–1658, 1659f pial, 1204–1205 postpartum recognition of, 556, 556f renal, 366–367, 367f renal transplantation complications from, 661–664, 667f–670f twinkling artifacts mimicking, 662–664, 668f Arteriovenous shunting, in fetal sacrococcygeal teratoma, 1238–1239 Arteritis alloimmune, ater pancreas transplantation, 677 of common carotid artery, 944–946, 947f Takayasu, aortic stenosis in, 444 Artery(ies). See speciic arteries Arthritis osteoarthritis, 869, 869f acromioclavicular joint, 893, 894f

Arthritis (Continued) psoriatic, of hand and wrist, injections for, 904 rheumatoid, 866 erosive, 867, 868f gout and, 867–869, 868f of hand and wrist, injections for, 904 joint efusion in, 867, 867f septic, pediatric, 1936, 1937f Arthrogryposis multiplex congenita elbow and knee dislocation and, 1933–1934 indings in, 1382 as limb reduction defect, 1401–1404, 1405f teratologic hip dislocation and, 1932 Arthropathy inlammatory, 866 shoulder and, 893–894, 894f shoulder and, 893–894 degenerative, 893, 894f inlammatory, 893–894, 894f Articular-sided rotator cuf tears, 888, 890f Artifacts anisotropic efect, 1517 blooming, 60–61 comet-tail, 202, 695 in benign and malignant thyroid nodule diferentiation, 712–713 in degenerative cysts of thyroid, 1646, 1647f Doppler ultrasound sources of, 29b empty stomach, 1838, 1839f enhancement as, 21, 22f lash, 60–61 loss of information from, 19–21 misregistration, 3f, 420–421 multipath, 19–21, 21f propagation velocity, 3, 3f, 420–421 refraction, 5, 6f reverberation, 19, 20f posterior, liver abscess and, 85–86, 87f ring-down, 266, 266f shadowing as, 19–21, 22f side lobe, 19, 20f tangential imaging, of pyloric muscle, 1834– 1835, 1836f TGC settings and, 19–21 thump, 60 tissue vibration, 973–974, 974f twinkling bezoars and, 1840 mimicking AVMs ater renal transplantation, 662–664, 668f renal calculi indicated by, 336, 337f Ascariasis biliary, 181 intestinal, pediatric, 1853, 1853f Ascites chylous, 508 exudate, 506–507 fetal cloacal exstrophy and, 1328 in hydrops, 1413, 1415f–1416f, 1435, 1436f meconium peritonitis and massive, 1418– 1419, 1421f parvovirus infection and massive, 1418–1419 urinary, from bladder rupture in posterior urethral valves, 1361, 1361f from gastrointestinal tract metastases, 266, 267f meconium peritonitis and, 1313 particulate, 507 pediatric, pleural luid diferentiated from, 1709 peritoneum and, 506–508, 507f–509f small bowel mesentery assessment with, 505, 505f transudate, 506–507 ASD. See Atrial septal defect

I-5

ASH. See Asymmetrical septal hypertrophy Asherman syndrome, 551 Aspergillosis, neonatal chylothorax from, 1704f Asphyxia intrauterine, near-total, acute, in difuse cerebral edema, 1553–1554, 1555f neonatal/infant brain and, duplex Doppler sonography of, 1580 pediatric, TCD sonography in, 1614, 1616f Asphyxiating thoracic dysplasia, 1398 Asphyxiating thoracic dystrophy, 1396 polydactyly in, 1382 Aspiration, for pyogenic liver abscesses, 1746–1747 Aspirin, 598–599 Asplenia, 159–160 in cardiosplenic syndrome, 1292, 1293b fetal, 1320 univentricular heart with, 1287–1288 Assisted reproductive technology, multifetal pregnancy incidence and, 1115 Astrocytomas, neonatal/infant brain and, 1562 Asymmetrical ibroglandular tissue, split-screen imaging and, 769, 769f Asymmetrical septal hypertrophy (ASH), 1292, 1294–1295 Asymptomatic Carotid Atherosclerosis Study (ACAS), 916 Atelectasis, pediatric, 1714, 1716f Atelencephaly, 1186 hydranencephaly diferentiated from, 1208 Atelosteogenesis, 1396 Atheromatous carotid plaques, characterization of, 919 Atherosclerosis, 432–433 renovascular disease and, 368 Atherosclerotic disease, peripheral arterial stenosis in, 968, 976, 978f Atherosclerotic disease, renal artery stenosis and, 447 Atherosclerotic plaque rupture, 919–920 Athletes, direct inguinal hernias in, 485–486 Athletic pubalgia. See Sports hernias ATN. See Acute tubular necrosis Atrazine, fetal gastroschisis and, 1322–1323 Atretic cephalocele, 1180 Atretic meningocele, tethered cord and, 1679 Atrial ibrillation, fetal, 1296 hydrops from, 1424 Atrial lutter, fetal, 1296 hydrops from, 1424 Atrial pacemaker, 1295–1296 Atrial septal aneurysm, PACs and, 1295 Atrial septal defect (ASD), 1277–1280, 1282f–1283f coronary sinus, 1280 ostium primum, 1279–1280, 1282f–1283f ostium secundum, 1279–1280, 1282f prenatal diagnosis of, 1280 sinus venosus, 1280, 1282f types of, 1282f Atrioventricular block (AVB), 1297 Atrioventricular (A-V) canal defects of, 1284 in trisomy 21, 1098f Atrioventricular septal defect (AVSD), 1279, 1282f, 1284–1286, 1284f–1285f balanced compared to unbalanced, 1285 complete compared to incomplete, 1284–1285, 1285f in trisomy 21, 1101, 1284 Atrioventricular valves, of fetal heart, 1274–1275 Atrium of lateral ventricles, neonatal/infant, in coronal imaging, 1515 Volume I pp 1–1014 • Volume II pp 1015–1968

I-6

Index

Attenuation coeicient, 36 of sound energy, 5–7, 7f, 35 Atypical hips, pediatric, 1932, 1933f Auditory response, in obstetric sonography, 1038 Auricular hillocks, 1134 Autoimmune cholangiopathy, 182 Autoimmune cholangitis, 182 Autoimmune pancreatitis, 236, 237f Autoimmune vasculitis, Henoch-Schönlein purpura and, 1853 Automated whole-breast ultrasound (ABUS), 760 Autopsy, in hydrops diagnosis, 1435 Autosomal dominant polycystic kidney disease (ADPKD), 83, 243, 361, 362f, 1346, 1348–1350, 1349f–1350f pediatric, 1814–1815, 1815f Autosomal recessive polycystic kidney disease (ARPKD), 359, 361f, 1799 pediatric, 1812–1813, 1814f AV anastomoses. See Arterial venous anastomoses A-V canal. See Atrioventricular canal A-V canal defects, 1284 AVB. See Atrioventricular block AVFs. See Arteriovenous istulas AVMs. See Arteriovenous malformations AVSD. See Atrioventricular septal defect Axial resolution, 16–19, 18f Axillary artery, 975 Axillary vein, 990–991, 990f Azimuth planes, 12f Azimuth resolution, 19, 19f Azoospermia, prostate and, 393 Azzopardi tumors, 824–825 B Bacille Calmette-Guérin (BCG), 390, 390f Backscatter, 3–4 CEUS increasing, 107, 111f Doppler ultrasound and, 21–22, 23f, 35 Bacteria pediatric infections from cervical lymphadenopathy in, 1660–1663 parotid gland, 1632–1633, 1632f thyroid, 1643–1645, 1645f pyogenic, liver abscesses from, 85–86, 87f pediatric, 1746–1747, 1751f Bacterial epididymitis, 841, 843f Baker cyst(s) injection for, 907–909, 908f ruptured, 870, 870f ultrasound techniques for, 870, 870f Ballottement, compression and, 768 Banana sign, in Chiari II malformation, 1183– 1185, 1184f spina biida screening and, 1221, 1228, 1230–1232 Band, of frequencies, 7 Band heterotopia, 1196 Bandwidth, 7–8 Barbotage, 909 Bardet-Biedl syndrome, hyperechogenic kidneys in, 1351 Bare area of liver, 77 sign, as pleural luid sonographic sign, 1709, 1709f Barlow test with adduction, in dynamic examination in coronal/lexion view, 1927 in transverse/lexion view, 1927 in determining hip stability, 1923 Basal cell nevus syndrome, 585 rhabdomyosarcoma associated with, 1908

Basal ganglia fetal, normal sonographic appearance of, 1168 vasculopathy, neonatal/infant brain and, 1556–1557 Basilar artery, 951 Basilic vein, anatomy of, 990–991, 990f Bat wing coniguration, in Chiari II malformation, 1526, 1527f Battledore placenta, 1484 B-cell lymphoma, AKI and, 1796 BCG. See Bacille Calmette-Guérin “Beads on a string” sign, 587–588 Beam steering, 10–11, 11f Beam width, 35 Beare-Stevenson syndrome, craniosynostosis in, 1136–1138 Beckwith-Wiedemann syndrome adrenocortical neoplasms and, 1827 CDH and, 1263 fetal hepatomegaly and, 1316 omphalocele and, 1325, 1327f pancreatic cysts and, 1320 hepatoblastomas and, 1746 macroglossia in, 1153 megalencephaly associated with, 1194–1195 mesenchymal dysplasia of placenta in, 1479, 1479f nesidioblastosis and, 1865 neuroblastoma with, pediatric, 1825 Wilms tumor screening with, 1818 Beemer-Langer syndrome, 1396 Behavioral changes, obstetric sonography and, 1040–1041 Bell-clapper deformity, 844, 844f pediatric, 1325 Benign ductal ectasia, prostate and, 387, 388f Benign follicular adenoma, 697 Benign mixed-cell tumors, 1638 Benign prostatic hyperplasia (BPH), 384, 385f–386f, 387–388 Bent-limb dysplasia, 1395 Beta angle, in hip joint classiication, 1924, 1924f–1925f β-hCG. See Human chorionic gonadotropin Bezoars of gastrointestinal tract, 300 pediatric, 1840, 1841f Biceps tendon, 878–879 dislocation of, 893 injection of, 904–905, 905f–906f long head of, 879, 880f–881f longitudinal split tear of, 893, 894f pathology of, 892–893 tenosynovitis and, 892–893, 893f ultrasound evaluation of, 880, 881f Bicornuate uterus, 534, 536f–537f, 538, 1881, 1881f Biid lamina, 1688 Biid scrotum, fetal, 1367 Bilateral hernias, 1262 Bile calcium, milk of, 194, 195f low extrahepatic obstruction to, 1734 stasis of, stone formation and, 1741 leakage of, ater liver transplantation, 627–629, 629f limey, 194, 195f Bile duct(s) aberrant, 167, 168f dilation of, in Caroli disease, 1736–1737, 1736f drainage of, 614–615 interlobular, paucity of, jaundice from, 1737 ischemia of, from post-liver transplant hepatic artery thrombosis, 628f

Bile duct(s) (Continued) necrosis of, post-liver transplantation, bile leaks from, 627 normal, 166–168, 166f spontaneous rupture of, neonatal jaundice caused by, 1734, 1737 strictures in, ater liver transplantation, 626–627, 627f–628f Biliary atresia extrahepatic, 1319 neonatal jaundice and, 1734–1735, 1737, 1738f Biliary cirrhosis, 92–93, 182 pediatric, 1741 Biliary cystadenomas, 82, 83f Biliary hamartomas, 83, 83f–84f Biliary rhabdomyosarcoma, in pediatric liver, 1746, 1749f Biliary sludge acute pancreatitis and, 221 complicating liver transplantation, 629, 631f gallbladder and, 194–195, 196f Biliary system, fetal, 1318–1319 Biliary tree, 166–188. See also Cholangiocarcinoma anatomy of, 166–168 ascariasis and, 181 autoimmune cholangitis and, 182 branching pattern of, 167, 167f Caroli disease of, 171, 171f cholangiocarcinoma and, 184–188 choledochal cysts of, 168–170, 169f–170f choledocholithiasis in, 172–173, 182 common bile duct stones and, 173–174, 173f intrahepatic, 173, 173f cirrhosis and, 182 clonorchiasis and, 178–179, 179f dilation of, in acute cholangitis, 176 fascioliasis and, 176–178, 177f–178f harmonic imaging of, 168, 169f hemobilia and, 174, 175f HIV cholangiopathy and, 181–182, 181f immune-related diseases of, 182–184 infection of, 176–182 liver lukes and, 176–179, 177f–179f ater liver transplantation complications involving, 625–629, 1767–1768, 1769f–1770f normal appearance of, 625 strictures in, 626–627, 627f–628f metastases to, 188, 192f Mirizzi syndrome and, 174, 174f obstruction of acute cholangitis and, 176, 177f causes of, 172b overview of, 171–172, 172f opisthorchiasis and, 178–179 pneumobilia and, 175–176, 176f primary sclerosing cholangitis and, 182, 183f, 184 recurrent pyogenic cholangitis and, 179–181, 180f sonographic technique for, 168, 169f trauma to, hemobilia from, 174, 175f variants of normal, 166–168 Bilobed placenta, 1481, 1482f Bilobed testis, 1891 Biloma, ater liver transplantation, 638 Bioefects. See also Acoustic cavitation; hermal index acoustic cavitation and, 40–46 AIUM on of diagnostic ultrasound with gas body contrast agents, 43, 44b in gas bodies, 45–46, 46b safety statements of, general, 47, 47b thermal, 40, 40b–41b

Index Bioefects (Continued) epidemiology of, 48 of HIFU, 31–33, 33f mechanical, 32 of obstetric sonography animal research and, 1038–1039 behavioral changes and, 1040–1041 birth weight and, 1040 childhood malignancies and, 1041 congenital malformations and, 1041 delayed speech and, 1040 Doppler ultrasound and, 1041 dwell time and, 1036 dyslexia and, 1040 human studies on, 1039–1041 instrument outputs and, 1035–1036 mechanical, 1038 neurologic development and, 1040–1041 nonright-handedness and, 1040 scanning mode and, 1035 system setup and, 1035–1036, 1035f–1037f thermal, 1036–1038 operating modes and, 30–31 output control and, 48–50, 49t output display standard and, 46–47, 46f output regulation and, 34–35 physical efects of sound and, 35 thermal, 32, 35–40 AIUM summary statement on, 40, 40b–41b bone heating and, 37, 37f, 37t estimating, 40 hyperthermia and safety and, 38, 38f mechanism of, 35 in obstetric sonography, 1036–1038 sot tissue heating and, 37–38, 37f spatial focusing and, 35 temporal considerations in, 36, 36f tissue type and, 36, 36f ultrasound output and, regulation of, 34–35 user concerns and, 31 Biometry, second-trimester, 1021, 1023f Biophysical proile (BPP), 1456–1458, 1457f, 1457t Biopsy(ies). See also Transrectal ultrasound, biopsy guided by chest wall lesion, ultrasound-guided, 1724–1725 ine-needle aspiration parathyroid adenoma and accuracy of, 746 of thyroid gland, 709–710, 710t, 722 interventional sonography devices for, 1950 liver, percutaneous, 132–133 post-transplant bile leaks from, 627–629 mediastinal mass, pediatric, 1956, 1959f percutaneous needle, 597–609 abscess complications with, 609, 610f of adrenal gland, 606–607, 608f of breast nodules, ultrasound-guided, 811–815, 813f–814f for cervical lymph nodes, 717–718, 718f color Doppler ultrasound for, 599 complications of, 608–609 computed tomography for, 599 contraindications to, 597–598 “freehand” technique for, 600, 602f hemorrhage complications with, 608, 609f imaging methods for, 599 indications for, 597–598 infection complications with, 609 of kidney, 605–606, 606f–607f of liver, 603–604, 603f–604f of lung, 607–608, 609f needle selection for, 599–600 needle visualization in, 601–603, 602f of pancreas, 604–605, 605f of parathyroid adenomas, 750–751, 753f

Biopsy(ies) (Continued) periprocedural antithrombotic management and, 598–599 procedure for, 600–601, 601f of spleen, 607, 608f for thyroid gland, 715–720, 718f–719f, 721f transducer sterilization for, 600 prostate PSA-directed, 395 ultrasound-guided, 407–411, 408f renal, pediatric, Doppler assessment of, 1809, 1810f–1811f of renal cell carcinoma staging, 343–344, 345f targeted organ lesion, 1961, 1961f–1962f ultrasound-guided of adrenal glands, 428, 429f of spleen, 161 Biparietal diameter (BPD) corrected, in gestational age determination, 1447, 1447t, 1448f femur length compared to, in heterozygous achondroplasia, 1398, 1398f in gestational age determination, 1446, 1447f long-bone lengths and, at diferent menstrual ages, 1379t nasal bones in trisomy 21 and, 1099–1100 in second-trimester, 1023f BI-RADS. See Breast Imaging Reporting and Data System Birth, preterm. See Preterm birth Birth weight discordance, in multifetal pregnancy, 1123 obstetric sonography and, 1040 Birt-Hogg-Dubé, hereditary oncocytosis, 348–350 Bladder. See also Cystitis adenocarcinoma of, 348 agenesis of, 322 anatomy of, 314 calculi in, 338–339, 339f pediatric, 1908 carcinomas of squamous cell, 348 transitional cell, 347–348, 350f cavernous hemangiomas of, 356 development of, 311, 312f congenital anomalies related to, 322 diverticula, 374, 374f identiication of, 592 drainage to, in pancreas transplantation, 668–672, 675f duplication of, 322 endometriosis of, 372, 372f exstrophy of, 322 fetal, 1339, 1340f cloacal exstrophy and inability to visualize, 1328 exstrophy of, 1365–1366, 1366f maximum volume of, 1339 nonvisualized, 1365, 1365b routine sonographic view of, 1026f rupture of, from posterior urethral valves, 1361, 1361f istulas of, 334, 335f function of, in spina biida, 1233 leiomyomas of, 356 leiomyosarcoma of, 356 lymphomas of, 353, 354f malacoplakia and, 333, 333f mesenchymal tumors of, 356 metastases to, 354–355, 355f neck of, 314 neuroibromas of, 356 neurogenic, 372–374, 373f

I-7

Bladder (Continued) pediatric augmentation of, 1912–1913, 1913f calculi in, 1908 dysfunctional, 1907–1908 neurogenic, 1907–1908 postoperative, 1912–1913, 1913f spontaneous rupture of, 1912 pheochromocytomas of, 356 rare tumors of, 356 rhabdomyosarcomas of, 356 schistosomiasis of, 331, 331f sonographic technique for, 314–315 trauma to, 366 urachal anomalies of, 322, 323f wall of causes of thickening of, 333b interstitial cystitis and thickening of, 372, 373f prune belly syndrome and thin walled, 1361–1362 Bladder, pediatric. See also Urinary tract, pediatric exstrophy of, hydronephrosis and, 1791, 1791f neurogenic, pediatric hydronephrosis and, 1788 normal anatomy of, 1783, 1783f outlet of, obstruction of, pediatric hydronephrosis and, 1788, 1789f–1790f postvoid scanning of, 1872 rhabdomyosarcoma of, 1820, 1823f tumors of, 1820, 1823f pediatric hydronephrosis and, 1788 volume of determination of, 1778, 1780f shape and correction coeicient for, 1780t wall thickness of, determination of, 1778–1781, 1780f Bladder exstrophy, fetal, 1326, 1328f Bladder lap hematomas, cesarean sections and, 556–557, 557f Bladder outlet obstruction, pediatric causes of, 1905–1906, 1905b epididymitis and, 1897 Blake pouch cerebellum and, 1189 cyst of arachnoid cysts diferentiated from, 1192–1193 sonographic appearance of, 1170, 1173f Dandy-Walker malformation diferentiated from, 1190 formation of, 1167 Blastocyst, 1049 Blastocyte stage, 1051, 1051f Bleeding adenoma and, 117, 118f endometrial abnormalities with, 544, 544b postmenopausal bleeding as, 545–546 intraamniotic, fetal echogenic bowel and, 1316 in placenta previa, 1469 uterine postpartum indings with, 554 vaginal, hydatidiform molar pregnancy and, 1078 Block vertebrae imperforate anus with, 1689, 1692f in scoliosis and kyphosis, 1235 Blood autologous, intratendinous injection of, 909–910, 912f fetal, sampling of in hydrops diagnosis, 1434–1435, 1435f in immune hydrops, 1421 incompatible, immune hydrops from, 1419–1421 Volume I pp 1–1014 • Volume II pp 1015–1968

I-8

Index

Blood low. See also Cerebral blood low, neonatal/ infant in carotid arteries internal, residual string of, detection of, 939, 940f normal transient reversal of, 933–934 patterns of, altered, misinterpretation of, 927, 928f patterns of, high-velocity, in stenoses, 928–932, 929f–931f, 931t pseudostring of, on power Doppler, 935 residual string of, in occlusion, detection of, 935 in MCA, PSV and, 1421–1423, 1421b, 1422t reversed, in ductus venosus, in aneuploidy screening, 1095, 1095f trophoblastic, 1083 venous absence of, in DVT, 992–994 slow moving, without DVT, 984, 988f Blood pool contrast agents, 55–56 encapsulated air bubbles as, 55–56, 55t free gas bubbles as, 55 second-generation, 56 selective uptake, 56, 57f Blood vessels. See also Carotid artery(ies); Internal jugular vein; Vascular malformations; Vertebral artery adrenal, 416–417, 417f cerebral extracranial, 917f IJV as, 955–956 malformations of, TCD sonography in, 1614, 1615f vertebral artery as, 950–955 chest, pediatric, 1716–1723, 1721f–1724f of fetal brain, malformations of, 1204–1208, 1206f hepatic, abnormalities in, 96–104 patency of, ater liver transplantation, 625 renal aberrant, 321–322 Doppler ultrasound of, 366 stenosis of, high-grade, waveforms in, 938 Blood-testis barrier, 827 Blooming artifacts, 60–61 “Blue dot” sign, 846 Blue rubber bleb nevus syndrome, in venous malformations of neck, 1657 Blue-dot sign, 1897 B-mode ultrasound, real-time, gray-scale, 9–10, 10f Bochdalek hernia, 1258 Body stalk anomaly, fetal, 1329 Bone marrow transplantation, for SCD, 1598 Bone(s) heating of, 37, 37f, 37t shear waves created in, 39 thermal index for, in late, 1039 wormian, 1139, 1139b, 1139f Bone(s), fetal appearance of, abnormal, sonographic evaluation for, 1381–1382 long abnormal length of, sonographic evaluation for, 1380–1384, 1381b, 1382f–1384f bowing of, 1381–1382 BPD and, at diferent menstrual ages, 1379t sonographic assessment of, 1387b–1388b Bone hermal Index (TIB), 39 Bony septum, in spinal cord in diastematomyelia, 1234–1235, 1236f Boomerang dysplasia, 1396 Borderline tumors, ovarian, 580f, 581 Bosniak classiication, malignant potential of renal cysts and, 359 Bossing, frontal, in skeletal dysplasias, 1382

“Bovine arch” coniguration, 916 Bowel. See also Echogenic bowel; Mechanical bowel obstruction; Small bowel dilated, fetal, 1313 dilated loops of, 1310, 1311f fetal gastroschisis and, 1323–1324 echogenic fetal, 1310, 1313–1316, 1315f in trisomy 21, 1100f, 1101 fetal, obstruction of, cloacal malformation and, 1363 function of, in spina biida, 1233 ischemic disease of, 297 neoplasms of, 592 obstruction of mechanical, 293 pediatric interventional sonography and anatomy of, 1950 necrosis of, with perforation, in NEC, 1854–1855 TRUS-guided biopsy and preparation of, 407 Bowing of femur, osteogenesis imperfecta type I and, 1380f of fetal long bones, 1381–1382 BPD. See Biparietal diameter BPH. See Benign prostatic hyperplasia BPP. See Biophysical proile BPS. See Bronchopulmonary sequestration Brachial artery, 975 high, bifurcation of, 975–976, 976f, 998, 999f Brachial plexus injury, pediatric, 1934–1936, 1936f–1937f Brachial vein anatomy of, 990–991, 990f DVT and chronic, 994–995, 996f nonocclusive, 994f Brachiocephalic artery, 916, 975 Brachiocephalic vein anatomy of, 990–991, 990f ultrasound examination of, 992f Brachmann-de Lange syndrome, CDH and, 1263 Brachycephaly, 1136, 1137f Brachydactyly, fetal, 1407, 1408f Brachytherapy, for prostate cancer, TRUS-guided, 401, 402f Bradycardia carotid low waveforms and, 936–937 embryonic, 1068–1069, 1068f fetal, 1297, 1297f hydrops from, 1423–1424 sinus, 1297 Brain, fetal. See also Ventriculomegaly abnormalities of, 1179 acrania and, 1179 Blake pouch cyst of, 1170, 1173f cavum veli interpositi of, 1170–1174, 1174f choroid plexus cysts of, 1170, 1173f cortical development malformations and, 1193–1203 absence of septi pellucidi as, 1201–1203 cerebrohepatorenal syndrome as, 1196 chondrodysplasia punctata as, 1196 classiication of, 1194b corpus callosum agenesis/dysgenesis as, 1199–1201, 1202f, 1203b focal changes in, 1196 hemimegalencephaly as, 1195 heterotopia as, 1196, 1199f intracranial calciications as, 1195f, 1203, 1204f lissencephaly as, 1195–1196, 1196f–1197f macrocephaly as, 1194–1195 megalencephaly as, 1194–1195 microcephaly as, 1194, 1195f

Brain, fetal (Continued) polymicrogyria as, 1196, 1198f schizencephaly as, 1196, 1199f SOD as, 1201–1203, 1203f TSC and, 1198, 1200f development of, stages of, 1525b, 1525f developmental anatomy of, 1167–1174, 1167t dorsal induction errors and, 1179–1186 amniotic band sequence as, 1180f, 1182–1183 anencephaly as, 1179, 1180f cephalocele as, 1179–1182 ciliopathies as, 1182 cranial changes in spina biida as, 1183–1186, 1184f–1185f, 1185t–1186t encephalocele as, 1179–1182, 1181f, 1182t exencephaly as, 1179 Joubert syndrome as, 1182 limb-body wall complex as, 1182–1183 Meckel-Gruber syndrome as, 1182 embryology of, 1167, 1167t hydrocephalus and, 1174–1178 infections of, 1203–1204, 1205f MRI evaluation of, 1166–1167, 1172f sonographic anatomy of, 1167–1170, 1168f, 1170f–1172f cerebellar view of, 1168–1169, 1169f median (midsagittal) view of, 1169, 1169f thalamic view of, 1168, 1169f ventricular view of, 1168, 1169f split, 1196 tumors and, 1208–1210, 1209f–1210f variants in (usually normal), 1170–1174 vascular malformations of, 1204–1208, 1206f dural sinus thrombosis as, 1205–1206, 1206f hydranencephaly as, 1208, 1208f intracranial hemorrhage as, 1206, 1207f ventral induction errors and, 1186–1203 arachnoid cysts as, 1192–1193, 1193f in cerebellum, 1189–1192 Dandy-Walker malformation as, 1190, 1190f HPE as, 1186–1189, 1187b, 1188f, 1189b mega-cisterna magna as, 1192, 1193f in posterior fossa, 1189–1192 rhombencephalosynapsis as, 1192 vermis hypoplasia or dysplasia as, 1190–1192, 1192f VM and, 1174–1178 Brain, neonatal/infant. See also Hypoxic-ischemic events, neonatal/infant brain and astrocytomas of, 1562, 1564f calcar avis of, development of, 1523f, 1524 cavum septi pellucidi of, development of, 1521, 1521f–1522f cavum veli interpositi of, development of, 1521–1522, 1521f cavum vergae of, development of, 1521, 1521f–1522f cellular migration disorders of, 1536–1537 cerebellar vermis of, development of, 1524 choroid plexus of in coronal imaging, 1514–1515, 1514f cysts of, 1565, 1566f development of, 1522–1523, 1522f–1523f papillomas of, 1562, 1565f cisterna magna of, development of, 1524 cleavage disorders of, 1532–1536 color Doppler ultrasound for, 1573–1574 congenital malformations of, 1524–1526, 1525b cystic encephalomalacia and, 1538, 1539f cystic intracranial lesions of, 1562–1565, 1565t cysts of arachnoid, 1563–1565, 1565b choroid plexus, 1565, 1566f frontal horn, 1522, 1522f, 1566 periventricular, 1566, 1566f

Index Brain, neonatal/infant (Continued) porencephalic, 1537, 1565 subependymal, 1566, 1567f death of, duplex Doppler sonography and, 1580, 1583f destructive lesions and, 1537–1538 developmental anatomy of, 1520–1524 diverticulation disorders and, 1532–1536 duplex Doppler sonography of, 1573–1576 approaches to, 1574, 1575f arterial blood low in, 1576, 1577t asphyxia and, 1580 brain death and, 1580, 1583f cerebral edema and, 1580 difuse neuronal injury and, 1580 ECMO and, 1578–1580, 1579f hemodynamics in, 1576–1580 HII and, 1580, 1581f–1582f hydrocephalus and, 1581–1583, 1584f intensive care therapies and, 1578–1580 intracranial hemorrhage and, 1580–1581, 1584f intracranial tumors and, 1585, 1587f measurements in, 1576, 1576f–1577f, 1576t mechanical ventilation and, 1578, 1579f near-ield structures and, 1585, 1588f optimization of, 1574, 1574b pitfalls of, 1585–1589, 1589f safety considerations for, 1574–1576 stroke and, 1580–1581, 1584f uncommon applications of, 1585, 1588f vascular malformations and, 1583–1585, 1585f–1587f venous blood low in, 1578, 1578f, 1578t ependymomas of, 1562 germinal matrix of, development of, 1524, 1524f HPE and, 1532–1536 alobar, 1534–1535, 1534b, 1536f classiication of, 1534f lobar, 1535 midline interhemispheric form of, 1535–1536 semilobar, 1535 hydranencephaly and, 1538, 1538f hydrocephalus and, 1538–1541 causes of, 1540b cerebrospinal luid production and circulation and, 1538–1541 hypoxic-ischemic injury to, 1541–1557 imaging of coronal, technique for, 1513–1515, 1513b, 1513f–1515f equipment for, 1512 mastoid fontanelle, 1512, 1517–1518, 1517f, 1519f pitfalls in, 1523b posterior fontanelle, 1512, 1517, 1517f–1518f sagittal, 1515–1517, 1516b, 1516f–1517f sonographic technique for, 1512–1518 standardized reports of, 1518–1520, 1520b 3-D ultrasound in, 1518 infections and, 1557–1560 acquired, 1560, 1561f–1563f CMV, 1558–1560, 1559f congenital, 1557–1560, 1559f ventriculitis as, 1560, 1563f lissencephaly and, 1537 in metabolic disorders, 1538 neural tube closure disorders of, 1526–1532 Chiari malformations and, 1526, 1526b, 1527f–1529f corpus callosum agenesis and, 1526–1528, 1529b, 1530f–1533f corpus callosum lipoma and, 1529, 1533f

Brain, neonatal/infant (Continued) Dandy-Walker malformation and, 1529–1532, 1530b, 1533f–1534f posttraumatic injury to, 1557, 1558f power mode Doppler ultrasound for, 1573–1574 premature coronal imaging of, 1515, 1515f hypoxic-ischemic events and, 1541, 1541t normal sonographic appearance of, 1521f ultrasound screening in, optimal, 1543b PVL and, 1550–1553, 1551f–1553f, 1566 schizencephaly and, 1536–1537, 1537f SOD and, 1532–1534, 1535f sulcation disorders of, 1536–1537 sulcus of, development of, 1520–1521, 1520f–1521f teratomas and, 1562 tumors of, 1560–1566, 1562b, 1564f–1565f primitive neuroectodermal, 1562 rhabdoid, 1562 supratentorial, 1562 vein of Galen malformations and, 1566, 1567f Brain, pediatric. See Transcranial Doppler sonography, pediatric Brain death neonatal/infant brain and, duplex Doppler sonography of, 1580, 1583f pediatric coma diferentiated from, 1618–1620, 1620f TCD sonography and, 1618–1620, 1618b, 1619f–1620f Brainstem, neonatal/infant, in difuse cerebral edema, 1555f Branchial arches, 1133–1134 anomalies of, 1651, 1651f–1653f Branchial clets, 1651 Branchial cysts type I, pediatric, 1639, 1651, 1651f type II, pediatric, 1639–1640, 1651, 1652f type III, pediatric, 1651, 1652f Branchial sinus abscess, type IV, 1643–1645, 1645f, 1651, 1653f Branchio-oto-renal syndrome, MCDK and, 1815 Breast Imaging Reporting and Data System (BI-RADS), 768 reporting categories of, 774, 774t Breast-ovarian cancer syndrome, 578 Breast(s) abscesses of, 803–804, 803f–804f anatomy of, 760–767 atrophy of, 763f benign sonographic indings of, 795–797 hyperechoic tissue in, 796–797, 796f parallel (wide-than-tall) orientation in, 797, 797f thin echogenic capsule in, 797 BI-RADS reporting categories for, 774, 774t cancer, staging of, 807–810, 808f–810f CEUS for assessment of, 773–774 cysts of, 774–785 acorn, 778f aspiration of, ultrasound-guided, 811, 813f clustered macrocysts and, 779, 780f clustered microcysts and, 782 with color streaking, 775, 776f complex, 780–785, 782f complicated, 775–780, 776f Doppler ultrasound for diferentiating, 769–770, 770f eggshell calciication and, 779, 780f fat-luid levels in, 775, 778f ibrocystic change and, 775 inlammation and infection of, 782–785, 785f lipid, 775–779, 779f

I-9

Breast(s) (Continued) microcysts and, 782, 784f milk of calcium and, 775, 776f–777f mural nodules and, PAM causing, 782, 783f–784f papillary lesions and, 782 septations within, 782, 783f simple, 774, 775f of skin origin, 779, 781f diagnostic ultrasound indications for, 797–803 breast pain as, 797–798 nipple discharge as, 798–799, 799f–801f palpable lumps as, 769, 769f, 798, 798f Doppler ultrasound for assessment of, 768–772, 770f–773f echogenicities of, 761 elastography for assessment of, 772–773, 773f implants of, evaluation of, 804–807, 804f–806f interventions for, ultrasound-guided, 811–815, 813f–814f lymphatic drainage of, 762–767, 767f mammographic indings of, 799–803 dense tissue in, 761–762, 763f location or position correlation in, 801 shape correlation in, 800, 802f–803f size correlation in, 800, 801f–802f sonographic-mammographic conirmation in, 803 surrounding tissue density correlation in, 801, 803f nipple discharge and, 798–799, 799f–801f pain in, 797–798 papillomas of, 769–771, 770f intracystic, 782, 783f intraductal, 799, 799f–800f peripheral, 799, 800f periductal mastitis of, 771, 771f physiology of, 760–767 solid nodules of, 780–786, 782f biopsy of, ultrasound-guided, 811–815, 813f–814f circumscribed, 786 heterogenicity of, 786, 786f papillary lesions and, 782 spiculated, 786 sonographic equipment for, 767, 767f sonographic techniques for, 768–774 for annotation, 768 CEUS as, 773–774 color Doppler ultrasound as, 769–772, 770f–773f Doppler ultrasound as, 768–772, 770f–773f elastography as, 772–773, 773f for lesion documentation, 768–769 patient position in, 768 special, 769–774 split-screen imaging for, 769, 769f 3-D ultrasound as, 773 suspicious sonographic indings of, 787–795, 787t acoustic shadowing in, 791–792, 793f angular margins in, 788–789, 790f architectural distortion in, 795 associated features in, 794–795 calciications in, 793–794, 795f duct extension in, 790–791, 792f edema in, 795 hypoechogenicity in, 792–793, 794f indistinct margins in, 787, 787f microlobulations in, 789, 791f not parallel orientation (taller-than-wide) in, 789–790, 792f skin changes in, 795 spiculation in, 787–788, 788f Volume I pp 1–1014 • Volume II pp 1015–1968

I-10

Index

Breast(s) (Continued) thick echogenic rim, with hyperechoic spicules in, 787–788, 789f TDLUs of, 760–761 sonographic appearance of, 762, 766f 3-D ultrasound for, 773 ultrasound examination of, 774–797 applications of, 760 automated whole-breast, 760 BI-RADS reporting categories for, 774, 774t diagnosis in, 760 Doppler ultrasound for, 768–772, 770f–773f equipment for, 767, 767f for guided intervention, 811–815, 813f–814f for implant evaluation, 804–807, 804f–806f for infection, 803–804, 803f–804f for interventional procedures, 760 for lymph node assessment, 807–810, 808f–810f niche applications for, 803–811 normal tissue and variations in, 774 for sonographic-MRI correlation, 810–811, 811f–812f suspicious indings in, 787–795, 787t technique for, 768–774 three dimensional, 788, 789f–790f water density tissue of, 761–762, 763f zones of, 761, 761f Breathing, sleep-disordered, 1611 Brenner tumor, 581–582, 582f Breus mole, 1471 Broad ligaments, 564–565 Broad-bandwidth, 7–8 Bronchogenic cysts fetal, 1255–1256, 1255f, 1255t pediatric, 1650, 1716, 1718f Bronchopulmonary foregut malformations, pediatric, 1716, 1718f Bronchopulmonary sequestration (BPS), 1246, 1248t, 1250–1251, 1251f extralobar, 1250 fetal, hydrops from, 1426 intralobar, 1250 Bruit, from carotid stenosis, color Doppler, 933, 934f Brunn epithelial nests, in chronic cystitis, 333, 333f Bubbles. See also Microbubbles acoustic cavitation generation of, 41–42, 42f behavior of, incident pressure and, 56–58, 57t Budd-Chiari syndrome, 98–103, 100f–103f in children, suprahepatic portal hypertension and, 1762–1763, 1763f IVC and, 463 “Buddha position,” fetal, 1401 Bulk modulus, 15–16 “Bunny” waveform, 953b, 954, 954f Burkitt lymphoma, pediatric, 1860 “Burned-out” tumors. See Germ cell tumors, testicular, regressed Bursal-sided partial-thickness rotator cuf tears, 888, 890f Bursitis, bursal injections for, 907–909, 908f Burst length, in output control, 48–50 Butterly vertebrae, in scoliosis and kyphosis, 1235 Bypass grat(s) coronary, radial artery evaluation for, 977–978, 980f of lower extremity peripheral arteries, 974–975, 975f PSV and dysfunction of, 974–975 of supericial femoral artery, 975f C CA. See Celiac artery CA 125, in ovarian cancer, 578

Cadaveric kidneys, paired, in transplantation, 643–644, 648f CAH. See Congenital adrenal hyperplasia “Cake” kidneys, pediatric, 1785 CAKUT. See Congenital anomalies of kidney and urinary tract Calcaneus, ossiication of, 1377–1378 Calcar avis, neonatal/infant, development of, 1523f, 1524 Calcarine issure, neonatal/infant, development of, 1520–1521, 1524 Calciic bursitis, 891 Calciic tendinitis injections for, 909, 911f of supraspinatus tendon, 891–892, 892f Calciication(s). See also Nephrocalcinosis abdominal, meconium peritonitis and, 1313, 1314f of adrenal glands, 423, 425f causes of, 424b in breast sonography, 793–794, 795f chronic DVT indicated by, 984, 987f in chronic pancreatitis masses, 233–236, 236f cystic meconium peritonitis with, 1842–1843, 1846f DCIS and, 793, 795f dystrophic, 339 pediatric urinary tract and, 1799 eggshell, breast cysts and, 779, 780f of endometrium, 533, 534f of gallbladder, 202, 202f intracranial, fetal, 1195f, 1203, 1204f liver, fetal, 1316–1318, 1317f, 1318b of meconium periorchitis, focal, 1904, 1904f of myometrium, 531–533, 533f–534f ovarian, focal, 566–568 of prostate, 387, 388f psammomatous, in peritoneal nodule, 510–511, 513f of radial arteries, evaluation for, 998, 998f renal artery, 336 of renal cysts, 358, 358f of renal parenchyma, 339–340, 340f scrotal, 833–834, 833b, 834f of seminal vesicles, 392 splenic, 150, 153f pediatric, 1769 of supericial femoral artery, 968, 970f of tendons, 859–861 of thyroid cysts, 695 in thyroid nodules diagnostic signiicance of, 713–714 in papillary carcinoma, 699, 702f of urinary tract, pediatric, 1798–1801 cortical nephrocalcinosis and, 1798, 1798b, 1798f dystrophic, 1799 medullary nephrocalcinosis and, 1798–1799, 1799f renal vein thrombosis and, 1799, 1800f urinary stasis and, 1799, 1800f urolithiasis and, 1799–1801, 1799f in uterine ibroids, 539f, 540, 540b of vas deferens, 392 yolk sac, 1067, 1068f Calciied metastases, of liver, 125, 128f Calcimimetics, for secondary hyperparathyroidism, 734 Calcitonin, secretion of, in medullary carcinoma of thyroid, 701 Calcium bile, milk of, 194, 195f Calcium hydroxyapatite, in calciic tendinitis, 909 Calculus(i) bladder, 338–339, 339f pediatric, 1908 caliceal, 334–335

Calculus(i) (Continued) liver transplantation complications with, 629, 632f renal, 334–336, 336f–337f entities that mimic, 336, 337b, 337f scrotal, extratesticular, 836–837, 837f staghorn tyrosinemia and, 1799, 1800f in xanthogranulomatous pyelonephritis, 328, 329f ureteral, 337–338, 338f–339f bladder augmentation and, 1912–1913 complicating renal transplantation, 659–660, 663f–664f urethral, pediatric, bladder outlet obstruction from, 1906, 1906f Calf veins, ultrasound imaging of, 982 Caliceal calculi, 334–335 Callosomarginal sulcus, neonatal/infant, development of, 1520–1521 Calvarium, fetal, compressibility of in osteogenesis imperfecta type II, 1382, 1392, 1393f in skeletal dysplasia, 1382 Calyceal diverticula, renal milk of calcium and, 1799, 1800f Calyces, dilation of, in hydronephrosis, 1354 Campomelic dysplasia, 1395, 1396f bowing of long bones in, 1381–1382 pulmonary hypoplasia and, 1384f ribs and, 1382–1384 sonographic appearance of, 1380f thanatophoric dysplasia diferentiated from, 1388–1389 Camptodactyly, fetal, 1404–1405, 1406f Campylobacter, 1852 Canal of Nuck cyst or hydrocele of, simulating groin hernia, 499–500, 501f delayed closure of, indirect inguinal hernia from, 476–477, 477f Canalization, in spine embryology, 1672, 1673f Candida albicans genitourinary tract infections from, 330–331, 331f neonatal urinary tract infection from, 1794, 1795f Candidiasis hepatic, 86–87, 88f hepatosplenic, splenic abscesses in, 150–152, 154f neonatal, 1794, 1795f Capillary malformations, tethered cord and, 1679 Capsular arteries, 821 Caput medusae, 1752 Carcinoid tumor, renal, 355–356 Carcinoma(s). See also Breast(s), solid nodules of; Ductal carcinoma in Situ; Hepatocellular carcinoma; Papillary carcinoma; Renal cell carcinoma; Transitional cell carcinoma acinic cell, parotid gland, pediatric, 1638, 1639f acoustic shadowing caused by, 791–792, 793f adenoid cystic, salivary gland, pediatric, 1638 adrenal, pediatric, 1827, 1827f adrenocortical, 424–425, 426f of bladder squamous cell, 348 transitional cell, 347–348, 350f cervical, 542, 543f hematometra in, 547f, 549 choriocarcinoma, testicular, 824, 825f circumscribed, 786 clear cell, 581, 582f colon, 261–264, 263f–264f pediatric, 1880

Index Carcinoma(s) (Continued) embryonal, 823, 825f ovarian, 1880 pediatric, testicular, 1899 endometrial, 544, 548–551, 550f polycystic ovarian disease and, 1877–1878 esophageal, staging of, endosonography in, 301 fallopian tube, 589 gallbladder, 206–207, 206f gastric, endosonographic identiication of, 301 mucoepidermoid, salivary gland, pediatric, 1638 of parathyroid glands adenomas diferentiated from, 735–736, 738f primary hyperparathyroidism from, 734 primary peritoneal serous papillary, 511–513, 515f prostate, transrectal sonography of, 302, 302f rectal, staging of, endosonography in, 301–302, 301f–304f spiculated, 786 TDLU, 789–790, 792f of thyroid gland, 695 anaplastic, 707–708, 708b, 709f follicular, 701, 701b, 706f–707f, 1648 incidence of, 722, 722f–723f medullary, 701–707, 707f–708f, 1648 nodular disease and, 698–708 papillary, 698–701, 701f–705f, 713, 1648, 1649f vaginal, pediatric, 1883 Carcinomatosis, peritoneal, 510–511, 510f–515f Cardiac output, reduced, carotid low waveforms and, 935f, 936–937 Cardioembolic stroke, 915–916 Cardiomyopathy(ies) carotid low waveforms and, 936–937, 936f fetal, 1295f adrenal glands and, 1353–1354 hydrops from, 1425 Cardiopulmonary bypass partial, in neonatal/infant brain, duplex Doppler sonography and, 1578–1579, 1579f pediatric TCD sonography in, 1621–1622 Cardiosplenic syndrome, 1292–1293, 1293b Cardiovascular disease, 432–433 Carney complex, 826 Carney triad, pheochromocytomas with, 1826 Caroli disease of biliary tree, 171, 171f pediatric, 1735 bile duct dilation in, 1736–1737, 1736f Carotid artery(ies). See also Plaque(s), carotid anatomy of, 916, 917f arthrosclerotic disease of, plaque characterization in, 919 color Doppler evaluation for stenosis of, 932–935 advantages and pitfalls of, 934–935, 934b, 934f bruit from, 933, 934f optimal settings in, low-low vessel evaluation, 933–934, 933b, 934f Takayasu arteritis of, 944–946, 947f common, 916, 917f aneurysm of, 947–948 carotid bifurcation and, 917–918, 918f ectatic, 947–948, 949f helical low in, 934 occlusion of, abnormal internal carotid artery waveform and, 941, 942f posttraumatic pseudoaneurysm of, 948, 950f stenosis of, grading of, 930 waveform of, 925–926, 925f disease of, preoperative strategies for, 941–942 dissection of, 946–947, 947b, 948f

Carotid artery(ies) (Continued) distal internal, as transtemporal approach landmark, 1592, 1594f Doppler spectral analysis for, 925–932 high-velocity blood low patterns in, 928–932, 929f–931f, 931t pitfalls in, 927–928, 928f spectral broadening in, 927, 927f standard examination in, 926–927, 926f endarterectomized, sonographic features of, 942, 944f external, 916 branching vessels of, 918, 918f collaterals of, intracranial circulation and, 939, 940f mistaking for internal carotid artery, 941, 941f stenosis of, grading of, 930 waveform of, 925–926, 925f low pattern in altered, misinterpretation of, 927, 928f high-velocity, in stenoses, 928–932, 929f–931f, 931t normal transient reversal of, 933–934 internal, 916 common carotid artery occlusion causing abnormal waveform in, 941, 942f ibromuscular dysplasia of, 944–946, 946f mistaking external carotid artery for, 941, 941f stenosis of, grading, 928–929, 929f–930f tardus-parvus waveforms in stenosis of, 934f, 938 waveform of, 925–926, 925f internal, occlusion of, 939–941 external carotid collaterals to intracranial circulation in, 939, 940f pitfall in diagnosis of, 941, 941f sonographic indings in, 939b string sign distinguished from, 939 kinked, carotid low waveforms and, 936–937, 936f lymph node masses near, 948, 949f neck masses of, 947–948, 949f–950f nonarthrosclerotic diseases of, 944–948 arteritis as, 944–946, 947f carotid body tumors as, 947–948, 949f from cervical trauma, 946, 948f extravascular masses as, 948, 949f ibromuscular dysplasia as, 944–946, 946f posttraumatic pseudoaneurysms as, 948, 950f ultrasound examination of, 916 postoperative ultrasound of, 942–944, 944f power Doppler evaluation for stenosis of, 935–939, 935b pitfalls and adjustments in, 935f–939f, 936–939, 937b pseudoulceration of, 923 revascularization of, ultrasound ater, 942–943, 945f stenosis of angiography and MRA for, 916 CEA for, 916 color Doppler evaluation of, 932–935 Doppler spectral analysis in, 925–932 external, grading of, 930 follow-up for, 941, 943t gray-scale, 923–924, 924f high-velocity blood low patterns in, 928–932, 929f–931f, 931t internal, grading of, 928–930, 929f–930f internal, tardus-parvus waveforms in, 934f, 938 power Doppler evaluation of, 935–939, 935b recurrent, grading of, 943–944, 945t

I-11

Carotid artery(ies) (Continued) stroke from, 915–916 ultrasound diagnostic criteria for, 930–932, 931t stenting of restenosis in, grading of, 943–944, 945t ultrasound ater, 942–943, 945f tandem lesions in, 937 TIA from embolism of, 919 tortuous carotid low waveforms and, 936–937, 937f spectral broadening in, 928 transcranial Doppler sonography for, 948–950, 950f ultrasound examination of color Doppler evaluation for, 932–935 diagnostic criteria for, 930–932, 931t Doppler spectral analysis for, 925–932 follow-up based on, 941, 943t indications for, 915–916, 916b interpretation of, 918–944 postoperative, 942–944, 944f techniques for, 917–918, 917f–918f transcranial Doppler sonography for, 948–950, 950f visual inspection of gray-scale images in, 918–924 visual inspection of gray-scale images for, 918–924 for intima-media thickening, 918–919, 919f for plaque characterization, 919–922, 920f–922f, 922b for plaque ulceration, 923, 923b, 923f–924f for stenosis evaluation, 923–924, 924f for vessel wall thickness, 918–919 walls of, dissections in, low disturbances in, 928 Carotid bifurcation, 917–918, 918f pathologic lymph node near, 948, 949f Carotid body tumors, 947–948, 949f Carotid bulb, 917 Carotid endarterectomy (CEA) for carotid stenosis, 916 pediatric, TCD sonography in, 1621 sonographic features following, 942, 944f Carotid Revascularization Endarterectomy Versus Stenting Trial (CREST), 916 Carotid-cavernous istulas, TCD sonography assessing, 1614 Carpal tunnel entrapment, of median nerve, 864–865, 866f Carpal tunnel syndrome, 865, 866f Carpenter syndrome, craniosynostosis in, 1136–1138 Cartilage, sonographic characteristics of, 1923 “Cartilage interface” sign, 886, 888, 888f Cataracts congenital, 1143, 1147b temperature increase in utero and, 1037 Catheterization central venous, IJV thrombosis complicating, 955 ESRD and, 994 Catheter(s) central, peripherally inserted, pediatric, insertion of, 1953 drainage for interventional sonography, 1948 placement of, 610–611, 611f removal of, 612 selection of, 610–611, 611f peripherally inserted central, 993f interventional sonography, pediatric, 1954, 1955f–1957f SVC, pediatric, position of, 1716–1721, 1722f Volume I pp 1–1014 • Volume II pp 1015–1968

I-12

Index

Cat-scratch disease, pediatric, 1633–1634 causes of, 1938, 1938f lymphadenopathy in, 1660–1663 Cauda equina, formation of, 1673, 1673f Caudal agenesis, 1674 closed spinal dysraphism and, 1689, 1690f maternal diabetes mellitus and, 1689 type 1, 1689, 1690f type 2, 1689 Caudal appendage, tethered cord and, 1679 Caudal cell mass, diferentiation of, in spine embryology, 1674 Caudal neuropore, in spine embryology, 1217 Caudal regression defects, 1218 fetal, 1237–1238, 1237f sequence, sacral agenesis in, 1237 syndromes as limb reduction defect, 1401, 1404f skeletal dysplasia and, 1382 Caudate lobe, 75–76, 76f Caudate nucleus, in sagittal imaging of neonatal/ infant brain, 1515, 1517f Caudothalamic groove, neonatal/infant in intraparenchymal hemorrhage, 1547, 1547f in sagittal imaging, 1516–1517, 1517f Causality, criteria for judging, 48 Cavernoma, portal, in portal vein thrombosis, 1757, 1761f Cavernous hemangiomas of bladder, 356 CEUS characterization of, 111, 113f Doppler ultrasound characterization of, 109–110 of liver, 108–112, 112f–113f percutaneous needle biopsy of, 603–604, 604f Cavitation. See Acoustic cavitation Cavum septi pellucidi fetal formation of, 1167 normal sonographic appearance of, 1168–1169 sonographic view of, 1024f neonatal/infant, development of, 1521, 1521f–1522f Cavum veli interpositi arachnoid cysts diferentiated from, 1192–1193 fetal, 1170–1174, 1174f neonatal/infant, development of, 1521–1522, 1521f Cavum Vergae formation of, 1167 neonatal/infant in coronal imaging, 1514–1515 development of, 1521, 1521f–1522f CBAVD. See Congenital bilateral absence of the vas deferens CCAM. See Congenital cystic adenomatoid malformation CDH. See Congenital diaphragmatic hernia CEA. See Carotid endarterectomy Cebocephaly alobar HPE and, 1534–1535, 1536f hypotelorism and, 1140 Celiac artery (CA) anatomy of, 451 duplex Doppler sonography of, 453–455, 455f in median arcuate ligament syndrome, 453, 453f occluded, 454–455, 458f stenosis of, ater liver transplantation, 634–635, 637f Celiac disease, in gastrointestinal tract, 300 Cell aggregation, in obstetric sonography, 1038 Cell membrane alteration, from obstetric sonography, 1038

Cell-free DNA, 1088–1089 aneuploidy screening with, 1107 Cellular migration disorders of, neonatal/infant brain and, 1536–1537 in organogenesis, 1524–1525 Cellulitis, 872–874, 873f–874f complicated lymphadenitis with, in children, 1658–1660, 1662f Center-stream sampling, true, in carotid occlusion diagnosis, 939 Central echo complex, in pediatric kidney, in renal duplication, 1783, 1784f Central hypoventilation syndrome, neuroblastoma with, pediatric, 1825 Central nervous system (CNS) anomalies of, 1166 MRI evaluation of fetal, 1166–1167 Central venous access, for interventional sonography, pediatric, 1954 Central venous catheterization DVT related to, 935, 995f IJV thrombosis complicating, 955 Centrum semiovale, neonatal/infant, 1514 Centrum(a), of vertebral body in lateral longitudinal scan plane, 1223f in lateral transaxial scan plane, 1222f ossiication of, 1218, 1219f in posterior longitudinal scan plane, 1224f in posterior transaxial scan plane, 1222f Cephalic vein, 990f, 991 Cephalocele(s) atretic, 1180 fetal brain and, 1179–1182 as spinal dysraphism, 1139–1140 Cerclage, cervical, for cervical incompetence, 1505–1507, 1506f Cerebellar hemispheres, fetal, normal sonographic appearance of, 1168–1169, 1169f Cerebellar hemorrhage, neonatal/infant brain and, 1548–1550, 1549f Cerebellar infarction, neonatal/infant brain and, 1555 Cerebellar vermis, 1167, 1515, 1516f neonatal/infant, development of, 1524 Cerebellum Blake pouch and, 1189 Dandy-Walker malformation in, 1190, 1190f embryology of, 1167 fetal, sonographic view of, 1024f hypoplasia of, 1190 mega-cisterna magna and, 1192, 1193f neonatal/infant, in coronal imaging, 1514–1515, 1514f rhombencephalosynapsis in, 1192 ventral induction errors in, 1189–1192 vermis hypoplasia or dysplasia in, 1190–1192, 1192f Cerebral artery. See Anterior cerebral artery; Middle cerebral artery; Posterior cerebral artery Cerebral blood low, neonatal/infant arterial, velocities in, range of, 1576, 1577t velocity of, determination of, 1576, 1576f venous, velocities in, range of, 1578, 1578f, 1578t Cerebral blood vessels, extracranial, 917f. See also Internal jugular vein; Vertebral artery IJV as, 955–956 vertebral artery as, 950–955 Cerebral cavernous malformation, in venous malformations of neck, 1657 Cerebral cortex. See also Cortical development malformations, fetal brain and development of, 1167 malformations of, 1193–1203

Cerebral edema neonatal/infant, 1550–1556 difuse, 1553–1555, 1554f–1555f duplex Doppler studies of brain and, 1580 pediatric, TCD sonography in, 1614, 1617f Cerebral hemisphere, neonatal/infant, in sagittal imaging, 1517, 1517f Cerebral infarction, neonatal/infant, 1550–1556 focal, 1555–1556, 1556b, 1556f luxury perfusion and, 1580–1581, 1584f Cerebral palsy pediatric, neurogenic bladder in, 1907 periventricular leukomalacia and, 1550 Cerebral peduncles, 1518 as transtemporal approach landmark, 1592, 1593f Cerebral sinovenous thrombosis, 1547–1548 Cerebrohepatorenal syndrome cortical malformations in, 1196 subependymal cysts from, 1566 Cerebroplacental ratio, MCA and, 1458, 1460f Cerebrospinal luid, hydrocephalus and production and circulation of, 1538–1541 Cerebrovascular accident, 915–916. See also Stroke Cerebrovascular disease, SCD indicators for, 1598, 1599b MCA and, 1600f, 1604f–1605f ophthalmic artery low as, 1599f stroke and, 1601f–1603f Cervical aortic arch, 1658 Cervical canal, dilation of, spontaneous PTB and, 1503 Cervical carcinoma, iliac veins and, 461f Cervical cerclage, for cervical incompetence, 1505–1507, 1506f Cervical ectopia cordis, 1295 Cervical ectopic pregnancy, 1073–1074, 1074f Cervical ectopic thymus, 1723 Cervical fascia, pediatric. See also Infrahyoid space, pediatric; Suprahyoid space, pediatric deep layers of, 1628, 1629f infrahyoid space in, 1628–1629, 1640–1650 suprahyoid space in, 1628–1629 Cervical kyphosis, in campomelic dysplasia, 1381–1382 Cervical lymph node(s) parathyroid adenomas confused with, 745 pediatric, inlammatory disease of, 1658–1663, 1661f–1663f percutaneous needle biopsies for, 717–718, 718f Cervical teratoma fetal, 1159, 1161f pediatric, 1654, 1654f Cervicothoracic vertebrae, campomelic dysplasia and, 1395 Cervix, 528–530 abnormalities of, 541–544, 543f management protocols for, 1507, 1507f–1508f transvaginal ultrasound indings on, 1503b assessment of, 1503–1507 for asymptomatic patients, 1503–1505 in cervical incompetence and cervical cerclage, 1505–1507, 1506f fetal therapy and, 1505 in general obstetric population screening, 1503–1504 in high-risk obstetric population screening, 1504–1505 in multiple gestations, 1504–1505 in pervious cervical surgery, 1505 in polyhydramnios, 1505 in preterm premature rupture of membranes, 1505 in prior PTB, 1504

Index Cervix (Continued) for symptomatic patients, 1505–1507 in uterocervical anomalies, 1505 carcinoma of, 542, 543f hematometra in, 547f, 549 duplicated, 538 dynamic changes in, spontaneous PTB and, 1501–1503, 1503f ectopic pregnancy implantation in, 1073–1074, 1074f funneling of, in spontaneous PTB prediction, 1501, 1502f incompetence of, 1495–1496 cervical cerclage and, 1505–1507, 1506f vaginal pessary and, 1507 length of, 1499–1500, 1499f in prediction of spontaneous preterm birth, 1500–1501, 1501t short, 1500–1501, 1500f, 1501t nabothian cysts of, 533, 535f in pregnancy, on second-trimester scan, 1021f pseudomass in, 533, 536f short, 1500–1501, 1500f, 1501t shortening of, progressive, spontaneous PTB and, 1501 sonography of, 1496–1501 technical limitations and pitfalls of, 1498– 1499, 1498b, 1499f transabdominal approach to, 1496–1497, 1496f transperineal/translabial approach to, 1497, 1497f transvaginal approach to, 1497–1498, 1497f–1498f surgery on, prior, cervical assessment and, 1505 trauma to, carotid artery damage from, 946, 948f Cesarean section(s) hematomas and bladder lap, 556–557, 557f subfascial, 556–557, 557f pediatric pregnancy and, 1884 postpartum indings on, 556–557, 557f–558f scars from, 557, 558f ectopic pregnancy implantation and, 1073, 1075f CEUS. See Contrast-enhanced ultrasound CF. See Cystic ibrosis CHAOS. See Congenital high airway obstruction Charcot triad, in acute cholangitis, 176 CHARGE syndrome, coloboma in, 1143 CHD. See Congenital heart disease Chemical peritonitis, 514 Chemical ventriculitis, in intraventricular hemorrhage, 1545–1547 Chemiluminescence, 42, 42f Chest, fetal. See also Congenital diaphragmatic hernia; Congenital pulmonary airway malformation; Lung(s) bronchogenic cysts in, 1255–1256, 1255f, 1255t CHAOS and, 1253–1255, 1254f congenital diaphragmatic hernia in, 1258–1264 development of structures in, 1243–1245 neurenteric cyst in, 1256 normal sonographic features of, 1244–1245, 1244f pericardial efusion in, 1258, 1258f pleural efusion in, 1256–1258, 1257f pleuropulmonary blastoma and, 1252–1253 pulmonary development in, 1243 pulmonary hypoplasia and, 1245–1246 pulmonary lymphangiectasia and, 1258, 1259f

Chest, pediatric. See also Pneumonia, pediatric atelectasis and, 1714, 1716f bronchopulmonary foregut malformations and, 1716, 1718f CPAM and, 1715–1716, 1717f diaphragm disorders of, 1716, 1718f–1720f empyema in, sonographic signs of, 1702–1711, 1707f lung abscess in, 1711, 1713f lung parenchyma and, 1711–1716 lymphatic malformations and, 1723 mediastinal masses in, 1723–1724 abnormal thymus location mimicking, 1723 anterior, 1723–1724 lymphadenopathy and, 1724 posterior, 1724 thymic index and, 1723, 1724t, 1725f, 1726t parapneumonic collections in, 1710–1711 pleural efusions in, sonographic signs of, 1702–1711, 1704f–1708f pleural luid in, sonographic signs of, 1709, 1709b, 1709f–1710f rib fractures in, 1727 sonography of CT compared to, 1709, 1710f–1711f indications for, 1701, 1702b pitfalls in, 1709–1710, 1712f technique for, 1701–1702, 1703f–1704f ultrasound-guided interventional procedures in, 1724–1726, 1726f–1727f vascular disorders of, 1716–1723 thrombosis, 1716–1721, 1721f–1723f wall of, lesion of, ultrasound-guided biopsy of, 1724–1725 Chiari malformation(s) I, 1526 II, 1190 banana sign in, 1183–1185, 1184f, 1221, 1228, 1230–1232 corpus callosum agenesis in, 1526, 1528f lemon sign in, 1183–1185, 1184f, 1221, 1232–1233 myelomeningoceles with no, 1526, 1529f normal sonographic appearance of fetal, 1168–1169 open spina biida and fetal, 1183, 1184f open spinal dysraphism with, pediatric, 1681–1682 sonographic indings in, 1526, 1526b, 1527f–1528f in spina biida screening, 1221, 1228 VM with, 1177 III, 1526 neonatal/infant neural tube closure disorders and, 1526, 1526b, 1527f–1529f Chiba needles, 1948 Child life specialists, 1776–1781 Childhood malignancies, obstetric sonography and, 1041 Chlamydia trachomatis, 846, 1633–1634 Chlamydial perihepatitis, PID and, 1887 Chloroma masseter muscle, 1641f pediatric, neck, 1667f Chocolate cysts, 574–575 Cholangiocarcinoma, 171 biliary tree and, 184–188 characterization of, with microbubble contrast agents, 106f distal, 188, 192f luke infections and, 178–179 hilar, 185–188 CEUS assessment of, 188, 191f criteria for unresectable, 187b

I-13

Cholangiocarcinoma (Continued) Doppler ultrasound assessment for, 187–188, 189f–191f treatment and staging for, 186–187 tumor growth patterns in, 186 intrahepatic, 184–185, 186f intraductal, 185, 186f–187f peripheral, 129 Cholangiography, transhepatic, 614–615 Cholangiohepatitis, Oriental, 179 Cholangiopathy autoimmune, 182 HIV, 181–182, 181f Cholangitis acute (bacterial), 176, 177f AIDS, 181 ascending, 629 autoimmune, 182 IgG4-related, 182–184, 185f pyogenic, recurrent, 179–181, 180f sclerosing causes of secondary, 182b primary, 182, 183f, 184 recurrent, ater liver transplantation, 629, 630f Cholecystectomy, gallbladder nonvisualization from, 190–194 Cholecystenteric istula, 207 Cholecystitis acalculous, 200 pediatric, 1741 acute, 195–200, 197f–199f, 197t, 201f hyperemia in, 197f, 198–199 pediatric, 1741 prominent cystic artery in, 197f, 198–199 sonographic indings in, 196, 197t chronic, 201–202 emphysematous, 175, 198f, 200 gallbladder nonvisualization from, 190–194, 193f gangrenous, 198f, 200 hemorrhagic, 200 percutaneous cholecystostomy for, ultrasoundguided, 613–614, 616f xanthogranulomatous, 202 Cholecystostomy, percutaneous, ultrasoundguided, 613–614, 616f Choledochal cysts of biliary tree, 168–170, 169f–170f fetal duodenal atresia mistaken for, 1309 of fetal gallbladder, 1319, 1320f neonatal jaundice and, 1735–1737, 1735f–1736f pediatric pancreatitis and, 1862–1864 Choledochocele, pediatric, 1735 Choledochoduodenal istula, 175–176, 177f Choledochoenteric istula, 175–176, 177f Choledochojejunostomy, for liver transplantation, 625 Choledocholithiasis, in biliary tree, 172–173, 182 common bile duct stones and, 173–174, 173f intrahepatic, 173, 173f Cholelithiasis, pediatric, 1741, 1741b, 1743f Chondrodysplasia punctata, 1399 cortical malformations in, 1196 sonographic appearance of, 1380f Chondroectodermal dysplasia, 1398–1399 Chondrolysis, complicating injectable steroids, 901 Chorioamnionitis, maternal, PVL and, 1551 Chorioangioma, 1476, 1478f–1479f Choriocarcinoma ovarian, pediatric, 1880 pseudoprecocious puberty and, 1887 PTN and, 1080–1082, 1083f testicular, 824, 825f, 1899 Chorion, amnion separation from, 1469, 1469f Chorion frondosum, 1465–1466 Volume I pp 1–1014 • Volume II pp 1015–1968

I-14

Index

Chorion laeve, 1465–1466 Chorionic bump, in gestational sac, 1065 Chorionic cavity, 1051, 1053f Chorionic plate, 1465–1466 Chorionic sac luid, 1054–1055, 1056f Chorionic villi, 1465–1466 formation of, 1051–1052, 1053f Chorionic villus sampling (CVS), 1107–1108, 1108f Chorionicity, in multifetal pregnancy, 1115–1116, 1116f sonographic determination of, 1117–1119, 1118f, 1119t, 1120f–1121f triplets and, 1122f Choroid plexus fetal fetal brain and cysts of, 1170, 1173f sonographic view of, 1024f spina biida and cysts of, 1233 trisomy 18 and cyst of, 1103f, 1104 trisomy 21 and cysts of, 1101 neonatal/infant in coronal imaging, 1514–1515, 1514f cysts of, 1565, 1566f development of, 1522–1523, 1522f–1523f papillomas of, 1562, 1565f papillomas of Aicardi syndrome and giant pigmented nevi in, 1209 in neonatal/infant brain, duplex Doppler sonography of, 1588f VM with, 1177–1178 Choroid(s) asymmetry of, in VM, 1178 separation of, from medial ventricle wall, in VM evaluation, 1176, 1176f Chromosomal abnormalities. See also Aneuploidy; Triploidy; Trisomy 13; Trisomy 18; Trisomy 21 diagnostic testing for, 1107–1109, 1108f Ebstein anomaly with, 1286 fetal, IUGR and, 1455 fetal hydrops from, 1429–1430, 1430f maternal age-related risks of, 1088, 1089f primary amenorrhea in, 1887 teratologic hip dislocation and, 1932 triploidy as, 1104–1106, 1104b, 1105f trisomy 13 as, 1104 trisomy 18 as, 1103–1104 trisomy 21 as, 1097–1103 Turner syndrome as, 1106–1107, 1106f Chromosomal anomalies, in CHD, 1270 Chromosomal microarray analysis (CMA), 1097 Chromosome 11p13, hepatoblastomas and, 1746 Chronic allograt nephropathy, 1810, 1812f Chronic autoimmune lymphocytic thyroiditis, 724, 725f–727f Chronic epididymitis, 841, 843f Chronic kidney disease (CKD), 1796–1798, 1797t, 1798f Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS), 389–390, 390f Chronic sclerosing pancreatitis, 236 Chylothorax congenital, fetal, hydrops from, 1425–1426 fetal in hydrops, 1413–1416 primary, 1256 neonatal, radiopaque hemithorax in, 1704f Chylous ascites, 508 Ciliopathies, 1182, 1346 Cingulate sulcus, 1515 neonatal/infant, development of, 1520–1521, 1521f Circumscribed carcinomas, 786 Circumvallate placenta, 1479–1480, 1480f–1481f

Cirrhosis biliary, 92–93, 182 pediatric, 1741 gallbladder wall thickening and, 199f hepatic vein strictures in, 95, 95f in inborn errors of metabolism, 1738 of liver, 92–96 Doppler ultrasound characteristics of, 95, 95f HCC and, 122, 122t intrahepatic portal hypertension from, 96 morphologic patterns of, 92–95, 94f pseudocirrhosis of, 125–128, 129f sonographic features of, 95b SWE and, 95–96 macronodular and micronodular, 92–93 pediatric, 1741, 1742f causes of, 1760b intrahepatic portal hypertension and, 1759–1762 post necrotic, 1741 Cistern, as transtemporal approach landmark, 1592, 1593f Cisterna magna fetal efacement of, in Chiari II malformation, 1183–1185, 1184f normal sonographic appearance of, 1168–1169 neonatal/infant clot in, in intraventricular hemorrhage, 1545, 1546f development of, 1524 mega, Dandy-Walker malformation diferentiated from, 1531, 1534f CKD. See Chronic kidney disease Classic diagnostic triad, for renal cell carcinoma, 340 Clavicle, 878–879, 878f growth of, normal, 1378 Clear cell carcinoma, 581, 582f Cleavage, neonatal/infant brain and disorders of, 1532–1536. See also Holoprosencephaly Clet lip/palate associated signs of, 1152b bilateral, 1152, 1156f–1157f hypertelorism and, 1144f Roberts syndrome and, 1401 complete compared to incomplete, 1151, 1153f–1154f deviation of vomer in, 1151 diferential diagnosis of, 1151b isolated clets of secondary palate in, 1153 median, 1152 as midface abnormality, 1151–1153 patterns of, 1152f Tessier category of, 1152–1153, 1153f trisomy 13 and 18 in, 1151 unilateral, 1152, 1155f midface hypoplasia with, 1149f Cleidocranial dysplasia ribs in, 1382–1384 wormian bones in, 1139 Clinodactyly, fetal, 1404–1405, 1406f Cliopathies, 1182 Clitoris, fetal, enlarged, 1367 CLO. See Congenital lobar overinlation Cloaca, 1337f, 1338, 1674 Cloacal exstrophy fetal abdominal wall and, 1328–1329, 1329f pediatric, risk of spinal dysraphism with, 1689 sacral agenesis in, 1237 Cloacal malformation, 1310–1311 fetal, lower urinary tract obstruction and, 1363, 1363f pediatric, risk of spinal dysraphism with, 1689

Clonorchiasis, biliary tree and, 178–179, 179f Clopidogrel (Plavix), 598 Closed-loop obstruction, mechanical bowel and, 293, 295f Cloverleaf-shaped skull, 1136 craniosynostosis with, 1137f–1138f in skeletal dysplasias, 1382 in thanatophoric dysplasia type 2, 1388–1389, 1389f Clubfoot fetal, 1407, 1407f body stalk anomaly and, 1329 campomelic dysplasia and, 1395 in skeletal dysplasia, 1382 spina biida and, 1233 pediatric, 1932 Clubhand, fetal, 1407 in skeletal dysplasias, 1382 Clustered macrocysts, in breast, 779, 780f Clustered microcysts, in breast, 782 CMA. See Chromosomal microarray analysis CMV. See Cytomegalovirus infection CNS. See Central nervous system CNVs. See Copy number variants Coagulation necrosis, from HIFU, 32 Coagulopathies, small bowel obstruction from, 1843 Coarctation of aorta, 1291, 1292f fetal, hydrops from, 1423–1424 hypoplastic let heart syndrome with, 1287 of frontal horn, 1522, 1522f of lateral ventricles, 1566 Coccygeal dimples, 1679, 1680f Coccyx agenesis of, 1689 development of, in infants, 1677, 1680f Cogwheel sign, 587–588 Colitis infectious, pediatric, 1852 pseudomembranous, 296–297, 298f tuberculosis, 287–288 ulcerative, 266–267 Collagen bundles, 859 Collagen vascular disease, maternal, fetal AVB from, 1297 Coloboma, 1143, 1146f Colon carcinoma of, 261–264, 263f–264f pediatric, 1880 diverticula of, 290, 291f fetal, 1308–1316 anorectal malformations and, 1310–1312, 1311f MMIHS and, 1362–1363 pediatric, 1847–1848 ectopic or imperforate anus and, 1847–1848, 1850f interventional sonography and anatomy of, 1950 normal anatomy of, 1847, 1850f sonographic technique for, 1847 Color assignments, changing, in color Doppler, 933 Color Doppler ultrasound, 24, 25b aliasing in, 28, 29f, 966 for breast assessment, 769–772, 770f–773f for carotid stenosis evaluation, 932–935 advantages and pitfalls of, 934–935, 934b, 934f bruit from, 933, 934f optimal settings in, low-low vessel evaluation, 933–934, 933b, 934f color assignments in, changing, 933 for Crohn disease, 268t, 269, 272f Doppler beam in, vessel paralleling, 933 for epididymitis, pediatric, 1896, 1896b in fetal heart assessment, 1275–1277, 1282f

Index Color Doppler ultrasound (Continued) green-tag feature in, 932–933 interpretation of, 28, 28f–29f interventional sonography, pediatric and, 1945 limitations of, 25b for neonatal/infant brain, 1573–1574 operating modes in, 30–31 for pancreatic carcinoma, 241, 241b, 241f–243f, 241t for percutaneous needle biopsies, 599 in placenta accreta diagnosis, 1471 in placenta blood low assessment, 1468–1469 in pleural luid imaging, 1709, 1710f power compared to conventional, 25, 26f PRF in, 28, 29f, 30–31 process of, 24, 26f prostate cancer and, 404f, 406 slow-low sensitivity settings on, 939 for testicular torsion, pediatric, 1895–1899, 1896b for testicular tumors, pediatric, 1901–1902 in ureteral calculi detection, 337, 339f for ureteral jets evaluation, 1781f weighted mean frequency in, 28 Color gain, in renal artery duplex Doppler sonography, 449 Color streaking, breast cysts with, 775, 776f Colpocephaly, 1202f in Chiari II malformation, 1526, 1527f in corpus callosum agenesis, 1528, 1530f Column of Bertin, in kidney development, 1781, 1783, 1784f Coma, brain death diferentiated from, 1618–1620, 1620f Comet-tail artifacts, 202, 695 in benign and malignant thyroid nodule diferentiation, 712–713 in degenerative cysts of thyroid, 1646, 1647f Common bile duct anastomosis of, for liver transplantation, 625 dilation of, cylindrical or saccular, pediatric, 1735, 1736f diverticula of, 1735 stones in, 173–174, 173f acute pancreatitis and, 221 liver transplantation complications with, 629, 632f Common femoral vein as landmark for femoral hernias, 482, 485f normal anatomy of, 500, 981f Complete molar pregnancy, 1078, 1079f Complete subclavian steal, 952–953, 953b, 953f Complete TGA, 1289, 1289f Complicated cysts, of breast, 775–780, 776f Compression of amplitudes, 9 ballottement and, 768 for breast sonography, 768, 772, 773f of femoral vein, normal, 982f maneuvers, for dynamic ultrasound of hernia, 474, 475f for parathyroid gland adenomas detection, 739 sot tissue ganglia causing, 865 in sound wave, 2, 2f Compression sonography, 258–260, 261f Computed tomography (CT) in abdominal aortic aneurysm rupture evaluation and, 438, 439f for screening and surveillance, 437 treatment planning with, 438 in interventional sonography, pediatric, 1943, 1943t parathyroid adenomas and accuracy of, 748, 748f

Computed tomography (CT) (Continued) pediatric chest, sonography compared to, 1709, 1710f–1711f for percutaneous needle biopsies, 599 three-dimensional, in skeletal dysplasia evaluation, 1384–1385 Concentric hypertrophy, 1294–1295 Conceptual age, deinition of, 1443–1444 ConirmMDx test, 396 Congenital adrenal hyperplasia (CAH) adrenal rests in, 832–833, 833f, 1824, 1900–1901 pediatric, 1822–1824, 1824f, 1900–1901 Congenital anomalies of kidney and urinary tract (CAKUT), 1336 Congenital bilateral absence of the vas deferens (CBAVD), 394 Congenital coxa vara, atypical hips and, 1932 Congenital cystic adenomatoid malformation (CCAM), 1246, 1248t fetal, hydrops from, 1426 Congenital diaphragmatic hernia (CDH), 1248t, 1258–1264 anomalies associated with, 1263 bilateral, 1262 fetal lung size and, 1244 FETO for, 1264 let-sided, 1258–1259, 1260f morbidity and mortality from, 1264, 1264t prognosis of, 1261–1262, 1262b right-sided, 1259, 1261f survival predictors in, 1262, 1262b in utero therapy for, 1264 Congenital heart block, fetal, 1297, 1297f hydrops from, 1425 Congenital heart defects, thickened NT in, 1095–1097, 1096f Congenital heart disease (CHD) chromosomal anomalies in, 1270 extracardiac malformations in, 1270 fetal arrhythmia and, 1270–1273 hydrops and, 1270 IVF and, 1270–1273 MCDA twins and, 1270–1273 risk factors associated with, 1270, 1271t–1272t recurrence, in ofspring, 1273t recurrence, in siblings, 1273t Congenital high airway obstruction (CHAOS), 1248t, 1253–1255, 1254f hydrops from, 1426 Congenital hypothyroidism, 694 pediatric ovarian cysts and, 1875 Congenital infantile myoibromatosis, 1664, 1665f Congenital lobar emphysema, 1246 Congenital lobar overinlation (CLO), 1246, 1251–1252, 1253f Congenital malformations, obstetric sonography and, 1041 Congenital myopathy, atypical hips and, 1932 Congenital nephrotic syndrome, CKD and, 1796–1798 Congenital pulmonary airway malformation (CPAM) classiication of, 1248 diferential diagnosis of, 1248t fetal, 1246–1252 hydrops development and, 1248–1249, 1426, 1427f pediatric, 1715–1716, 1717f pleuropulmonary blastoma diferentiated from, 1252–1253 sonographic diagnosis of, 1248, 1249f volume ratio of, 1248, 1250

I-15

Congestive heart failure gallbladder wall thickening and, 199f neonatal/infant, 1566 Conglomerate masses, Crohn disease and, 269 Conjoined tendon insuiciency direct inguinal hernia and, 479–481, 483f–484f sports hernia and, 485–486, 489f Conjoined twins, 1115–1116 complications with, 1129–1130, 1130f Conn syndrome, adrenal adenomas in, 419 Connatal cysts, 1566 Connective tissue, dense ibrous, homogeneous plaque and, 920–921 Conradi-Hünermann syndrome, 1399 Constrictive amniotic bands, 1182–1183 Continuous ambulatory peritoneal dialysis, 521 Continuous wave (CW) devices, 8 Continuous wave Doppler, 24, 25f Continuous wave probes, with duplex pulsed Doppler, 939 Continuous wave ultrasound, 36 Contraceptive devices, intrauterine, 529, 552–554, 553f Contraceptives, oral, hepatic adenomas and, 1746 Contrast, speckle efect on, 13–15, 14f Contrast agents, 41–42. See also Blood pool contrast agents acoustic cavitation and, 43, 44b avoidance of, in obstetric sonography, 1038 blood pool, 55–56 disruption-replenishment imaging and, 66–67, 67f echo enhancing, 57f harmonic imaging with, 58–64 in hydrosonovaginography, 1870–1871, 1871f intermittent harmonic power Doppler imaging and, 66, 66f intermittent imaging with, 64–67, 66f intravenous Doppler, 1749–1750 intravenous ultrasound, 1746 microbubbles as, 53–54, 54f behavior of, incident pressure and, 56–58, 57t disruption of, 64–67, 66f FNH characterization with, 106, 106f, 108t, 109f future of technology for, 68–69, 69f–70f HCC characterization with, 106, 106f hemangioma characterization with, 106, 106f–107f, 108t inertial cavitation and, 67–68 lesional enhancement with, 105, 106f–107f, 109f liver mass characterization with, 105–106, 106f–107f, 108t, 109f–110f MI and, 58, 58b, 105 need for, 56–58, 57f regulation of, 68 safety of, 67–68 in musculoskeletal interventions, 898 nonlinear echoes and, 58–64 amplitude and phase modulation imaging and, 64, 65f harmonic B-mode imaging and, 60 harmonic spectral and power Doppler and, 60–61, 60f–62f plane-wave contrast imaging and, 64 pulse inversion Doppler imaging and, 63–64 pulse inversion imaging and, 62–63, 62f–63f temporal maximum intensity projection imaging and, 64, 65f tissue harmonic imaging and, 61–62 perluorocarbons in, 56 for liver mass detection, 107, 111f requirements for, 54–56 Volume I pp 1–1014 • Volume II pp 1015–1968

I-16

Index

Contrast agents (Continued) triggered imaging and, 65 types of, 54–56 in water enema technique, 1870–1871, 1871f Contrast efect, of steroid anesthetic mixture, 899, 899f Contrast pulse sequence (CPS), 64 Contrast-enhanced ultrasound (CEUS) adenoma diagnosis with, 116–117, 117f backscatter increased with, 107, 111f for breast lesions, 773–774 cavernous hemangioma characterization with, 111, 113f for Crohn disease, 269, 273f Crohn disease identiication with, pediatric, 1853, 1854f in fatty liver diagnosis, 91–92 FNH diagnosis with, 113–115, 115f gut wall and, 261 HCC detection with, 120–122, 123f Hilar cholangiocarcinoma assessment with, 188, 191f liver metastases diagnosis with, 128–129, 130f for pancreas, 251 for pancreas transplantation, 676 for prostate cancer, 406 for thyroid gland assessment, 692, 714–715 Contrast-to-noise ratio, spatial compounding and, 13–15, 15f Conus medullaris determining position of, 1677, 1679f fetal, location of, 1218–1221, 1221f, 1673, 1673f low and tethered, caudal agenesis type II and, 1689 Conus septum, TOF and, 1288 Cooper ligaments, 761, 761f–763f Copy number variants (CNVs), 1088 Coracoacromial ligament, 878–879 Coracobrachialis muscle, 878–879 Coracoclavicular ligaments, 878–879 Coracohumeral ligament, 878–879 Coracoid process, 878–879, 879f Cordocentesis, 1434, 1434f Cornelia de Lange syndrome, microcephaly in, 1194 Cornua hematometra and, 551–552 “Cornual pregnancy”, 1073 Coronary bypass grat, radial artery evaluation for, 977–978, 980f Corpora amylacea, 387 Corpora quadrigemina, 1518 Corpus callosum agenesis of in Chiari II malformation, 1526, 1528f fetal brain and, 1199–1201, 1202f, 1203b neonatal/infant neural tube closure disorders and, 1526–1528, 1529b, 1530f–1533f periventricular nodular heterotopia and, 1199f VM and, 1177 dysgenesis of, fetal brain and, 1199–1201, 1203b lipoma of, 1529, 1533f in rhombencephalosynapsis, 1192 thinning of, in PVL, 1552 Corpus luteum angiogenesis of, 1063 cysts of, 570 pediatric, 1875 development of, 568 formation of, 1049 Corrected TGA, 1290, 1290f Cortical development malformations, fetal brain and, 1193–1203 absence of septi pellucidi as, 1201–1203 cerebrohepatorenal syndrome as, 1196 chondrodysplasia punctata as, 1196

Cortical development malformations, fetal brain and (Continued) classiication of, 1194b corpus callosum agenesis/dysgenesis as, 1199–1201, 1202f, 1203b focal changes in, 1196 hemimegalencephaly as, 1195 heterotopia as, 1196, 1199f intracranial calciications as, 1195f, 1203, 1204f lissencephaly as, 1195–1196, 1196f–1197f macrocephaly as, 1194–1195 megalencephaly as, 1194–1195 microcephaly as, 1194, 1195f polymicrogyria as, 1196, 1198f schizencephaly as, 1196, 1199f SOD as, 1201–1203, 1203f TSC and, 1198, 1200f Cortical nephrocalcinosis, 339 pediatric, 1798, 1798b, 1798f Corticosteroids, for musculoskeletal injections, 900 Cortisol, secretion of, 417 Couinaud anatomy, of liver, 76–77, 77t, 78f Coxa vara, congenital, atypical hips and, 1932 Coxsackie virus, 1203–1204 Coxsackie virus infection, fetal hydrops from, 1431 Coxsackievirus B, endocardial ibroelastosis from, 1294 CPAM. See Congenital pulmonary airway malformation CP/CPPPS. See Chronic prostatitis/chronic pelvic pain syndrome CPS. See Contrast pulse sequence Cranial Bone hermal Index (TIC), 39–40 Cranial hairy tut, diastematomyelia and, 1689 Cranial neuropore, in spine embryology, 1217 Craniocervical junction, in pediatric spine, 1674, 1675f Cranioectodermal dysplasia, 1395 Craniolacunia, in Chiari II malformation, 1526 Craniopharyngioma, intracranial, fetal, 1208 Craniorachischisis, 1179, 1218 Cranioschisis, deinition of, 1225t Craniosynostosis with cloverleaf-shaped skull deformity, 1137f–1138f cranial contour indicating, 1382 intracranial compliance in, evaluation of, 1581–1582 metopic, 1137f syndromes associated with, 1136–1139, 1137f–1138f Cranium, in skeletal dysplasias, 1382 Crass position, for shoulder ultrasound modiied, 881, 883f–884f original, 881, 883f Creeping fat, Crohn disease and, 269, 271f Cremasteric (external spermatic) artery, 821, 821f Cremasteric relex, 846 CREST. See Carotid Revascularization Endarterectomy Versus Stenting Trial CRL. See Crown-rump length Crohn disease anatomy afected by, 268 appendicitis associated with, 285, 287f, 1862f CEUS for, 269, 273f classic features of, 269 color Doppler ultrasound for, 268t, 269, 272f complications of, 269–276 istula formation as, 276, 279f–280f incomplete mechanical bowel obstruction as, 274, 276f inlammatory masses as, 275–276, 278f–279f localized perforation with phlegmon as, 274–275, 277f perianal inlammation as, 276, 281f, 305–306 strictures as, 269–274, 275f–276f

Crohn disease (Continued) conglomerate masses and, 269 creeping fat and, 269, 271f diagnosis of, 267–268 gastrointestinal tract and, 266–269 gut wall thickening and, 269, 270f–271f hyperemia and, 269, 272f–273f intramural sinus tract in, 269, 274f lymphadenopathy in, 269, 272f management of, 266–267 mucosal abnormalities and, 269, 274f pediatric, 1853, 1854f sonographic assessment of, 268, 268b, 268t transperineal scanning in, 276 Crossed-fused ectopia, 318, 318f pediatric, 1784–1785, 1785f Crouzon syndrome craniosynostosis in, 1136–1138 midface hypoplasia in, 1148 Crown-rump length (CRL), 1054 accurate, criteria for, 1092, 1092b early pregnancy failure and, no heartbeat and, 1063, 1064f embryos with less than 7 mm, and no heartbeat, 1064 in gestational age determination, 1445, 1446f, 1446t in gestational age estimation, 1062 gestational sac with small MSD in relationship to, early pregnancy failure and, 1066, 1067f NT compared to, 1089, 1090f Cryptorchid testes, 823 Cryptorchidism testicular microlithiasis and, 1904 testis and, 851, 851f pediatric, 826 Crystalline form, of injectable steroids, 900 CT. See Computed tomography Cubital tunnel, 865–866 Cul-de-sac anterior, 528 luid in, 568–569, 569f posterior, 528, 566 Cumulus oophorus, 1049 Currarino triad, 1689 Curved array transducers beam steering in, 10–11, 11f use and operation of, 12 Cushing disease, adrenal adenomas in, 419 Cushing syndrome, 832–833 adrenal adenomas in, 419 pediatric, adrenal rests in, 1900–1901 Cutaneous rapidly involuting congenital hemangiomas, 1742–1743 CVS. See Chorionic villus sampling CW devices. See Continuous wave devices Cyclopia, 1140 alobar HPE and, 1534–1535 Cystadenocarcinoma(s) mucocele of appendix and, 299 ovarian mucinous, 580f, 581 pediatric, 1880 serous, 580–581, 580f Cystadenoma(s) biliary, 82, 83f epididymal, paratesticular, 1904 mucocele of appendix and, 299 ovarian mucinous, 580f–581f, 581 pediatric, 1880 serous, 580–581, 580f papillary, of epididymis, 840–841 Cystic adenomatoid malformations, pediatric, 1715

Index Cystic artery, 194 prominent, in acute cholecystitis, 197f, 198–199 Cystic dysplasia, testicular, 830 pediatric, 1891–1892, 1891f Cystic encephalomalacia, 1538, 1539f Cystic ibrosis (CF) fatty iniltration of liver in, 1740f fetal, hydrops from, 1428 fetal echogenic bowel and, 1316 fetal liver calciications and, 1316–1318 gastrointestinal tract and, 300 ileal obstruction and, 1310 inborn errors of metabolism and, 1738 ovarian cysts and, pediatric, 1875 pediatric pancreatitis and, 1862–1864 Cystic hygroma(s). See also Lymphatic malformations in aneuploidy screening, 1093, 1093f hydrops from, 1425 thickened NT and, 1096f in Turner syndrome, 1106–1107, 1106f Cystic kidney disease, CKD and, 1796–1798 Cystic meconium peritonitis, 1842–1843, 1846f Cystic metastases, 82 of liver, 125, 128f Cystic periventricular leukomalacia, 1551–1552, 1552f Cystic presacral lesions, pediatric, 1915 Cystic teratomas, ovarian, 582–584, 582b, 583f Cystic tumor(s) arachnoid cysts diferentiated from, 1192–1193 cavum veli interpositi cysts diferentiated from, 1170 Cystinosis, CKD and, 1796–1798 Cystitis chronic, 333, 333f cystica, pediatric, 1908 emphysematous, 333, 334f genitourinary, 333 glandularis, pediatric, 1908 granulomatous, pediatric, 1908 hemorrhagic, pediatric, 1908, 1910f infectious, 333, 334f interstitial, 372, 373f pediatric urinary tract infection and, 1794, 1796f–1797f, 1908, 1910f–1911f pseudopolyps and, 333, 333f Cystitis cystica, 333 Cystitis glandularis, 333 Cystogenesis, 1524, 1525b Cystoscopy, for lower urinary tract obstruction, 1363–1365 Cyst(s). See also Dermoid cyst(s); Duplication cysts; Epidermoid cyst(s); Kidneys, fetal, cystic disease of; Kidneys, pediatric, cystic disease of; Kidney(s), cysts of; Pancreas, cystic neoplasms of; Pseudocyst(s) in adenomyosis, 540b, 541, 542f adnexal, in pregnancy, 1020 adrenal, 421–422, 422b, 423f amnion inclusion, 1061 anechoic, 331 arachnoid cavum veli interpositi cysts diferentiated from, 1170 corpus callosum agenesis and, 1526–1528 fetal brain and, 1192–1193, 1193f of neonatal/infant brain, 1563–1565, 1565b spinal canal and, pediatric, 1695–1697, 1696f Baker, 870, 870f injection for, 907–909, 908f

Cyst(s) (Continued) Blake pouch arachnoid cysts diferentiated from, 1192–1193 sonographic appearance of, 1170, 1173f branchial type I, pediatric, 1639, 1651, 1651f type II, pediatric, 1639–1640, 1651, 1652f type III, pediatric, 1651, 1652f breast, 774–785 acorn, 778f aspiration of, ultrasound-guided, 811, 813f clustered macrocysts and, 779, 780f clustered microcysts and, 782 with color streaking, 775, 776f complex, 780–785, 782f complicated, 775–780, 776f Doppler ultrasound for diferentiating, 769–770, 770f eggshell calciication and, 779, 780f fat-luid levels in, 775, 778f ibrocystic change and, 775 foam, 779, 781f inlammation and infection of, 782–785, 785f lipid, 775–779, 779f microcysts and, 782, 784f milk of calcium and, 775, 776f–777f mural nodules and, PAM causing, 782, 783f–784f papillary lesions and, 782 septations within, 782, 783f simple, 774, 775f of skin origin, 779, 781f bronchogenic, pediatric, 1650, 1716, 1718f chocolate, 574–575 choledochal of biliary tree, 168–170, 169f–170f fetal duodenal atresia mistaken for, 1309 of fetal gallbladder, 1319, 1320f neonatal jaundice and, 1735–1737, 1735f–1736f pediatric pancreatitis and, 1862–1864 choroid plexus fetal brain and, 1170, 1173f neonatal/infant brain and, 1565, 1566f spina biida and, 1233 in trisomy 18, 1103f, 1104 in trisomy 21, 1101 connatal, 1566 corpus lutein, 570 pediatric, 1875 daughter, 331, 332f in Echinococcosis, 1748 decidual, 1054 dorsal midline, in corpus callosum agenesis, 1528, 1531f ejaculatory duct, 392 embryonic, 1077, 1077f endometrial, 547–548 epididymal, 839, 842f pediatric, 1902–1903, 1903f esophageal, pediatric, 1650 fetal bronchogenic, 1255–1256, 1255f, 1255t cortical, in renal dysplasia, 1347–1348 neurenteric, 1256 ovarian, 1369, 1369f pancreatic, 1320 renal, 1346–1352 splenic, 1320–1322, 1322f ilar, in newborn, 1674–1675, 1678f follicular, 568 pediatric, 1875 foregut, pediatric, 1650

I-17

Cyst(s) (Continued) frontal horn, neonatal/infant brain and, 1522, 1522f, 1566 ganglion, 869–870, 869f injection for, 907–909, 909f Gartner, pediatric, 1883–1884 gastrointestinal congenital, 297, 298f pediatric, 1860–1862, 1863f–1864f gel, 779, 781f hydatid, 89, 89f–90f in Echinococcosis, 1748 renal, 331, 332f splenic, 147, 150f inclusion amnion, 1061 epidermal, 779 peritoneal, 508–509, 509f, 573, 573f surface epithelial, 569, 573 vaginal, pediatric, 1883–1884 infrahyoid space, pediatric, 1650 inspissated, 779, 781f interhemispheric, in corpus callosum agenesis, 1201 intratesticular, 829, 830f of kidneys, 356–365 percutaneous management of, 617–618, 619f of kidneys, pediatric, congenital, 1816–1818 dialysis and acquired, 1816–1818, 1817f ater liver transplantation, 1816–1818 in TSC, 1816, 1817f in VHL disease, 1816 liver, 82, 82f–83f autosomal dominant polycystic kidney disease and, 83 benign, 82 fetal, 1318, 1318f percutaneous management of, 618 peribiliary, 82–83 mesenteric fetal, ovarian cysts diferentiated from, 1369 gastrointestinal cysts diferentiated from, 1860, 1863f pediatric, ovarian cysts diferentiated from, 1875 peritoneal, 509–510, 510f milk of calcium, 653, 657f müllerian duct, 392 pediatric, 1908, 1910f nabothian, 533, 535f, 1499 neurenteric, pediatric, 1686–1688, 1724 omental, pediatric ovarian cysts diferentiated from, 1875 ovarian dermoid, 582–584, 583f fetal, 1369, 1369f functional, 570–571, 571f hemorrhagic, 570–571, 571f, 575 menstrual cycle and follicular, 568 neonatal, 1876f paratubal, 573 parovarian, 573 percutaneous management of, 618–619 peritoneal inclusion, 573, 573f postmenopausal, 569–570, 571f surface epithelial inclusion, 569, 573 in triploidy, 1105f ovarian, pediatric, 1873–1877 hemorrhagic, 1877, 1878f–1879f in polycystic ovarian disease, 1877–1878, 1879f torsion and, 1875–1876, 1876b, 1877f pancreatic, 242–248, 243f congenital, 1865 fetal, 1320 Volume I pp 1–1014 • Volume II pp 1015–1968

I-18

Index

Cyst(s) (Continued) simple, 243, 244f VHL disease and, 243, 244f paralabral, injection for, 907–909, 910f–911f parameniscal, 907–909 paramesonephric duct, pediatric, 1883–1884 paraurethral, pediatric, 1883–1884 parovarian, pediatric, 1875, 1876f percutaneous management of, 617–619, 619f peritoneal inclusion, 508–509, 509f mesenteric, 509–510, 510f periventricular, of neonatal/infant brain, 1566, 1566f pineal, 1170 popliteal, pediatric, 1939 porencephalic, neonatal/infant brain and, 1537, 1565 posterior fossa subarachnoid, Dandy-Walker malformation diferentiated from, 1190, 1531, 1531b prostate, 388, 390–392, 391f in renal cell carcinoma, 343, 343f rhombencephalon, 1077, 1077f round ligament, simulating groin hernias, 500, 501f scrotal, extratesticular, 839, 842f sebaceous, 779, 781f seminal vesicle, 392, 393f pediatric, 1908, 1910f simulating groin hernias, 499–500, 501f spermatic cord, pediatric, 1902–1903 splenic, 146–148, 146b, 148f–151f endothelial-lined, 148 epidermoid, 146–147, 148f–149f false, 146–147, 149f fetal, 1320–1322, 1322f hydatid, 147, 150f pediatric, 1769 primary congenital, 146–147, 148f–149f pseudocysts as, 146–147, 149f subchorionic maternal loor infarction with, 1474, 1476f placental, 1474, 1477f subependymal, 1543–1544 of neonatal/infant brain, 1566, 1567f of suprahyoid space, pediatric, 1639–1640, 1640b, 1640f–1641f tailgut, 297, 298f testicular, 829, 829b cystic dysplasia and, 830 epidermoid, 830f, 831 intratesticular, 829, 830f simple, pediatric, 1901–1902 tubular ectasia of rete testis and, 829–830, 830f theca lutein, 570, 572 pediatric, 1875 thymic, 1652, 1653f, 1723–1724 thyroglossal, duct, pediatric, 1640, 1643, 1644f–1645f thyroid calciications of, 695 pediatric, 1646, 1647f tunica albuginea, 829, 830f tunica vaginalis, 829, 830f pediatric, 1902–1903 umbilical cord, 1483, 1483f sonographic appearance of, 1061, 1061f in trisomy 18, 1103f urachal, 322, 323f ovarian cysts diferentiated from, 1369 pediatric, 1907–1908, 1909f pediatric hydronephrosis and, 1791, 1792f–1793f pediatric ovarian cysts diferentiated from, 1875

Cyst(s) (Continued) utricle, 391f, 392 vallecula, pediatric, 1640, 1641f of vas deferens, 842f Cytogenesis, 1513b, 1524 Cytomegalovirus (CMV) infection, 91 in acute typhlitis, 287–288, 289f congenital, neonatal/infant brain and, 1558– 1560, 1559f fetal brain development and, 1203–1204, 1205f hydrops from, 1431–1432 hyperechogenic kidneys in, 1351 fetal echogenic bowel and, 1315f neonatal/infant, schizencephaly from, 1536– 1537, 1558 Cytopathologists, deinition of, 600 Cytotrophoblast cells, 1466f D Dabigatran, 598 Dacryocystocele, 1143, 1147f Damping materials, in transducers, 8 “Dancing megasperm”, 841 Dandy-Walker complex, VM and, 1177 Dandy-Walker continuum, 1190–1191 Dandy-Walker malformation, 1190 arachnoid cysts diferentiated from, 1192–1193 in cerebellum, 1190, 1190f corpus callosum agenesis and, 1526–1528 diferential diagnosis of, 1190, 1192–1193, 1531–1532, 1531b etiology of, 1530 mega-cisterna magna diferentiated from, 1192 neonatal/infant neural tube closure disorders and, 1529–1532, 1530b, 1533f–1534f sonographic indings of, 1530b in triploidy, 1105f ventriculoperitoneal shunting for, 1530 Dandy-Walker spectrum, 1530–1531 Dandy-Walker variant, 1190–1191, 1530 Dartos fascia, 846 Daughter cysts, 331, 332f in Echinococcosis, 1748 DCIS. See Ductal carcinoma in Situ DDH. See Development dysplasia of the hip de la Chapelle dysplasia, 1396 de Morsier syndrome, 1201–1203. See also Septo-optic dysplasia de Quervain disease, 724 de Quervain tendinosis, injection for, 904, 905f de Quervain thyroiditis, 1645 Decibel, 5–7 Decidua, 1466f Decidua basalis, 1054, 1465–1466 Decidua basalis–chorion frondosum, 1054 Decidua capsularis, 1054, 1465–1466 Decidua vera, 1054, Decidual cysts, 1054 Decidual reaction, 1049 Deep venous thrombosis (DVT). See also Peripheral veins acute brachial veins and nonocclusive, 994f in GSV, 984, 984f lower extremity, 983–984, 983f–985f upper extremity, 992–994, 994f–995f blood low and absent, 992–994 slow, 984, 988f of calf, 982 central venous catheterization related to, 935, 995f chronic in brachial vein, 994–995, 996f calciications indicating, 984, 987f

Deep venous thrombosis (DVT) (Continued) of IJV, 994f lower extremity, 984, 986f–987f nonocclusive, 992, 994f in profunda femoris vein, 987f upper extremity, 994–995, 995f–996f in femoral vein, duplicated, detecting, 988, 988f follow-up recommendations for, 989 pulmonary embolism from lower extremity, 979, 981f upper extremity, 994 ultrasound examinations of indications in, 979 limitations of, 989 venous insuiciency caused by, 989, 990f Default output power, for obstetric sonography, 1035 Deferential artery, 821, 821f Deinity, 56 Deformations, deinition of, 1399 Delivery. See also Preterm birth fetal hydrops and, 1436 preterm, 1495–1496 Deltoid muscle, 878–879, 878f Demineralization, of spine, in skeletal dysplasias, 1382 Depigmentation, complicating injectable steroids, 901 Depth gain compensation, 8 Dermal sinus tract dorsal, pediatric, 1686, 1688f focal, 1674 tethered cord and, 1679 Dermoid cyst(s) hemorrhagic ovarian cyst diferentiated from, 1877 neck, pediatric, 1652–1654, 1654f ovarian, 582–584, 583f in suprahyoid area, 1640 Dermoid mesh, 582–583, 583f Dermoid plug, 582, 583f DES. See Diethylstilbestrol Desmoid tumors, simulating anterior abdominal wall hernias, 500–501, 502f Desmoplastic small round cell tumors, 1860 Detrusor arelexia, 372–374, 373f Detrusor hyperrelexia, 372–374, 373f Development dysplasia of the hip (DDH), 1920–1930 causes of, 1921 clinical overview of, 1920–1921 dynamic sonographic technique for, 1922–1927 anterior view for, 1927, 1929f coronal/lexion view for, 1925–1927, 1926f coronal/neutral view for, 1923–1924, 1924f–1925f history of, 1922 stress maneuvers for, 1923 technical factors in, 1922–1923 transverse/lexion view for, 1927, 1928f transverse/neutral view for, 1927 evaluation during treatment and, 1929–1930 evaluation of infant at risk and, 1927–1929 incidence of, 1920–1921 mechanism of, 1921 minimum standard examination for, 1922b risk factors of, 1921b screening for, 1921 Dextrocardia, 1273 Dextroposition, 1273, 1274f Dextrotransposition, of great arteries, 1289–1290 DFI. See Direction of low index

Index Diabetes mellitus chronic renal failure in, 372 maternal caudal agenesis and, 1689 LGA fetus and, 1454, 1455t NTDs from, 1218 Dialysis acquired cystic kidney disease associated with, 364 acquired renal cysts in, pediatric, 1816–1818, 1817f peritoneal, continuous ambulatory, 521 postoperative ultrasound evaluation for, 996 preoperative ultrasound for, 996 Diamond-Blackfan syndrome, 1401 Diaphragm duodenal, 1841–1842, 1844f eventration of, 1716 fetal agenesis of, 1258 defect of anterior, pentalogy of Cantrell and, 1329 development of, 1244f, 1245 eventration of, 1258, 1262–1263 gastric, pediatric, 1839, 1840f interventional sonography and anatomy of, pediatric, 1950, 1950f pediatric disorders of, 1716, 1718f–1720f paralysis of, 1716, 1719f–1720f rupture of, 1716, 1720f Diaphragm sign, as pleural luid sonographic sign, 1709 Diaphragmatic hernia congenital, 1248t, 1258–1264 anomalies associated with, 1263 bilateral, 1262 fetal lung size and, 1244 FETO for, 1264 let-sided, 1258–1259, 1260f morbidity and mortality from, 1264, 1264t prognosis of, 1261–1262, 1262b right-sided, 1259, 1261f survival predictors in, 1262, 1262b in utero therapy for, 1264 fetal, hydrops from, 1425 pediatric, 1716, 1718f thickened NT in, 1095–1096 Diaphragmatic pericardium, pentalogy of Cantrell and, 1329 Diaphragmatic slips, 80 Diastasis recti abdominis, 489–490, 489f Diastematomyelia, 1674, 1681 closed spinal dysraphism and, 1688–1689, 1688f fetal, 1234–1235, 1236f Diastolic runof, prolonged, carotid low waveforms and, 936–937 Diastrophic dwarism indings associated with, 1382 hitchhiker thumb in, 1382, 1406 Diastrophic dysplasia, 1398, 1398f DICA. See Distal internal carotid artery Dichorionic diamniotic twins, 1019f, 1115–1116, 1116f growth discrepancy in, 1123f placental indings in, 1119 sonographic indings of, chorionicity and, 1119, 1120f Didelphys uterus, 534, 536f–537f, 1881 Diencephalon, 1077 Diethylstilbestrol (DES) cervical assessment in, 1505 uterus exposure to, 534, 536f, 1881 Difuse relectors, 4, 5f

Difuse steatosis, 91, 92f Difusion tensor imaging, in PVL, 1553 DiGeorge syndrome, 1196 neuroblastoma with, pediatric, 1825 DiGeorge syndrome, fetal thymus evaluation for, 1245 Digestive tube, embryology of, 1304–1305 Digital rectal examination (DRE), 381–382, 387 Dilated bowel, fetal, 1313 Dilated distal ureter, 592 Dilated loops of bowel, 1310, 1311f fetal gastroschisis and, 1323–1324 Dilated loops of small bowel, 1311–1312 Dilated stomach, fetal, 1307, 1308f Diploid karyotype, complete molar pregnancy and, 1078 Diplomyelia, in diastematomyelia, 1236f Direct controls, 48, 49t Direction of low index (DFI), 1618 Discriminatory level, for seeing gestational sac, 1056 Disjunction, in spine embryology, 1672–1673 Dislocations, pediatric. See also Developmental dislocation and dysplasia of hip frank, of hip, 1927 of hip, developmental, 1920–1930 Displaced-crus sign, as pleural luid sonographic sign, 1709 Disruption-replenishment imaging, 66–67, 67f Disruptions, deinition of, 1376, 1377t, 1399 Dissection complications, renal artery stenosis and, 447, 448f Distal cholangiocarcinoma, 188, 192f Distal internal carotid artery (DICA) SCD and stenosis of, 1606f as transtemporal approach landmark, 1592, 1594f Diuretic therapy, medullary nephrocalcinosis and, 1798 Diverticulation. See also Holoprosencephaly neonatal/infant brain and disorders of, 1532–1536 in organogenesis, 1524, 1525f Diverticulitis acute, 288–290 classic features of, 288–290 muscular hypertrophy from, 290, 291f pericolonic changes in, 290, 292f sonography of, 290, 290b focally inlamed fat in, 521 right-sided, 285–287, 288f Diverticulosis, spastic, 288–290 Diverticulum(a) bladder, 374, 374f identiication of, 592 calyceal, renal milk of calcium and, 1799, 1800f colonic, 290, 291f of common bile duct, 1735 Hutch, 310 Meckel intussusception and, 1844–1845, 1849f pediatric appendicitis diferentiated from, 1858–1860, 1862f urachal, 322, 323f pediatric, 1907–1908, 1909f urethral, 323, 323f anterior, pediatric, bladder outlet obstruction from, 1906 urinary bladder, transitional cell carcinoma in, 348 ventricular, 1294 vesicourachal, pediatric, 1775, 1791 Dizygotic (fraternal) twins, 1115–1116, 1116f Dolichocephaly, 1136

I-19

Donor renal vein, anastomosis, in renal transplantation, 643 Doppler angle, 21–22, 24f, 29b, 30 Doppler angle theta. See Angle theta, Doppler Doppler beam, vessel paralleling, in color Doppler, 933 Doppler efect, 21–22, 23f Doppler frequency, 29 Doppler frequency shit, 21–22, 23f–24f Doppler gain, 30, 33f Doppler indices, 27–28, 27f Doppler spectrum, 925 interpretation of, 25–28, 27f Doppler ultrasound. See also Carotid artery(ies), Doppler spectral analysis for; Color Doppler ultrasound; Duplex Doppler sonography; Kidneys, pediatric, vascular disease of, Doppler assessment of; Liver, pediatric, Doppler assessment of; Obstetric sonography; Power Doppler ultrasound; Transcranial Doppler sonography aliasing in, 29b, 32f artifact sources in, 29b backscatter and, 21–22, 23f, 35 bioefects of obstetric sonography and, 1041 for breast assessment, 768–772, 770f–773f cysts in, 769–770, 770f cavernous hemangiomas characterized by, 109–110 cirrhosis of liver characteristics in, 95, 95f complete venous, for lower extremity peripheral veins, 989 continuous wave, 24, 25f Doppler angle and, 21–22, 24f, 29b, 30 Doppler efect and, 21–22, 23f Doppler equations and, 21–22, 23f–24f Doppler frequency and, 29 Doppler frequency shit and, 21–22, 23f–24f Doppler gain and, 30, 33f Doppler indices and, 27–28, 27f Doppler spectrum and, interpretation of, 25–28, 27f for ductus venosus assessment, 1458, 1459f for fetal well-being assessment, 1458–1460, 1459f–1460f FNH characterized by, 113 gut wall evaluation with, 260–261, 262f harmonic spectral and power, 60–61, 60f–62f hilar cholangiocarcinoma assessment with, 187–188, 189f–191f instrumentation for, 24–25, 25b, 25f–26f for intussusception, pediatric, 1849f of liver transplantation recipient, pediatric, 1764–1769 lymphadenopathy assessment with, 771–772, 772f for MCA in fetal alloimmunization detection, 1421, 1422f fetal assessment of, 1458–1460, 1460f for musculoskeletal system, 857, 857f obstetric, sample volume and velocity range in, 1036 operating modes in, 30–31 overview and physics of, 21–30 pediatric kidney assessment with, 1778 pediatric liver assessment with, 1748–1764 placental vascularity and, 1467–1469 portal hypertension assessment with, 1748–1764 for PTN, 1083 pulse inversion, 63–64 pulsed wave, 24, 25f testicular low, 1890 Volume I pp 1–1014 • Volume II pp 1015–1968

I-20

Index

Doppler ultrasound (Continued) renal arterial stenosis diagnosis from, falsepositive, 658, 661f for renal cell carcinoma detection, 343, 344f for renal transplant assessment, 648, 651f–652f pediatric, 1807–1812 renal vascular, 366 sample volume size and, 29b, 30 signal processing and display in, 23–24, 24f spatial focusing and, 35 spectral, 60–61, 60f–62f in carotid artery analysis, 925–932 for fetal heart assessment, 1275, 1281f spectral broadening in, 24, 24f, 29, 29b, 31f spectral display in, 25 technical considerations in, 28–30 thermal efects in, 31 for umbilical arteries assessment, 1458, 1459f wall ilters in, 29, 30f Dorsal dermal sinus, pediatric, 1686, 1688f Dorsal enteric istula, pediatric, 1686–1688 Dorsal induction errors, fetal brain and, 1179–1186 amniotic band sequence as, 1180f, 1182–1183 anencephaly as, 1179, 1180f cephalocele as, 1179–1182 ciliopathies as, 1182 cranial changes in spina biida as, 1183–1186, 1184f–1185f, 1185t–1186t encephalocele as, 1179–1182, 1181f, 1182t exencephaly as, 1179 Joubert syndrome as, 1182 limb-body wall complex as, 1182–1183 Meckel-Gruber syndrome as, 1182 Dorsal midline cyst, in corpus callosum agenesis, 1528, 1531f Dorsal rectum, in bladder development, 311, 312f Dorsalis pedis artery, 966 DORV. See Double-outlet right ventricle “Double contour sign”, 867–869, 868f “Double-bubble” sign, in fetal duodenal atresia, 1309, 1310f Double-decidual sign, 1054, 1056f “Double-duct” sign, 231, 231f Double-outlet right ventricle (DORV), 1288–1289, 1289f Down syndrome, testicular microlithiasis and, 1904. See also Trisomy 21 Drainage, ultrasound-guided, 609–617 of abscesses abdominal, 612 liver, 612–613, 614f–615f pediatric, 1953 pediatric, appendiceal, 1956, 1960f pelvic, 612, 613f renal, 617, 618f splenic, 617 transrectal, 1953–1954, 1954f of bile duct luids, 614–615 of biliary tract luids, 613–615 catheters for for interventional sonography, 1948 placement of, 610–611, 611f removal of, 612 selection of, 610–611, 611f contraindications to, 609–610 diagnostic aspiration in, 611 of empyemas, pediatric, 1954, 1958f follow-up care for, 612 of gallbladder luids, 613–614, 616f imaging methods for, 610, 610f indications for, 609–610 of pancreatic pseudocysts, 615–617, 617f patient preparation for, 611 percutaneous cholangiography and, 1956, 1959f

Drainage, ultrasound-guided (Continued) of pleural and peritoneal luids, pediatric, 1954–1956, 1958f of pleural efusion, 1724–1725 procedure for, 612 DRE. See Digital rectal examination Drop metastasis, 266, 267f Drugs fetal hydrops from, 1432 illicit use of, fetal gastroschisis and, 1322–1323 nephrotoxic, AKI and, 1796 toxicity of, renal transplantation abnormalities and, 1809 Duct extension, of DCIS, 790–791, 792f Ductal arch, fetal, 1275, 1279f Ductal carcinoma in Situ (DCIS), 789–790, 792f calciications and, 793, 795f duct extension of, 790–791, 792f Ductal ectasia, mammary ducts and, 762 Duct(s). See also Bile duct(s) mammary normal sonographic appearance of, 762, 764f subareolar and intranipple, scanning of, 762, 765f pancreatic, 215–218, 219f–220f of Santorini, 218, 219f thymopharyngeal, formation of, 1652 of Wirsung, 218, 219f Ductus arteriosus, 1273–1274, 1275f Ductus venosus, 1273–1274, 1275f fetal, Doppler ultrasound assessment of, 1458, 1459f reversed low in, in aneuploidy screening, 1095, 1095f Duodenal atresia, fetal dilated fetal stomach diferentiated from, 1307 “double-bubble” sign in, 1309, 1310f echogenic bowel and, 1315f small bowel obstruction and, 1308–1309, 1310f Duodenal diaphragm, 1841–1842, 1844f Duodenal duplication cysts, fetal duodenal atresia mistaken for, 1309 Duodenal leaks, ater pancreas transplantation, 682 Duodenal stenosis, 1308–1309 Duodenal web, 1841, 1844f Duodenum, 219 atresia of, in trisomy 21, 1097, 1098f pediatric, 1841–1847 anatomy of, 1841, 1841f atresia of, 1841, 1842f congenital obstruction of, 1841–1842, 1842f–1844f hematoma of, 1842, 1845f sonographic technique for, 1841 stenosis of, 1841 ulcer in, perforated, gallbladder wall thickening signs in, 201f Duplex Doppler sonography in Budd-Chiari syndrome, 102–103 celiac artery, 453–455, 455f mesenteric artery, 453–455, 455f interpretation of, 454–455, 456f–458f of neonatal/infant brain, 1573–1576 approaches to, 1574, 1575f arterial blood low in, 1576, 1577t asphyxia and, 1580 brain death and, 1580, 1583f cerebral edema and, 1580 difuse neuronal injury and, 1580 ECMO and, 1578–1580, 1579f hemodynamics in, 1576–1580 HII and, 1580, 1581f–1582f hydrocephalus and, 1581–1583, 1584f intensive care therapies and, 1578–1580 intracranial hemorrhage and, 1580–1581, 1584f

Duplex Doppler sonography (Continued) intracranial tumors and, 1585, 1587f measurements in, 1576, 1576f–1577f, 1576t mechanical ventilation and, 1578, 1579f near-ield structures and, 1585, 1588f optimization of, 1574, 1574b pitfalls of, 1585–1589, 1589f safety considerations for, 1574–1576 stroke and, 1580–1581, 1584f uncommon applications of, 1585, 1588f vascular malformations and, 1583–1585, 1585f–1587f venous blood low in, 1578, 1578f, 1578t obesity and renal artery in, 447 in portal hypertension, 98 renal artery, 447–450, 450f false-positive/false-negative results with, 450, 450f interpretation of, 450 in ureteral calculi detection, 337–338 Duplex scanner, 24 Duplication anomalies, fetal, 1359–1360, 1359f, 1360b Duplication cysts, 297 duodenal, fetal duodenal atresia mistaken for, 1309 enteric, fetal, 1312–1313, 1313f ovarian cysts diferentiated from, 1369 esophageal, 1256 gastrointestinal, pediatric, 1860, 1863f ovarian cysts diferentiated from, 1875 Dural sinus fetal malformations of, 1205 thrombosis of, 1205–1206, 1206f neonatal/infant, thrombosis of, 1585 Duty factor, 36 DVT. See Deep venous thrombosis Dwarism, diastrophic indings associated with, 1382 hitchhiker thumb in, 1382, 1406 Dwell time, 36 in obstetric sonography, 1036 Dynamic contrast-enhanced ultrasound, 66–67 Dynamic maneuvers, for hernia imaging, 473–474, 474f–475f Dynamic range, of amplitudes, 9 Dysgerminomas, ovarian, 584, 584f pediatric, 1880 pseudoprecocious puberty and, 1887 Dyslexia, obstetric sonography and, 1040 Dysostoses, deinition of, 1376, 1377t Dysplastic kidneys, pediatric, 1798, 1798f Dysraphic hamartomas, 1682 Dysraphic lesions, 1679–1680 Dysraphism. See Spinal dysraphism, fetal; Spinal dysraphism, pediatric Dyssegmental dysplasia, 1399 Dystrophic calciication, 339 pediatric urinary tract and, 1799 Dystrophic facies, in Miller-Dieker syndrome, 1195 E Eagle-Barrett syndrome. See Prune belly syndrome Early pregnancy failure. See Pregnancy, irst trimester of, early failure of Ear(s) embryology of, 1134 fetal abnormalities of, 1148, 1148f length of, in trisomy 21, 1101 low-set, 1148 Ebstein anomaly, 1286–1287, 1286f Echinococcal disease adrenal, 423 genitourinary, 331, 332f

Index Echinococcal disease (Continued) peritoneal, 517 splenic, 147, 150f Echinococcosis, in pediatric liver, 1748 Echinococcus granulosus, 613 hepatic infestation by, 88–89 Echinococcus multilocularis, parasitic infestation by, 90 Echocardiography, fetal ive-chamber view in, 1275, 1279f four-chamber view in apical, 1274–1275, 1277f subcostal, 1274–1275, 1277f indications for, 1270–1273, 1273b M-mode, 1275, 1280f–1281f three-vessel and trachea view in, 1275, 1279f timing of, 1274 Echoendoscope, 428–429 Echoes, 3–4. See also Nonlinear echoes fundamental, 58–59 Echogenic bowel fetal aneuploidy and, 1315–1316, 1315f bowel obstruction and, 1316 CF and, 1316 conditions associated with, 1315b fetal growth restriction and fetal demise with, 1316 infection and, 1316 intraamniotic bleeding and, 1316 meconium peritonitis and, 1313 in trisomy 21, 1100f, 1101 Echogenic capsule, thin, in breast sonography, 797 Echogenic intimal lap, in carotid artery dissection, 946, 948f Echogenic lines, nearly parallel, in normal carotid wall, 918–919, 919f Echogenic metastases, of liver, 125, 128f Echogenic rim, in breast sonography, with hyperechoic spicules, 787–788, 789f Echogenicity, in liver mass detection, 106–107 Echo-ranging, 3 Echovist, 55–56 ECMO. See Extracorporeal membrane oxygenation ECST. See European Carotid Surgery Trial Ectasia, aortic, 440 Ectoderm layer, of trilaminar embryonic disc, 1216–1217, 1217f Ectodermal-neuroectodermal tract, focal, 1674 Ectopia cordis, fetal abdominal wall and, 1329, 1329f pentalogy of Cantrell and, 1329 structural cardiac anomalies and, 1295, 1296f, 1329 Ectopic pregnancy, 1069–1076 abdominal, 1074, 1075f cervical, 1073–1074, 1074f clinical presentation of, 1069–1070 heterotopic gestation and, 1070–1071, 1072f implantation sites of, 1072–1073 abdominal, 1074, 1075f cervical, 1073–1074, 1074f cesarean scar, 1073, 1075f interstitial, 1073, 1074f infertility and, 1070 interstitial, 1073, 1074f management of, 1075–1076 conservative, 1076 failure of, 1076, 1076f laparoscopy for, 1076 medical, 1076 nonspeciic sonographic indings in, 1072–1073 adnexal mass and, 1072, 1073f ectopic tubal ring as, 1072, 1073f

Ectopic pregnancy (Continued) endometrium and, 1072–1073 free pelvic luid and, 1072, 1073f pediatric, 1884–1885, 1885f prevalence of, 1070 risk of, 1070b ruptures, hemoperitoneum in, 508f serum β-hCG levels and, 1071 sonographic diagnosis of, 1070–1071, 1070f–1071f speciic sonographic indings in, 1071–1072, 1072f of unknown location, 1075 Ectopic thyroid tissue, 694 Ectrodactyly, fetal, 1406–1407, 1406f EDD. See Expected date of delivery Edema breast sonography and, 795 cerebral neonatal/infant, 1550–1556, 1554f–1555f, 1580 pediatric, TCD sonography in, 1614, 1617f gut, 295, 297f of ovaries, massive, 578 pediatric, 1878–1879, 1879f scrotal, idiopathic, 846 pediatric, 1898–1899, 1898f subcutaneous, fetal, in hydrops, 1417, 1419f–1420f Edematous cord, 1484f Edwards syndrome. See Trisomy 18 EF. See Endocardial ibroelastosis EFSUMB. See European Federation of Societies of Ultrasound in Medicine and Biology Eggshell calciication, breast cysts and, 779, 780f EHE. See Epithelioid hemangioendothelioma Ejaculatory ducts, 382f–383f, 384 cysts of, 392 obstruction of, 393–394 transurethral resection of, 393 Elastography basic points in, 15–16, 16b for breast assessment, 772–773, 773f gut wall and, 261 for musculoskeletal system, 857 for prostate cancer, 407 shear wave, 16, 17f–18f, 772 cirrhosis of liver and, 95–96 for pediatric liver, 1764, 1765f strain, 16, 17f, 772 for thyroid gland assessment, 692, 714–715, 715f–716f transient, 1764 Elbow injection of, 901 pediatric, dislocations of, 1933–1934 ulnar nerve dislocation at, 865–866, 866f Electronic beam steering, 10–11 “Elephant trunk” sign, fetal cloacal exstrophy and, 1328 Elevation planes, 12f Elevation resolution, 19, 19f Ellis-van Creveld syndrome, 1396, 1397f, 1398–1399 polydactyly in, 1382 Emboli showers, 1621–1622 Embolism carotid artery, TIAs from, 919 pulmonary, DVT causing lower extremity, 979, 981f upper extremity, 994 Embolization, uterine artery, for uterine ibroids, 540

I-21

Embolus, renal artery stenosis and, 447 Embryo. See also Aneuploidy, screening for, irst-trimester; Chromosomal abnormalities abnormal, 1077 anencephaly in, 1077 cardiac activity of, normal sonographic appearance of, 1058–1059, 1060f with CRL less than 7mm and no heartbeat, 1064 deinition of, 1445 early pregnancy failure and gestational sac with no, 1063–1065, 1065f evaluation of, 1076–1077 heartbeat of, in gestational age determination, 1445, 1445f, 1446t intracranial cystic structures in, 1077, 1077f normal development of, mimicking pathology, 1077, 1077f normal sonographic appearance of, 1057, 1059f–1060f physiologic anterior abdominal wall herniation in, 1077, 1077f, 1322, 1323f omphalocele confused with, 1325, 1327f sonographic appearance of, normal, 1018f transfer, 1070 in yolk sac, 1058f Embryonal carcinoma, 823, 825f ovarian, 1880 pediatric, testicular, 1899 Embryonal rhabdomyosarcoma, pediatric, paratesticular, 1903–1904, 1903f Embryonal sarcoma, undiferentiated, in pediatric liver, 1746, 1748f Embryonic bradycardia, 1068–1069, 1068f Embryonic disc, trilaminar, in spinal development, 1216–1217, 1217f Embryonic period, 1053–1054 Emphysema, lobar, congenital, 1251, 1253f Emphysematous cholecystitis, 175, 198f, 200 Emphysematous cystitis, 333, 334f Emphysematous pyelitis, 326–327, 327f Emphysematous pyelonephritis, 325–326, 326f Empty stomach artifact, 1838, 1839f Empyemas, pediatric, 1702–1711 abscess diferentiated from, 1725, 1726f drainage of, 1954, 1958f lung abscess compared to, 1711, 1713f parapneumonic collections and, 1710–1711 from pneumonia, 1707f sonographic appearance of, 1707f Encephalitis CMV, neonatal, 1559f pediatric, neurogenic bladder in, 1907 Encephalocele(s) corpus callosum agenesis and, 1526–1528 fetal amniotic band syndrome and, 1330 anencephaly diferentiated from, 1179 fetal brain and, 1179–1182, 1181f, 1182t pentalogy of Cantrell and, 1329 sloped forehead in, 1139–1140 Encephaloclastic schizencephaly, 1196 Encephalomalacia, cystic, 1538, 1539f End diastolic ratio, in internal carotid artery stenosis evaluation, 937 End diastolic velocity in assessing degree of carotid stenosis, 929 in mesenteric duplex Doppler sonography interpretation, 454 Endarterectomy, carotid for carotid stenosis, 916 pediatric, TCD sonography in, 1621 sonographic features following, 942, 944f Endocardial cushion defects, 1284 Volume I pp 1–1014 • Volume II pp 1015–1968

I-22

Index

Endocardial cushion(s), 1279, 1282f development of, 1284, 1284f Endocardial ibroelastosis (EF), 1292 fetal, 1294, 1295f heart block and, 1425 Endocervical canal, normal sonographic appearance of, 1497f, 1499 Endocrine disorders, fetal hydrops from, 1432 Endocrine drainage, in pancreas transplantation, 672, 675f Endocrine tumors, pancreatic, 248–249, 249f–250f, 249t Endoderm layer, of trilaminar embryonic disc, 1216–1217, 1217f Endodermal sinus tumor ovarian, 585 pediatric, 1880 testicular, 823–824, 825f pediatric, 1899 vaginal, pediatric, 1883 Endoleaks, ater AAA repair, 438–439, 440f–442f Endoluminal grat, 438 Endometrial carcinoma, 544, 550f polycystic ovarian disease and, 1877–1878 Endometrial plaques, 523, 524f Endometrioid tumors, ovarian, 581 Endometrioma(s) appearances of, 574–575, 575f in pouch of Douglas, 524f sonographic evaluation of, 521–523 Endometriosis of bladder, 372, 372f in ovaries, 574–576, 575f–576f in peritoneum, 521–523, 524f Endometritis, 554 PID and, 1885 postpartum recognition of, 555–556 Endometrium abnormalities of, 544–552 ablation as, 551–552, 552f adhesions as, 551, 552f atrophy as, 547–548 bleeding as, 544, 544b carcinoma as, 544, 548–551, 550f hematometrocolpos as, 546–547, 546f hormone use and postmenopausal, 544–545, 544b, 545f hydrometrocolpos as, 546–547 hyperplasia as, 544, 547–548, 548f polyps as, 544, 548, 549f postmenopausal bleeding as, 545–546 postmenopausal luid and, 546–547, 546b, 547f sarcoma as, 551, 551f thickening, 544, 544b calciications of, 533, 534f cysts of, 547–548 ectopic pregnancy and, 1072–1073 layers of, sonographic appearance of, 531, 532f lining of, in menstrual cycle, 1050f phases of, sonographic appearance of, 531, 532f proliferation of, 1049, 1050f sonographic appearance of, 531, 532f thickness of measurement for, 531 transvaginal ultrasound assessment for, 545–546 Endoscopic ultrasound for adrenal glands, 428–429, 429f for percutaneous needle biopsy of pancreas, 423 Endosonography, of gastrointestinal tract, 300–307 for anal canal, 302–307, 304f–307f, 306b for rectum, 301–302, 301f–304f for upper gastrointestinal tract, 300–301 Endotracheal suctioning, in neonatal/infant brain, 1578

Endovascular aortic repair (EVAR), 438 End-stage renal disease (ESRD) catheterization and, 994 hemodialysis for, 996 relux nephropathy and, 327, 327f Enhancement artifacts, 21, 22f Entamoeba histolytica, 613 hepatic infection by, 87 Enteric drainage, in pancreas transplantation, 672 Enteric duplication cysts, fetal ovarian cysts diferentiated from, 1369 small bowel and, 1312–1313, 1313f Enterobius vermicularis organisms, 1853 Enterocolitis, necrotizing, pediatric, 1854–1855, 1855b, 1856f Enterocutaneous istulas, 612 Entertainment videos, 49b, 50 Enthesis, 902 Eosinophilic gastritis, gastric mucosa thickening in, 1839–1840 Ependymomas, neonatal/infant brain and, 1562 Epicondylitis, 861 Epidermal inclusion cysts, 779 Epidermal nevus syndrome, hemimegalencephaly associated with, 1195 Epidermoid cyst(s) pediatric neck and, 1652–1654 in suprahyoid area, 1640 testicular, 1900–1901, 1901f splenic, 146–147, 148f–149f testicular, 830f, 831 Epidermolysis bullosa, pyloric atresia and, 1307 Epididymis anatomy of, 819–820, 820f appendices of, 820–821, 820f cystadenomas of, paratesticular, 1904 cysts of, 839, 842f inlammation of, 846 lesions of, 839–841 papillary cystadenomas of, 840–841 pediatric, 1890 appendix, 1897, 1897f cysts of, 1902–1903, 1903f postvasectomy changes in, 841, 843f sarcoidosis and, 841, 843f sperm granuloma and, 841, 843f tumors of, extratesticular, 840–841, 840f Epididymitis acute, 846 scrotum pain from, 846, 847f–848f, 1895– 1896, 1896f chronic, 841, 843f pediatric bladder outlet obstruction and, 1897 chronic, 1896 color Doppler ultrasound for, 1896, 1896b following trauma, 1897 infarction and, 1896 ischemia and, 1896 orchitis and, 1896 testicular torsion and, 1323–1324, 1895–1896, 1896f Epididymo-orchitis, acute scrotal pain from, 846, 847f–849f Epidural hematomas, neonatal/infant, 1557 Epigastric hernias, 488–491, 490f–491f Epigastrium, free air in, 526 Epignathus, 1159 Epinephrine, secretion of, 417 Epineurium, 864–865, 865f Epiphysis slipped capital femoral, 1931–1932 stippled, 1399 Epiploic foramen, 211–212 Epispadias, bladder exstrophy with, 1326

Epispadias, fetal cloacal exstrophy and, 1328 Epithelial cell tumors, ovarian, pediatric, 1879 Epithelioid hemangioendothelioma (EHE), 123–124 Epstein-Barr virus difuse lymphadenitis in, 1660, 1662f PTLD and, 682 Erb palsy, 1934 ERSPC (European Randomized Study of Screening for Prostate Cancer), 397 Erythroblastosis fetalis, 1419. See also Hydrops, fetal, immune Escherichia coli, 846, 1852 Esophageal atresia, 1305–1306, 1305f–1306f, 1305t Esophageal cysts, pediatric, 1650 Esophageal duplication cysts, 1256 Esophageal pouch sign, 1305–1306, 1306f Esophagus carcinoma of, staging of, endosonography in, 301 fetal, 1305–1306 esophageal atresia and, 1305–1306, 1305f– 1306f, 1305t parathyroid adenomas confused with, 745 pediatric, 1833–1840 anatomy of, 1834, 1834f sonographic technique for, 1833–1835 ESRD. See End-stage renal disease ESWL. See Extracorporeal shockwave lithotripsy Ethanol ablation of cervical nodal metastasis from papillary carcinoma, 720, 721f for secondary or recurrent hyperparathyroidism, 751–754, 754f for thyroid nodules autonomously functioning, 719–720 benign functioning, 719, 719f solitary solid benign “cold”, 720 Ethanol sclerotherapy, 719 Ethmocephaly alobar HPE and, 1534–1535 hypotelorism and, 1140 European Carotid Surgery Trial (ECST), 916 European Federation of Societies of Ultrasound in Medicine and Biology (EFSUMB), 1041 European Randomized Study of Screening for Prostate Cancer (ERSPC), 397 EVAR. See Endovascular aortic repair Ex utero intrapartum treatment (EXIT) procedure, 1159, 1255 Exencephaly, 1179, 1218 EXIT procedure. See Ex utero intrapartum treatment procedure Exorbitism, 1140 craniosynostosis and, 1136–1138 hypertelorism with, in Pfeifer syndrome, 1145f Expected date of delivery (EDD) determination of, 1022 ultrasound changing, 1022–1029 External beam radiotherapy, for prostate cancer, 400–401, 401f External spermatic (cremasteric) artery, 821, 821f Extracardiac malformations, in CHD, 1270 Extracorporeal membrane oxygenation (ECMO) complications of, 1548 in neonatal/infant brain, duplex Doppler sonography and, 1578–1580, 1579f TCD sonography in monitoring, 1622 Extracorporeal shockwave lithotripsy (ESWL), 42 Extravaginal torsion, 844, 844f Extremities fetal measurements of, 1378–1379, 1379t, 1380f–1381f routine sonographic views of, 1021, 1028f right lower, amputation of, 1403f

Index Exudate ascites, 506–507 Exudates, pleural, sonographic appearance of, 1702 F Face abnormalities of, craniosynostosis and, 1136–1138 midface abnormalities of, 1148–1153 Face, fetal. See also Midface abnormalities; Neck, fetal; Orbits, fetal embryology and development of, 1133–1134, 1134f forehead abnormalities in, 1137f, 1139–1140, 1139b, 1140f–1141f hemangiomas of, 1154, 1160f HPE changes to, 1189, 1189b lower, abnormalities of, 1153–1154 macroglossia as, 1153, 1153b, 1158f micrognathia as, 1153–1154, 1158f retrognathia as, 1153–1154 midface abnormalities of, 1148–1153 normal, sonography of, 1134–1135, 1135f orbital abnormalities in, 1140–1143 routine sonographic views of, 1021, 1024f sot tissue tumors of, 1154, 1160f Facial nerve, pediatric, anatomy of, 1630 Falciform ligament, 77, 79f pediatric, 1731, 1731f–1732f Fallopian tube(s), 585–589 anatomy of, 565, 565f carcinoma in, 589 hydrosalpinx of, 585–587, 587f normal sonographic appearance of, 568 pediatric, torsion of, 1875–1876 PID and, 587–589, 588f torsion of, 589 Falx sign, bright, in osteogenesis imperfecta type II, 1392 Familial hypocalciuric hypercalcemia, primary hyperparathyroidism distinguished from, 734 Familial juvenile nephronophthisis, 359 Familial paraganglioma syndromes, pheochromocytomas with, 1826 Fanconi anemia, 1746 Fanconi pancytopenia, 1400, 1402f Far ield, of beam, 8 Fasciitis necrotizing, of perineum, 846–847 planter, injection for, 902, 904f Fascioliasis, 176–178, 177f–178f FAST. See Focused abdominal sonography for trauma FASTER. See First and Second Trimester Evaluation of Risk Fastigial point, 1189–1190 Fat, Crohn disease and creeping, 269, 271f Fat necrosis injectable steroid complications with, 901 simulating anterior abdominal wall hernias, 500, 502f Fat-luid levels, in breast cysts, 775, 778f Fatty liver, 91–92, 92f–93f Fecal incontinence, anal endosonography in, 305, 305f Fecaliths, in acute appendicitis, 1857, 1859f Feet. See Foot Feminization, testicular, 1368 dysplastic gonads and, 1899 primary amenorrhea in, 1887 Feminizing adrenal tumors, pseudoprecocious puberty and, 1888

Femoral artery common, 966 AVF of, 974f normal appearance of, 966–967, 967f pseudoaneurysms of, 973f stenosis of, 969f supericial, 966 bypass grat of, 975f calciication of, 968, 970f normal appearance of, 966–967 occlusion of, 967f, 969f stenosis of, 969f, 971f Femoral canal, as landmark for femoral hernias, 482, 485f Femoral hernias, 471, 481–483. See also Hernia(s), femoral Femoral vein bifurcation of, 980–981 common as landmark for femoral hernias, 482, 485f normal anatomy of, 500, 981f ultrasound examination of, 982–983 compression of, normal, 982f DVT in duplicated, detecting, 988, 988f normal, 989f phasicity, 459, 459f–460f Femur, fetal bowing of, 1380f deiciency of, proximal focal, 1400, 1400f hypoplasia of, in caudal regression, 1237–1238 length of assessment of, 1378, 1379t, 1380f BPD in heterozygous achondroplasia compared to, 1398, 1398f in gestational age determination, 1448, 1449f, 1449t in second-trimester, 1023f short, etiology of, 1381 subtrochanteric, absence of, 1400 “telephone receiver”, 1380f Femur, head of, pediatric avascular necrosis of, 1930 in DDH assessment, 1923 position of, in evaluation of infant at risk, 1927 in sonogram of hip from transverse/lexion view, 1927, 1928f Femur-ibula-ulnar complex, 1400 Femur/foot length ratio, 1379 Femur-tibia-radius complex, 1400 Fertilization, cycle of, 1051, 1051f Fetal akinesia sequence, 1401 Fetal alcohol syndrome, 1194 rhabdomyosarcoma associated with, 1908 Fetal artery, aberrant, sirenomelia from, 1238 Fetal Echocardiography, indications for, 1270– 1273, 1273b Fetal endoscopic tracheal occlusion (FETO), 1264 Fetal ibronectin (FFN), 1501 Fetal growth restriction, echogenic bowel and, 1316 Fetal hemoglobin deicit, immune hydrops and, 1419. See also Hemoglobin, fetal Fetal hydrops. See Hydrops, fetal Fetal lobation, in kidneys, 317, 1781, 1781f Fetal period, 1054 Fetal renal hamartomas, 1818–1820 Fetal therapy, cervical assessment and, 1505 FETO. See Fetal endoscopic tracheal occlusion Fetomaternal transfusion, maternal serum alpha-fetoprotein elevation in, 1228 Fetter syndrome, craniosynostosis in, 1136–1138

I-23

Fetus. See also speciic organs adrenal glands of masses in, 1353–1354, 1353f, 1353t normal, 1353, 1353f assessment of, for alloimmunization, 1421–1423, 1421b, 1422f, 1422t assessment of well-being of, 1455–1460 BPP for, 1456–1458, 1457f, 1457t Doppler ultrasound for, 1458–1460, 1459f–1460f “Buddha position” of, 1401 coexistent hydatidiform molar pregnancy and, 1078–1080, 1081f death of echogenic bowel and, 1316 maternal serum alpha-fetoprotein elevation in, 1228 deinition of, 1445 ears of abnormalities of, 1148, 1148f length of, in trisomy 21, 1101 low-set, 1148 foot of, deformities of, 1404–1407 gestational age determination and measurements of, 1016, 1016b, 1444–1449 age assignment and, 1449, 1450t in irst trimester, 1444–1445, 1445f–1446f, 1445t–1446t in second and third trimesters, 1446–1448, 1447f–1450f, 1447t–1449t growth of abnormalities of, 1453–1455 assessment of, 1022–1029 curves depicting, 1453, 1453f restriction of, 1455 growth restriction of, echogenic bowel and, 1316 hand of, deformities of, 1404–1407 keepsake imaging of, 49b, 50 large-for-gestational age, 1453–1454 diabetic mothers and, 1454, 1455t incidence of, 1453–1454 sonographic criteria for, 1454t–1455t malformations of, diagnostic accuracy of, 1030 megacystis in, 1360, 1360b, 1360f movements of, musculoskeletal development and, 1378 MRI of, 1031–1032, 1031f presentation of, determination of, 1021, 1022f situs of, determination of, 1021, 1022f small-for-gestational age, 1454–1455, 1454b sonographic appearance of, normal, 1018f weight assessment for, 1450–1453 in relation to gestational age, 1451–1453, 1452t, 1453f weight estimation for, 1450–1453 formulas in, 1451, 1451t gestational age compared to, 1453, 1453f recommended approach in, 1451, 1452t FFN. See Fetal ibronectin Fibrinous peritonitis, 509f Fibroadenoma, 797, 797f Fibrochondrogenesis, 1396 Fibroelastosis, endocardial, fetal, 1294, 1295f heart block and, 1425 Fibroglandular tissue, asymmetrical, split-screen imaging and, 769, 769f Fibroids, uterine, 538–540, 539f, 540b Fibrolamellar carcinoma, 122–123 Fibrolipomas, coccygeal dimples and, 1679 Fibroma(s) cardiac, fetal, 1294 gastrointestinal, endosonographic identiication of, 301 ovarian, 585, 586f Volume I pp 1–1014 • Volume II pp 1015–1968

I-24

Index

Fibroma(s) (Continued) paratesticular, 1903–1904 simulating anterior abdominal wall hernias, 500–501, 502f Fibromatosis, ovarian edema diferentiated from, 1878–1879 Fibromatosis coli, pediatric, inlammatory disease and, 1663–1664, 1663f Fibromuscular dysplasia carotid low disturbances in, 928 of internal carotid artery, 944–946, 946f renal artery stenosis and, 447, 447f renovascular disease and, 368 Fibronectin, fetal, 1501 Fibrosarcomas paratesticular, 1903–1904 simulating anterior abdominal wall tumors, 500–501, 502f Fibroscan, 1764 Fibrosis retroperitoneal, 464–465, 465f testicular, ater orchitis, 846, 849f tubulointerstitial, 359 Fibrothorax, sonographic appearance of, 1702 Fibrous cap thinning, microRNAs and, 920 Fibrous pseudotumors, 838, 840f Field of view (FOV), 105, 505–506 musculoskeletal system and extended, 857 in obstetric sonography, 1036, 1036f Filar cyst, in newborn, 1674–1675, 1678f Filum terminale formation of, 1673, 1673f lipomas of, 1674 closed spinal dysraphism and, 1684–1685, 1686f normal anatomy of, 1674–1675, 1677f Fine-needle aspiration biopsy parathyroid adenoma and accuracy of, 746 of thyroid gland, 709–710, 710t, 722 Fingers, syndactyly of, 1105f Finite amplitude distortion, in sot tissue heating, 37–38, 37f First and Second Trimester Evaluation of Risk (FASTER), 1090–1091, 1095 Fistula(s). See also Arteriovenous istulas aortoenteric, 438 bladder, 334, 335f cholecystenteric, 207 choledochoduodenal, 175–176, 177f choledochoenteric, 175–176, 177f Crohn disease and formation of, 276, 279f–280f dorsal enteric, pediatric, 1686–1688 enterocutaneous, 612 in imperforate anus, 1847–1848, 1850f neurenteric, 1674 perianal, perianal inlammatory disease in, 305–306 tracheoesophageal, fetal CHAOS and, 1254–1255 esophageal atresia and, 1305 vesicocolic, 1310–1312 vesicocutaneous, 334 vesicoenteric, 334 vesicoureteral, 334 vesicouterine, 334 vesicovaginal, 334 Fitz-Hugh-Curtis syndrome, PID and, 1887 Flash artifacts, 60–61 Flexor hallucis longus tendon, injection of, 902, 903f Flexor retinaculum, thickening of, 865 Fluid, in neonatal/infant brain imaging, 1512 Fluorescent in situ hybridization, in hydrops diagnosis, 1433–1434 Fluoroscopic guidance, for drainage catheter placement, 610

FNH. See Focal nodular hyperplasia Foam cysts, in breast, 779, 781f Focal depth, in obstetric sonography, 1036, 1036f Focal hypertrichosis, tethered cord and, 1679 Focal nodular hyperplasia (FNH) adenoma diferentiated from, 116–117 CEUS for diagnosis of, 113–115, 115f characterization of, with microbubble contrast agents, 106, 106f, 108t, 109f Doppler ultrasound characterization of, 113 of liver, 112–115, 114f–115f pediatric, 1746 sulfur colloid scanning and, 115 Focal subcortical heterotopia, 1196 Focal therapy, for prostate cancer, 400 Focal zone, 505–506 Focused abdominal sonography for trauma (FAST), 508 Folic acid, in spina biida prevention, 1224–1225 Follicular adenomas, thyroid, pediatric, 1646–1648, 1647f Follicular carcinoma, of thyroid gland, 701, 701b, 706f–707f pediatric, 1648 Follicular cysts menstrual cycle and, 568 pediatric, 1875 Fondaparinux, 598 Fontanelle mastoid, neonatal/infant brain imaging through, 1512, 1517–1518, 1517f, 1519f duplex Doppler, 1574, 1575f posterior, neonatal/infant brain imaging through, 1512, 1517, 1517f–1518f duplex Doppler, 1574, 1575f Fontanelle, anterior cerebral artery, compression of, in hydrocephalus, RI and, 1582, 1584f neonatal/infant brain imaging through, 1512–1513 coronal planes in, 1513f duplex Doppler, 1574, 1575f sagittal planes in, 1516f Foot (Feet). See also Clubfoot fetal deformities of, 1404–1407 length of, measurement of, 1379, 1381f rocker-bottom, 1406f, 1407 in skeletal dysplasia, 1382 injection of, 901 supericial peritendinous and periarticular, 902–904, 903f–904f pediatric, congenital deformities of, 1932–1933 club foot as, 1932 vertical talus as, 1932–1933, 1932f Foramen magnum approach for duplex Doppler ultrasound of neonatal/ infant brain, 1574, 1575f for TCD sonography, 1592, 1595f Foramen of Magendie, neonatal/infant, in mastoid fontanelle imaging, 1517–1518 Foramen ovale, 1273–1275, 1275f, 1279, 1282f sonographic appearance of, 1280, 1283f Foraminal lap, sonographic appearance of, 1283f Forearm muscle, hernia of, 859f Forearm veins, sonographic evaluation of, 996–998, 998f Foregut, 1304–1305 bronchopulmonary malformations of, pediatric, 1716, 1718f cysts of, 1650 Forehead, fetal, abnormalities of, 1137f, 1139–1140, 1139b, 1140f–1141f Foreign body(ies) embedded in sot tissue, 872, 873f in gastrointestinal tract, 300

Foreign body(ies) (Continued) interventional sonography, pediatric, for deep removal of, 1961, 1965f in vagina, pediatric, 1887 Fornices cavum septi pellucidi mistaken for, 1521 fetal, normal sonographic appearance of, 1168 4Kscore, 396 Four-dimensional ultrasound, for fetal heart assessment, 1277 Fournier gangrene, acute scrotal pain from, 846–847 FOV. See Field of view Fracture(s) fetal, in skeletal dysplasias, 1380f, 1381–1382 in osteogenesis imperfecta, 1392, 1393f pediatric, rib, 1727 testicular, 850, 850f Frame rate in obstetric sonography, 1036 in renal artery duplex Doppler sonography, 449 Frank dislocation, of hip, 1927 Fraser syndrome, 1253 Fraternal twins. See Dizygotic twins Fraunhofer zone, of beam, 8 Free air, pneumoperitoneum and, 525f, 526 “Freehand” technique, for percutaneous needle biopsies, 600, 602f Frequency compounding, 7–8 Frequency spectrum bandwidth, 7–8 Frequency(ies) acoustic, 2 band of, 7 in sound waves, 2, 2f Fresnel zone, of beam, 8 Frontal bossing, 1137f, 1139, 1139b in skeletal dysplasia, 1382 Frontal horns, of ventricles in Chiari II malformation, 1526, 1527f–1528f in corpus callosum agenesis, 1528, 1530f–1531f neonatal/infant in coronal imaging, 1514, 1514f–1515f cysts of, 1522, 1522f, 1566 Frontonasal prominence, 1134 Frontothalamic distance, in trisomy 21, 1101 Fryn syndrome, CDH and, 1263 Fukuyama syndrome, cobblestone lissencephaly in, 1195 Full-thickness rotator cuf tears, 886–887, 887f–888f Fundal adenomyomas, 202, 204f Fundamental echo, 58–59 Fundus, uterine, 530 Fungal diseases genitourinary, 330–331 hepatic, 86–87, 88f Fungus balls in collecting systems, 330–331, 331f formation of, in neonatal candidiasis, 1794, 1795f Fused vertebrae, pediatric, 1688 Fusiform dilatation, 283 G G6PD. See Glucose-6-phosphate dehydrogenase deiciency Gadopentetate dimeglumine, as pregnancy category C drug, 1032 Gain settings, 505–506 Galactoceles, 775 Galactography, 799 Galactosemia, inborn errors of metabolism and, 1738 Gallbladder, 188–207. See also Cholecystitis absent or small, in biliary atresia, 1734–1735, 1737, 1738f

Index Gallbladder (Continued) adenomas of, 203–204, 205f adenomyomas of, 202–204, 204f–205f adenomyomatosis of, 202, 203f–205f agenesis of, 190–194 anatomy of, 188–194, 193f aspiration of, 614, 616f biliary sludge and, 194–195, 196f calciication of, 202, 202f carcinoma of, 206–207, 206f drainage of, 613–614, 616f duplication of, 194 fetal, 1318–1319, 1319f choledochal cysts and, 1319, 1320f enlarged, 1318 gallstones and, 1319, 1320f nonvisualization of, 1318–1319 gallstone disease of, 194, 195f hepatization of, 195 hourglass, 202, 205f intrahepatic, 188–190, 193f malignancies of, 204–206 milk of calcium bile and, 194, 195f pediatric, wall thickening in, 1741 perforation of, 198f, 200 polyps of, 203–206, 203b cholesterol, 203, 205f inlammatory, 203–204, 205f porcelain, 202, 202f small, in biliary atresia, 1737, 1738f sonographic nonvisualization of, causes of, 190–194, 194b sonographic technique for, 194 variants of, normal, 188–194 volvulus of, 201 wall thickening in causes of, 198, 199f, 200b in children, 1741 hyperemia in, in acute cholecystitis, 197f, 198–199 sympathetic, 199–200, 201f Gallstone disease, 194, 195f Gallstones acute pancreatitis and, 221 fetal, 1319, 1320f pediatric, 1741, 1743f diseases associated with, 1741b Gamma-glutamyl transpeptidase (GGTP), 1318 Gamna-Gandy bodies, in spleen, 157 Ganglion cysts injection for, 907–909, 909f ultrasound techniques for, 869–870, 869f subacromial-subdeltoid bursa thickening with, 889–891, 892f Ganglioneuroblastoma, pediatric, 1825 Ganglioneuromas, adrenal, 427–428 benign, pediatric, 1825 Gangrene, Fournier, 846–847 Gangrenous appendix, pediatric, 1857, 1861f Gangrenous cholecystitis, 198f, 200 Gartner cyst, pediatric, 1883–1884 Gas, free intraperitoneal, in acute abdomen, 277–281, 282f Gas bubbles, free, as blood pool contrast agents, 55 Gastric diaphragm, pediatric, 1839, 1840f Gastric ulcers, pediatric, 1839–1840, 1840f Gastric vein, let, pediatric Doppler studies of, best approach for, 1752 low direction of, in portal hypertension, 1752, 1757 in intrahepatic portal hypertension, 1761 Gastritis, pediatric, 1839–1840, 1840f Gastrocolic trunk, pancreatic head and, 212

Gastroduodenal artery, pancreatic head and, 211–212, 213f Gastroesophageal relux, sonographic detection, 1834, 1834f Gastrointestinal tract. See also Acute abdomen; Crohn disease acute abdomen and, 277–290 anatomy of, 257–261 CF and, 300 Crohn disease and, 266–269 endosonography of, 300–307 for anal canal, 302–307, 304f–307f, 306b for rectum, 301–302, 301f–304f for upper gastrointestinal tract, 300–301 gut edema and, 295, 297f gut signature and, 257, 257f–259f, 257t infections of, 295–300 AIDS patients and, 296 bezoars and, 300 celiac disease and, 300 congenital cysts and, 297, 298f hematomas and, 299 intraluminal foreign bodies and, 300 ischemic bowel disease and, 297 mucocele of appendix and, 299, 299f peptic ulcer and, 299, 300f pneumatosis intestinalis and, 297–299, 299f pseudomembranous colitis and, 296–297, 298f layers of, 257, 257f–258f masses of, 592 mechanical bowel obstruction and, 293 neoplasms of, 261–266 adenocarcinoma as, 261–264, 263f–264f lymphoma as, 264–266, 266f metastases as, 266, 267f stromal tumors as, 264, 265f paralytic ileus and, 294f, 295 pediatric cysts of, 1860–1862, 1863f–1864f duplication cysts of, 1860, 1863f, 1875 neoplasms of, 1860–1862, 1864f sonographic technique for, 257–261, 262f Gastrointestinal tract, fetal, 1304–1322. See also speciic organs anomalies of, hydrops from, 1427–1428, 1428f Gastroschisis fetal, 1322–1325 associated conditions of, 1324–1325 epidemiology of, 1322–1323 management of, 1325 pathogenesis of, 1323 prenatal diagnosis of, 1323–1324, 1324f maternal serum alpha-fetoprotein elevation in, 1228 Gastrulation, 1053 disorders of, 1686–1689 in spine embryology, 1672 Gaucher disease, spleen and, 157, 158f Gel cysts, 779, 781f Gender fetal, identiication of, 1367, 1367f in multifetal pregnancy, chorionicity and, 1119 pediatric kidney length according to, 1776–1778, 1778t pediatric kidney volume according to, 1776–1778, 1778t TCD sonography velocity evaluation and, 1595 Genetic amniocentesis, 1108–1109, 1108f Genetic disorders, fetal hydrops from, 1432 Genital tract, fetal, 1366–1369 abnormal, 1367–1368, 1368f hydrocolpos and, 1368 normal, 1366–1367, 1366f–1367f ovarian cysts and, 1369, 1369f

I-25

Genitalia, fetal abnormal, 1367–1368, 1368f ambiguous, 1365, 1368f normal, 1366–1367, 1366f–1367f Genitourinary tract. See also Bladder; Kidney(s); Renal artery(ies); Renal cell carcinoma; Renal vein(s); Transitional cell carcinoma; Ureter; Urethra; Urinary tract abnormalities of, in Miller-Dieker syndrome, 1195 anatomy of, 311–314 bladder diverticula and, 374, 374f congenital anomalies of, 317–323 bladder development and, 322 kidney ascent and, 318 kidney growth and, 317–318 ureteral bud and, 318–321 urethral development and, 323, 323f vascular development and, 321–322 duplex collecting system and, 319, 320f embryology of, 311 infections of, 323–333 AIDS and, 331–333, 332f–333f alkaline-encrusted pyelitis as, 324–325 Candida albicans as, 330–331, 331f cystitis as, 333 echinococcal disease as, 331, 332f fungal, 330–331 papillary necrosis as, 328–329, 329b, 329f parasitic, 331 pyelonephritis as, 323–328 pyonephrosis as, 325, 326f schistosomiasis as, 331 tuberculosis as, 329–330, 330f medical diseases of, 369–372 acute cortical necrosis as, 370, 372f acute interstitial nephritis as, 370 acute tubular necrosis as, 370 amyloidosis as, 372 diabetes mellitus as, 372 endometriosis as, 372, 372f glomerulonephritis as, 370, 371f interstitial cystitis as, 372, 373f neurogenic bladder and, 372–374, 373f obstruction of hydronephrosis and, 316, 317b pitfalls in assessment of, 317 postsurgical evaluation of, 374–375 sonographic technique for, 314–315 stones in, 334–340 trauma to, 365–366 tumors of, 340–356 adenocarcinoma as, 348 angiomyolipoma as, 351–352, 351f–352f leukemia as, 353–354 lymphoma as, 352–353 metastases as, 354–355 oncocytoma as, 348–351 rare, 355–356 renal cell carcinoma as, 340–344 squamous cell carcinoma as, 348 transitional cell carcinoma as, 346–348 urachal adenocarcinomas as, 355 vascular abnormalities of, 366–369 AVF and malformation as, 366–367, 366f renal vascular Doppler ultrasound and, 366 Germ cell tumors ovarian, 582–585 pediatric, 1879 testicular, 822–825, 822b mixed, 822–823, 825f nonseminomatous, 823–824, 825f regressed, 824–825, 825f–826f thymus, 1723–1724 Volume I pp 1–1014 • Volume II pp 1015–1968

I-26

Index

Germinal epithelium, 565 Germinal matrix hemorrhage, hypoxic-ischemic injury in premature infant and, 1541–1543, 1542f, 1543b, 1543t Germinal matrix of, neonatal/infant, development of, 1524, 1524f Gerota fascia, 314 Gestational age alpha-fetoprotein levels compared to, 1227f calculation of, 1049 cervical length and, 1499–1500, 1499f spontaneous PTB prediction based on, 1500–1501, 1501t deinition of, 1443–1444 determination of accuracy of, 1449, 1450t composite formulas for, 1448–1449 routine ultrasound screening in, 1022–1029 estimation of CRL in, 1062 in irst trimester, 1061–1062 gestational sac size in, 1061, 1061f MSD in, 1061, 1061f, 1444–1445, 1445t routine ultrasound screening in, 1022–1029 extremity long-bone lengths and BPD at, 1379t fetal measurements for determining, 1016, 1016b, 1444–1449 age assignment and, 1449, 1450t in irst trimester, 1444–1445, 1445f–1446f, 1445t–1446t in second and third trimesters, 1446–1448, 1447f–1450f, 1447t–1449t fetal weight assessment in relation to, 1451– 1453, 1452t, 1453f fetal weight estimation compared to, 1453, 1453f for heterozygous achondroplasia detection, 1381 kidney length compared to, 1776–1778, 1780f PSV blood low in MCA as function of, 1421, 1422t thermal efects of ultrasound and, 1037–1038 thoracic circumference and length correlated with, 1247t usage of term, 1167 Gestational sac, 1017f abnormal size of, 1063 chorionic bump in, 1065 chorionic sac luid of, 1054–1055, 1056f discriminatory level for seeing, 1056 early pregnancy failure and appearance concerns in, 1065, 1066f no embryo in, 1063–1065, 1065f small MSD in relationship to CRL in, 1066, 1067f identiication of, in gestational age determination, 1444, 1445f, 1446t mean diameter of CRL and, early pregnancy failure and, 1066, 1067f in gestational age determination, 1444–1445, 1445t normal sonographic appearance of, 1054–1055, 1055f–1056f size of, in gestational age estimation, 1061, 1061f threshold level for seeing, 1056 transvaginal ultrasound for identiication of, 1054–1055 β-hCG levels and, 1056–1057 Gestational trophoblastic disease, 556, 1077–1084, 1479 hydatidiform molar pregnancy and, 1078–1080 complete, 1078, 1079f partial, 1078, 1080f vaginal bleeding and, 1078

Gestational trophoblastic disease (Continued) PTN and, 1078, 1080–1084, 1082f choriocarcinoma and, 1080–1082, 1083f diagnosis and treatment of, 1083–1084 Doppler ultrasound for, 1083 ater hydatidiform molar pregnancy, 1080, 1081f invasive mole, 1080, 1081f PSTT and, 1082 sonographic features of, 1082–1083 “Geyser sign”, 889–891, 892f GGTP. See Gamma-glutamyl transpeptidase Ghost triad, biliary atresia and, 1737, 1738f Giant pigmented nevi, choroid plexus papillomas in, 1209 Giant-cell tumors, in TSC, 1200f Glenohumeral joint, 878–879, 878f efusion of, 893–894, 894f Glenohumeral joint, injection of, 901, 901f Glenoid fossa, 878–879, 878f Glial scarring, in PVL, 1552–1553 Glioependymal cysts, cavum veli interpositi cysts diferentiated from, 1170 Gliomas, hypothalamic, precocious puberty and, 1887 Glisson capsule, 77 Glomerulonephritis, 370, 371f CKD and, 1796–1798 Glomus, choroid plexus, neonatal/infant, development of, 1522–1523, 1523f Glomuvenous malformation, in venous malformations of neck, 1657 Glucocorticoid, secretion of, 417 Glucose, plasma levels of, high, NTDs from, 1218 Glucose-6-phosphate dehydrogenase (G6PD) deiciency, 1431 Glutaric aciduria type 1, 1540–1541 Glycogen storage disease (GSD) inborn errors of metabolism and, 1738 liver in, 92 pediatric type I, adenomas in, 1746 tyrosinemia and, 1740f Goiter(s) adenomatous, sonographic appearance of, 727 fetal, 1159–1163, 1162f multinodular, 711, 711f in children, 1648, 1648f parathyroid adenomas detection and, 746 sonographic appearance of, 727 in thyroid gland nodular disease, 695–697, 695f–699f Goitrous hypothyroidism, 694 Goldenhar syndrome, clets of secondary palate in, 1153 Gonadal dysgenesis, primary amenorrhea in, 1887 Gonadal stromal tumors, testicular, 826, 827f Gonadal veins, anatomic variants of, 457 Gonadoblastoma(s), 826, 827f pediatric, 1880 in dysplastic gonads, 1899–1901 Gonads diferentiation of, 1887 dysplastic, 1899–1901 Gonococcal perihepatitis, PID and, 1887 Gorlin syndrome, 585 Gout, rheumatoid arthritis and, 867–869, 868f Graaian follicle, 1049 Graded compression sonography, 283 Grat infarction, pediatric renal transplantation and, 1807–1809, 1808f Grat-dependent hyperparathyroidism, 742–744, 743f Grat-versus-host disease, pediatric, intestinal wall thickening in, 1853–1854, 1855f

Granulocytic sarcomas, pediatric, neck, 1666, 1667f Granuloma(s) of liver, pediatric, 1748 silicone, in extracapsular breast implant rupture, 805–807, 806f sperm, 841, 843f splenic, pediatric, 1771f stitch, ater herniorrhaphy, 494–496, 495f Granulomatous cystitis, pediatric, 1908 Granulomatous disease, chronic, gastric mucosa thickening in, 1839–1840 Granulomatous mastitis, 803–804 Granulomatous peritonitis, 514 Granulomatous prostatitis, 390, 390f Granulosa cell tumor, ovarian, 585 pediatric, 1880 pseudoprecocious puberty and, 1887 Graves disease fetal goiter in, 1159–1163 thyroid gland and, 727, 727f pediatric, 1646, 1646f Gray-scale median level, for echolucency of plaque, 922 Great arteries, transposition of, 1289–1290, 1289f–1290f Great saphenous vein (GSV) acute DVT in, 984, 984f anatomy of, 981–982, 981f vein mapping of, 989–990 Great vessels, fetal, short-axis view of, 1275, 1278f Green-tag feature, in color Doppler, 932–933 Groin deinition of, 471 hernias of, dynamic ultrasound of contents of, 472–473 entities stimulating, 499–500, 501f key sonographic landmarks for, 474 maneuvers for, 473–474, 474f–475f recurrent, 494–496 report for, 471–472 technical requirements for, 471 pain, 470–471 Growth. See Fetus, growth of; Intrauterine growth restriction Growth discordance, in multifetal pregnancy, 1123, 1123f GSD. See Glycogen storage disease GSV. See Great saphenous vein Gubernaculum testis, 851 Guidewire exchange technique, for drainage catheter placement, 610 Gut edema, 295, 297f primitive, 1057 signature, 257, 257f–259f, 257t strictures in, in Crohn disease, 269–274, 275f–276f Gut wall CEUS and, 261 Doppler ultrasound evaluation of, 260–261, 262f elastography and, 261 layers of, 257, 257f–258f masses in, 258 pathology of, 257–258, 260f pseudokidney sign in, 257, 260f target pattern in, 257, 260f thickening of Crohn disease and, 269, 270f–271f pathology related to, 257 Gynecology. See also Fallopian tube(s); Uterus anatomy in, 564–570, 565f nongynecologic pelvic masses and, 591–592 Gynecomastia, in testicular choriocarcinoma, 824 Gyral interdigitation, in Chiari II malformation, 1526, 1528f

Index Gyri abnormalities of, in lissencephaly, 1195 development of, 1167 normal sonographic appearance of, 1169, 1171f H HAART. See Highly active antiretroviral therapy Haglund deformity, 903f Hamartoma(s) biliary, 83, 83f–84f dysraphic, 1682 fetal renal, 1818–1820 hypothalamic, precocious puberty and, 1887 pediatric, mesenchymal, 1744 splenic, 153–156, 156f testicular, 829, 829f in TSC, 1200f Hamstring tendon, injection of, 905–907, 907f–908f Handedness, obstetric sonography and, 1040 Hand(s). See also Clubhand clenched, in trisomy 18, 1103, 1103f fetal amputation of, in amniotic band sequence, 1403f deformities of, 1404–1407 in skeletal dysplasia, 1382 injection of, 901 supericial peritendinous and periarticular, 904, 905f persistent clenched, 1404 “trident” coniguration of, achondroplasia and, 1407, 1408f Harmonic imaging of biliary tree, 168, 169f B-mode, 60 contrast agents with, 58–64 spectral and power mode Doppler, 60–61, 60f–62f tissue, 13, 13f–14f, 38, 61–62 Harmonic power angio, 66 Harmonics, generation of, 13, 13f Hartmann pouch, 188 Hashimoto thyroiditis, 724, 725f–727f fetal goiter in, 1159–1163 pediatric, 1645, 1646f HCB. See Hypertrophied column of Bertin HCC. See Hepatocellular carcinoma hCG. See Human chorionic gonadotropin Head, fetal abnormalities of, 1135–1140 craniosynostosis and, 1136–1139, 1137f–1138f in shape, 1136–1139, 1137f in size, 1135–1136 wormian bones as, 1139, 1139b, 1139f circumference of in gestational age determination, 1446–1447, 1447f–1448f, 1448t in second-trimester, 1023f measurements of, in gestational age determination, 1446–1448, 1447f–1448f, 1447t–1448t oblong, 1136–1138 sonographic views of, 1021, 1024f Head, pediatric, lesions of, 1961, 1966f Headaches, pediatric TCD sonography for, 1610–1611, 1612f Healing response, impaired, injectable steroid complications with, 901 Heart. See also Congenital heart disease congenital defects of thickened NT in, 1095–1097, 1096f in trisomy 18, 1103 in trisomy 21, 1097, 1098f

Heart (Continued) disease of carotid low waveforms and, 936–937, 936f CDH and, 1263 ischemic, 433 in Miller-Dieker syndrome, 1195 early pregnancy failure and absence of beating, 1063, 1064f echogenic focus in, in trisomy 21, 1100f, 1101 embryonic activity of, normal sonographic appearance of, 1058–1059, 1060f beating of, in gestational age determination, 1445, 1445f, 1446t embryos with CRL less than 7mm and no beating, 1064 rate, TCD sonography velocity evaluation and, 1595 Heart, fetal. See also Echocardiography, fetal arrhythmias of, 1295–1297 bradycardia as, 1297, 1297f CHD and, 1270–1273 congenital heart block as, 1297, 1297f hydrops from, 1424, 1425f PACs and PVCs as, 1295–1296 tachycardia as, 1296–1297, 1296f atrioventricular valves of, 1274–1275 axis of, 1245 abnormal, mortality rate with, 1273 dimensions of, 1276f disease of, congenital recurrence risks in ofspring for, 1273t recurrence risks in siblings for, 1273t risk factors associated with, 1271t–1272t dysfunction of, from Ebstein anomaly, 1286 failure of, in sacrococcygeal teratoma, 1238–1239 malformations of, with AVSD, 1285–1286 normal anatomy of, 1273–1277 position of, 1245 abnormal, mortality rate with, 1273 routine sonographic views of, 1021, 1025f scanning techniques for, 1273–1277 four-chamber view of, 1273–1275, 1277f situs of, 1245 structural anomalies of, 1277–1295 aortic stenosis as, 1292 APVR as, 1290, 1291f ASD as, 1277–1280, 1282f–1283f AVSD as, 1284–1286, 1284f–1285f cardiac tumors as, 1293–1294, 1293f–1294f cardiomyopathy as, 1295f cardiosplenic syndrome as, 1292–1293, 1293b coarctation of aorta as, 1291, 1292f DORV as, 1288–1289, 1289f Ebstein anomaly as, 1286–1287, 1286f ectopia cordis as, 1295, 1296f, 1329 hydrops from, 1423–1424 hypoplastic let heart syndrome as, 1287, 1287f hypoplastic right ventricle as, 1287, 1287f pentalogy of Cantrell and, 1329 pulmonic stenosis as, 1292 TGA as, 1289–1290, 1289f–1290f TOF as, 1288, 1288f truncus arteriosus as, 1288, 1289f univentricular heart as, 1287–1288, 1287f VSDs as, 1281–1284, 1283f–1284f tumor of, 1293–1294, 1293f–1294f hydrops from, 1424 ultrasound assessment of color Doppler, 1275–1277, 1282f spectral Doppler, 1275, 1281f

I-27

Heart, fetal (Continued) three-dimensional and four-dimensional, 1277 univentricular, 1287–1288, 1287f valves of, morphology of, 1285f valvular stenosis of, 1275–1277 ventricles of, short-axis view of, 1275, 1278f Heart block, fetal complete, hydrops from, 1423–1424 congenital, 1297, 1297f hydrops from, 1425 Heating of bone, 37, 37f, 37t of sot tissue, 37–38, 37f Heerfordt disease, chronic pediatric sialadenitis in, 1634–1635 Height, pediatric, kidney length compared to, 1776–1778, 1777f Hemangioblastoma, intracranial, fetal, 1208 Hemangioendothelioma(s) epithelioid, hepatic, 123–124 infantile, 1319f liver and, 1743–1744, 1745f Hemangioma(s) cardiac fetal, 1294 in infants, 1293 cavernous of bladder, 356 CEUS characterization of, 111, 113f Doppler ultrasound characterization of, 109–110 of liver, 108–112, 112f–113f percutaneous needle biopsy of, 603–604, 604f characterization of, with microbubble contrast agents, 106, 106f–107f, 108t cutaneous rapidly involuting cogenital, 1742–1743 dacryocystocele diferentiated from, 1143 fetal cardiac, 1294 face, 1154, 1160f of liver, 1319f infantile of neck, 1655, 1656f parotid gland, 1636, 1637f tethered cord and, 1679 intraspinal, pediatric, 1689–1691 paratesticular, 1903–1904 pediatric gastrointestinal, 1862, 1864f liver and, 1742–1743, 1744f sclerosis of, 112 segmental, tethered cord and, 1679 splenic, 148, 153–157, 156f subcutaneous, spinal canal and, 1697, 1697f umbilical cord, 1483 Hemangiopericytoma renal, 356 splenic lesions in, 153 Hemangiosarcoma, of liver, 123 Hematoceles, scrotal, 835f, 836 pediatric, 1902 Hematoma(s) in AVF for hemodialysis, 1002–1003, 1005f bladder augmentation and, 1912–1913 bladder lap, cesarean sections and, 556–557, 557f duodenal, pediatric, 1842, 1845f epidural, neonatal/infant, 1557 of gastrointestinal tract, 299 intestinal, small bowel obstruction from, 1843 intraparenchymal, 638 ater liver transplantation, 638, 644f Volume I pp 1–1014 • Volume II pp 1015–1968

I-28

Index

Hematoma(s) (Continued) pelvic, 591 perinephric luid collections and, 1809 preplacental, 1471, 1475f renal, 365–366 ater renal transplantation, 665, 671f simulating anterior abdominal wall hernias, 500, 502f splenic, 158, 159f pediatric, 1770, 1771f stitch, ater herniorrhaphy, 494–496, 495f subamniotic, 1474 subchorionic, 1474 placental abruption diferentiated from, 1471, 1474f subdural, neonatal/infant, 1557, 1558f subfascial, cesarean sections and, 556–557, 557f subplacental, 1471, 1474f in synthetic arteriovenous grat for hemodialysis, 1002–1003 testicular, 848–850, 850f pediatric, 1897–1898 Hematometra cervical carcinoma and, 546, 547f, 549 cornual, 551–552 Hematometrocolpos, 1882f from imperforate hymen, 546–547, 546f Hematopoiesis, in yolk sac, 1057 Hematospermia, prostate and, 394, 394b Hematotrachelos, 546 Hemidiaphragm, eventration of, 1263f Hemihypertrophy hepatoblastomas and, 1746 Wilms tumor screening with, 1818 Hemimegalencephaly, 1195 Hemithorax, pediatric, radiopaque in neonatal chylothorax, 1704f partially, 1705f Hemivertebrae pediatric, 1688–1689 scoliosis and kyphosis from, 1235–1237 Hemobilia, 174, 175f Hemodialysis, 996–1006 AVF and aneurysms near, 1003, 1005f arm and leg swelling with, 1006, 1009f hematomas near, 1002–1003, 1005f maturation of, evaluating, 1003 occlusion of, 1006 palpable focal masses near, 1002–1003 placement for, 996, 997f pseudoaneurysms near, 1003, 1005f stenoses associated with, 1003–1006, 1007f–1008f ultrasound evaluation of, 1000–1006, 1002f–1003f for ESRD, 996 sonographic examination technique for, 996 synthetic arteriovenous grat and aneurysms near, 1003 arm and leg swelling with, 1006, 1009f hematomas near, 1002–1003 occlusion of, 1006, 1010f palpable focal masses near, 1002–1003 placement of, 996, 997f pseudoaneurysms near, 1003, 1006f stenoses associated with, 1006, 1008f ultrasound examination of, 1002, 1004f ultrasound examination and protocol for, 1000 thigh grat and, preoperative mapping for, 1000, 1001f vein mapping before, 996–1000 upper extremity, 996–998, 998f–1000f Hemoglobin, fetal deicit in, immune hydrops and, 1419

Hemolysis fetal, hydrops from, 1431 from obstetric sonography, 1038 Hemolytic anemia, fetal, hepatomegaly, and, 1316 Hemolytic-uremic syndrome (HUS), pediatric Doppler assessment of, 1805, 1807f intestinal wall thickening in, 1851f, 1853–1854 Hemoperitoneum, 507–508, 508f Hemorrhage(s) adrenal, 422–424, 424f fetal, 1354 ater liver transplantation, 638, 645f neonatal, 1824–1825, 1825f arachnoid cysts diferentiated from, 1192–1193 cavum veli interpositi cysts diferentiated from, 1170 cerebellar, neonatal/infant brain and, 1548–1550, 1549f fetal, hydrops from, 1431 hypoxic-ischemic events and cerebellar, 1548–1550, 1549f germinal matrix, 1541–1543, 1542f, 1543b, 1543t intraparenchymal, 1547–1548, 1547f–1549f intraventricular, 1544–1545, 1544f–1546f, 1545b intraventricular, with hydrocephalus, 1545–1547, 1546f–1547f subarachnoid, 1550, 1550f subependymal, 1543–1544, 1543f–1544f intracranial fetal, 1206, 1207f neonatal/infant brain and, duplex Doppler sonography of, 1580–1581, 1584f intramural, pediatric, in Henoch-Schönlein purpura, 1853, 1855f intraparenchymal IUFD and, 1124f neonatal/infant brain and, 1547–1548, 1547f–1549f intraplacental, thick placenta in, 1466 intraplaque, in heterogenous plaque, 920–921 intraventricular from germinal matrix hemorrhage, 1541 with hydrocephalus, 1545–1547, 1546f–1547f neonatal/infant brain and, 1544–1545, 1544f–1546f, 1545b signs of, 1545b pediatric ovarian cysts and, 1877, 1878f–1879f spinal canal, 1695, 1695f–1696f thyroid, 1646, 1647f percutaneous needle biopsy complications with, 608, 609f placental, 1474 posterior fossa, 1548–1550 postpartum, in fetal hydrops, 1436 subarachnoid, neonatal/infant brain and, 1550, 1550f subchorionic early pregnancy failure and, 1069, 1069f fetal echogenic bowel and, 1315f subdural, fetal, bilateral, 1207f subependymal, neonatal/infant brain and, 1543–1544, 1543f–1544f Hemorrhagic cholecystitis, 200 Hemorrhagic cystitis, pediatric, 1908, 1910f Hemorrhagic ovarian cysts, 570–571, 571f, 575 Hemothorax, sonographic appearance of, 1702, 1707f Henoch-Schönlein purpura, 845–846, 1842 pediatric, 1853, 1855f scrotal and testicular involvement in, 1899 Heparin, 598 Hepatic alveolar echinococcus, 90

Hepatic artery anastomosis of, for liver transplantation, 624 aneurysms of, ater liver transplantation, 1768, 1769f–1770f anomalies of, 80–81 liver circulation and, 78 ater liver transplantation normal appearance of, 625 occlusion of, 626–627 pseudoaneurysms of, 634, 636f resistive index elevation in, 634 stenosis of, 631–634, 634f–635f, 1766 thrombosis of, 627, 628f, 631, 633f pediatric, Doppler studies of, best approaches for, 1752–1754, 1755f pseudoaneurysm of, 104 ater liver transplantation, 634, 636f Hepatic vein(s) anatomic variants of, 457 anomalies of, 81–82 fetal liver calciications and, 1316–1318 liver circulation and, 80 normal, 76, 76f, 77t occlusion of, in Budd-Chiari syndrome, 100–102, 100f–101f pediatric anatomy of, 1733–1734, 1734f Doppler studies of, best approaches for, 1752 thrombosis of, suprahepatic portal hypertension and, 1763, 1763f stenosis of, ater liver transplantation, 637, 643f strictures of, in cirrhosis, 95, 95f Hepatitis, 1203–1204 A, 83 acute, 84–85, 85f–86f, 172 gallbladder wall thickening signs in, 201f B, 83–84 maternal hydrops from, 1432 C, 84 chronic, 85 from congenital herpes, hepatitis from, 1739f D, 84 E, 84 neonatal, jaundice and, 1734, 1737–1738, 1739f viral, 83–85 Hepatization, of gallbladder, 195 Hepatoblastomas, pediatric, 1746, 1747f pseudoprecocious puberty and, 1888 Hepatocellular carcinoma (HCC) CEUS for detection of, 120–122, 123f characterization of, with microbubble contrast agents, 106, 106f in cirrhotic liver, characterization of, 122, 122t ibrolamellar subtype of, 122–123 inborn errors of metabolism and, 1738 of liver, 118–123, 120f–121f, 122t, 123f pediatric, 1746 portal vein thrombosis from, 120, 121f sonographic appearance of, 119–120, 120f Hepatocyte nuclear factor 1β–related (HNF1β) disease, 1350–1351 Hepatoduodenal ligament, 77, 79f Hepatofugal portal venous low, 1750, 1757 Hepatolithiasis, 179 Hepatomegaly, fetal, 1316, 1317f Hepatopetal portal venous low, 1750 Hepatosplenomegaly from CMV, 1204 fetal, 1317f in immune hydrops, 1422 Hereditary hemorrhagic telangiectasia, 104 Hereditary lymphedema, fetal, 1403–1404, 1405f Hereditary nonpolyposis colorectal cancer syndrome, 578 Hermaphroditism, true, pediatric, 1891, 1899

Index Hernia(s). See also Diaphragmatic hernia Amyand, 472–473, 473f anterior abdominal wall, dynamic ultrasound of contents of, 472–473 entities stimulating, 500–501, 502f maneuvers for, 473–474, 474f–475f technical requirements for, 471 types of, 471, 471f ventral, 488–494 bilateral, 1262 Bochdalek, 1258 complications of, 496–499 congenital diaphragmatic, 1248t direct inguinal in athletes, 485–486 bilateral, 480–481, 484f characteristics of, 479–481 classiication of, 475 conjoined tendon insuiciency and, 479–481, 483f–484f incidence of, 479–480, 482f key indings with, 476t location of, 474–475, 476f–477f dynamic maneuvers for imaging of, 473–474, 474f–475f femoral, 471 characteristics of, 481–483 diagnostic accuracy with, 481 with inguinal hernia, 493–494, 495f key indings with, 476t key sonographic landmarks of, 474–475, 477f locations of, 482, 485f strangulated, 500f Teale, 482, 485f Valsalva maneuver and, 472f, 483 forearm muscle, 859f groin, dynamic ultrasound of contents of, 472–473 entities stimulating, 499–500, 501f key sonographic landmarks for, 474 maneuvers for, 473–474, 474f–475f recurrent, 494–496 report for, 471–472 technical requirements for, 471 at Hesselbach triangle, inferior aspect, 476t hiatal, sonographic appearance of, 1834, 1834f incarcerated, 496–497 incisional, 492–493, 494f indirect inguinal Canal of Nuck delayed closure from, 476–477, 477f characteristics of, 476–479 classiication of, 475 inferior epigastric artery relationship to, 476–477, 478f key indings with, 476t location of, 474–475, 476f–477f nonsliding, 477–478, 478f pediatric, 1902 round ligaments relationship to, 476–479, 480f into scrotum, 478–479, 482f sliding, 477–478, 478f spermatic cord relationship to, 476–479, 479f, 481f inguinal, 471, 475–488 Amyand, 472–473, 473f bowel-containing, 472–473, 473f classiication of, 475 dynamic ultrasound of, Valsalva maneuver for, 473, 474f, 483 with femoral hernia, 493–494, 495f luid-containing, 472–473, 473f indirect, 472f

Hernia(s) (Continued) key sonographic landmarks of, 474–475, 476f–477f pediatric, 1899, 1902, 1902f types of, 476t linea alba, 488–491 diagnosing, 490 diastasis recti abdominis and, 489–490, 489f epigastric, 488–491, 490f–491f hypogastric, 488–489, 491, 491f periumbilical, 492, 494f spectrum of appearances of, 489, 489f strangulated, 499f of liver, 80 Morgagni, 1258, 1718f multiple, 493–494, 495f obstructed, 496–497 of omentum, 1902 pantaloon, 493–494, 495f paraumbilical, 492 pericardial, 1258, 1262 periumbilical linea alba, 492, 494f strangulated, 500f repair of mesh in, sonography and, 496, 497f–498f pain ater, 494–496, 495f spiral clips in, pain from, 497, 498f scrotal, 836, 836f pediatric, 1902 shape of, complication potential and, 497, 499f spigelian, 471 characteristics of, 483–484 key indings with, 476t key sonographic landmarks of, 474–475, 476f–477f location of, 483, 486f shape in, 483–484, 487f strangulated, 483–484, 488f torn aponeurosis and abdominis tendon in, 483–484, 487f sports, 484–488, 488f–489f strangulated femoral, 500f indings in, 498–499, 499t linea alba, 499f periumbilical, 500f spigelian, 483–484, 488f umbilical, 491–492, 492f–493f ventral, 488–494 Herniation midgut, physiologic, in embryo, 1077, 1077f, 1322, 1323f omphalocele confused with, 1325, 1327f of thymus, superior, 1723 Herniorrhaphy, 470–471 Herpes simplex virus congenital hepatitis from, 1739f neonatal/infant brain and, 1560 fetal brain development and, 1204 hydrops from, 1432 Hertz, deinition of, 2 Hesselbach triangle, herniation at inferior aspect of, 476t Heterotaxy syndrome, right-sided stomach and, 1307, 1309f Heterotopia, 1196, 1199f Heterotopic gestation, 1070–1071, 1072f Heterozygous achondroplasia, 1396–1398, 1398f detection of, gestational age for, 1381 inheritance pattern for, 1379–1380

I-29

Hiatal hernias, sonographic appearance of, 1834, 1834f HIFU. See High-intensity focused ultrasound High pass ilters, 29, 30f Higher harmonics, 58–59 High-intensity focused ultrasound (HIFU), 31–33, 33f for prostate cancer, 400 Highly active antiretroviral therapy (HAART), 331–333 High-velocity jets, color Doppler, in carotid stenosis, 926, 926f, 933 aliasing, 933 HII. See Hypoxic ischemic injury Hilar cholangiocarcinoma, 185–188 CEUS assessment of, 188, 191f criteria for unresectable, 187b Doppler ultrasound assessment for, 187–188, 189f–191f treatment and staging for, 186–187 tumor growth patterns in, 186 Hindgut, 1304–1305 Hip(s) dislocated, campomelic dysplasia and, 1395 fetal, dislocation of, spina biida and, 1233 injection of, 900f, 901–902 Hip(s), pediatric. See also Developmental dislocation and dysplasia of hip atypical, 1932, 1933f capsule of, echogenic, 1923 DDH and, 1920–1930 dislocation of deinition of, 1923 teratologic, 1932 joint efusion in, 1930–1932, 1931f nondevelopmental dysplasia abnormalities of, 1930–1932 normal, 1923 painful, 1930–1932 sonography of, indications for, 1922b stability of in evaluation of infant at risk, 1927 tests determining, 1923 subluxation of, 1923 Hirschsprung disease, 1312, 1312f neuroblastoma with, pediatric, 1825 Histiocytosis Langerhans cell in infant, 1751f metastasis of, to testes, 1901 sinus, metastasis of, to testes, 1901 Histogenesis, 1524, 1525b Histopathologists, deinition of, 600 Histoplasmosis adrenal glands in, 423 pediatric, lymph nodes and, 1660–1663 Hitchhiker thumb in diastrophic dwarism, 1382, 1406 diastrophic dysplasia and, 1398, 1398f HIV. See Human immunodeiciency virus HIV cholangiopathy, 181–182, 181f HIV-associated nephropathy (HIVAN), 332–333, 333f HNF1β. See Hepatocyte nuclear factor 1β–related disease Hodgkin lymphoma, pediatric, neck, 1665, 1665f Hodgkin’s disease, splenic lesions in, 152–153, 154f Holoprosencephaly (HPE) agnathia and, 1154, 1159f alobar, 1187, 1188f ball type of, 1187–1189 classiication of, 1187b cup type of, 1187–1189, 1188f hydranencephaly diferentiated from, 1208 Volume I pp 1–1014 • Volume II pp 1015–1968

I-30

Index

Holoprosencephaly (HPE) (Continued) neonatal/infant, 1534–1535, 1534b, 1536f pancake type of, 1187–1189 classiication of, 1187b corpus callosum agenesis and, 1526–1528 factors associated with, 1187b fetal brain and, 1186–1189, 1187b, 1188f, 1189b fetal facial changes associated with, 1189, 1189b hypotelorism and, 1140 lobar, 1187–1189 classiication of, 1187b neonatal/infant, 1535 microforms of, 1187 midline interhemispheric form of, 1187, 1189 classiication of, 1187b neonatal/infant, 1535–1536 neonatal/infant, 1532–1536 alobar, 1534–1535, 1534b, 1536f classiication of, 1534f lobar, 1535 midline interhemispheric form of, 1535–1536 semilobar, 1535 semilobar, 1187–1189, 1188f classiication of, 1187b neonatal/infant, 1535 thickened NT and, 1096f in trisomy 13, 1104, 1105f Holosystolic valvular insuiciency, in AVSD, 1285–1286 Holt-Oram syndrome, 1401 Homozygous Achondroplasia, thanatophoric dysplasia diferentiated from, 1389, 1389f Hormonal states, decreased, primary amenorrhea in, 1887 Hormone replacement therapy (HRT), 529 endometrium abnormalities ater menopause and, 544–545, 544b, 545f Hormonogenesis, disorders of, thyroid hyperplasia from, 695 Horseshoe kidneys, 159–160, 318, 319f fetal, 1345–1346, 1345f with megalourethra, 1362 pediatric, 1784, 1785f Hourglass gallbladder, 202, 205f HPE. See Holoprosencephaly HPS. See Hypertrophic pyloric stenosis HRT. See Hormone replacement therapy Human chorionic gonadotropin (β-hCG), 1049, 1884–1885 concentration of, in trisomy 21, 1089–1090 ectopic pregnancy and, 1071 free, 1089–1090 gestational sac and, 1056–1057 normal ultrasound appearance of, 1055–1057, 1057b Human immunodeiciency virus (HIV), 331 chronic parotitis in children with, 1635, 1636f fetal brain and, 1203–1204 nephropathy associated with, 332–333, 333f Humerus length, in trisomy 21, 1101 HUS. See Hemolytic-uremic syndrome Hutch diverticula, 310 Hydatid abscesses, 613 Hydatid cysts in Echinococcosis, 1748 renal, 331, 332f splenic, 147, 150f Hydatid disease, hepatic, 88–90, 89f–90f Hydatid sand, 88–89 Hydatidiform molar pregnancy, 1078–1080. See also Persistent trophoblastic neoplasia coexistent normal fetus and, 1078–1080, 1081f complete, 1078, 1079f partial, 1078, 1080f pediatric, 1884, 1884f

Hydatidiform molar pregnancy (Continued) PTN ater, 1080, 1081f vaginal bleeding and, 1078 Hydranencephaly fetal, 1208, 1208f neonatal/infant, 1538, 1538f Hydrocele(s), scrotal, 834–836, 835f fetal, 1367 in fetal hydrops, 1413, 1416f pediatric, 1899, 1902, 1902f Hydrocephalus, 1681 communicating, 1177–1178 extraventricular obstructive, 1538 fetal brain and, 1174–1178 from germinal matrix hemorrhage, 1541 HPE diferentiated from, 1189 hydranencephaly diferentiated from, 1208 intraventricular obstructive, 1538 in neonatal/infant, duplex Doppler sonography and, 1581–1583, 1584f neonatal/infant brain and, 1538–1541 causes of, 1540b cerebrospinal luid production and circulation and, 1538–1541 intraventricular hemorrhage with, 1545–1547, 1546f–1547f obstructive, 1177–1178 in Dandy-Walker malformation, 1529–1530 pediatric, TCD sonography in monitoring of, 1611–1614, 1613f postmeningitis, 1887 in trisomy 18, 1103 VM diferentiated from, 1611–1612 X-linked, 1177 Hydrocephalus ex vacuo, 1177–1178 Hydrocolpos fetal, 1368 pediatric, 1881, 1882f Hydrometra, 546, 547f Hydrometrocolpos, 546–547 cloacal malformation and, 1363 pediatric, 1881 Hydromyelia in myelocystocele, 1233 pediatric, 1688 Hydronephrosis causes of, 316, 317b deinition of, 1354 fetal degree of, risk of postnatal pathology by, 1355, 1356t in duplication anomalies, 1359–1360, 1359f, 1360b grading system for, 1354, 1355f from UPJ obstruction, 1358, 1358f VUR and, 1360 genitourinary tract obstruction and, 316, 317b pediatric, causes of, 1785–1791 bladder exstrophy and, 1791, 1791f bladder outlet obstruction and, 1788, 1789f–1790f MMIHS and, 1788–1791 prune belly syndrome and, 1788 UPJ obstruction and, 1786, 1787f urachal anomalies and, 1791, 1792f–1793f ureteral obstruction and, 1786–1788, 1787f VUR and, 1788, 1790f in pregnancy, 316 Hydrops, fetal adrenal glands and, 1353–1354 AVSD associated with, 1285–1286 in CHD, 1270 chorioangioma management and, 1476 from CMV, 1204 CPAM and development of, 1248–1249, 1426, 1427f

Hydrops, fetal (Continued) delivery and, 1436 diagnostic approach to, 1432–1435 fetal investigations in, 1433–1435 history in, 1432 maternal investigations in, 1433 obstetric sonography in, 1432–1433 postnatal investigations in, 1435 workshop for, summary of, 1433t etiology of, 1418–1419, 1421f immune, 1419–1423 deinition of, 1413 noninvasive assessment of alloimmunization for, 1421–1423, 1421b, 1422f, 1422t RhoGAM and, 1418 maternal complications in, 1436 nonimmune, 1423–1432 anemia and, 1431 arrhythmias and, 1424, 1425f cardiac tumors and, 1424 cardiovascular causes of, 1423–1425, 1424f causes and associations of, 1412, 1414t chromosomal abnormalities and, 1429–1430, 1430f deinition of, 1413 drugs and, 1432 endocrine disorders and, 1432 fetal welfare assessment in, 1435 gastrointestinal tract anomalies and, 1427–1428, 1428f genetic disorders and, 1432 idiopathic disorders and, 1432 infection and, 1431–1432, 1431f lymphatic dysplasia and, 1428, 1436f metabolic disorders and, 1432 mortality rate in, 1435 neck abnormalities and, 1425, 1426f pathophysiology of, 1423, 1423f skeletal dysplasia and, 1432 thoracic anomalies and, 1425–1427, 1427f tumors and, 1430–1431 twins and, 1429, 1429f urinary tract anomalies and, 1428, 1429f obstetric prognosis in, 1435–1437 postnatal outcome of, 1437 predelivery aspiration procedures in, 1437 in sacrococcygeal teratoma, 1238–1239 sonographic features of, 1413–1418 ascites and, 1413, 1415f–1416f pericardial efusion and, 1416, 1418f placentomegaly and, 1418, 1420f pleural efusions and, 1413–1416, 1417f, 1425 polyhydramnios and, 1418, 1420f, 1432–1433 subcutaneous edema and, 1417, 1419f–1420f thick placenta in, 1466, 1467f Hydrops tubae proluens, 589 Hydrosalpinx, 573 of fallopian tubes, 585–587, 587f PID and, 1885 Hydrosonourethrography, 1872 Hydrosonovaginography, 1870–1871, 1871f Hydrostatic reduction, of intussusception, ultrasound-guided, 1844–1845 Hydrothorax, fetal, hydrops from, 1425–1426 Hygromas. See Cystic hygroma(s) Hymen, imperforate, hematometrocolpos form, 546–547, 546f Hypercalcemia familial hypocalciuric, 734 medullary nephrocalcinosis and, 1798 Hypercalciuria, medullary nephrocalcinosis and, 1798 Hyperechogenic kidneys, 1351–1352, 1352f Hyperechoic caudate nuclei, neonatal/infant brain and, 1557, 1557f

Index Hyperechoic tissue, in breast sonography, 796–797, 796f Hyperemia in acute cholecystitis, 197f, 198–199 Crohn disease and, 269, 272f–273f reactive, in testicular detorsion, 1895 testicular, pediatric, 1896 Hyperoxaluria, primary, CKD and, 1796–1798 Hyperparathyroidism grat-dependent, 742–744, 743f pediatric, 1650 persistent, 741–744, 744f imaging importance in, 749, 751f–752f primary, 733–735 causes of, 734b diagnosis of, 734 MAP for, 749 pathology of, 734 prevalence of, 733–734 treatment of, 734–735 recurrent, 741–744, 743f ethanol ablation for, 751–754, 754f secondary, 744–745 calcimimetics for, 734 ethanol ablation for, 751–754, 754f tertiary, 751 Hyperreactio luteinalis, 572 Hyperrelexia, detrusor, 372–374, 373f Hypertelorism conditions associated with, 1140, 1141b, 1144f–1145f midface hypoplasia with, 1149f in skeletal dysplasias, 1382 Hypertension. See also Portal hypertension carotid low waveforms and, 935f, 936–937 fetal, adrenal glands and, 1353–1354 maternal, IUGR and, 1455 pulmonary, with CDH, 1264 renovascular clinical indings suggesting, 446b renal artery stenosis and, 446–447 renovascular disease and, 368 Hyperthermia NTDs from, 1218 safety and, 38, 38f teratogenic efects from, 38 Hyperthyroidism fetal goiter in, 1163 Graves disease and, 727, 727f Hypertrichosis, focal, tethered cord and, 1679 Hypertrophic cardiomyopathy, 1294–1295 Hypertrophic obstructive cardiomyopathy, 1292 Hypertrophic pyloric stenosis (HPS), 1835–1838, 1835b, 1837f–1838f pitfalls in diagnosis of, 1838, 1838b, 1839f pylorospasm and minimal muscular, 1836–1838, 1838f Hypertrophied column of Bertin (HCB), 313–314, 314b, 315f Hypertrophy of adrenal glands, 416–417 concentric, 1294–1295 kidney and compensatory, 317–318 Hyperventilation, arterial velocities and, 1595 Hyperventilation therapy, pediatric, TCD sonography and, 1614 Hypoalbuminemia, gallbladder wall thickening and, 199f Hypochondrogenesis, achondrogenesis type 2 diferentiated from, 1391 Hypoechogenicity, in breast sonography, 792–793, 794f Hypoechoic metastases, of liver, 125, 127f–128f Hypogastric hernias, 488–489, 491, 491f

Hypophosphatasia, 1383f achondrogenesis diferentiated from, 1391 anencephaly diferentiated from, 1179 calvarial compressibility in, 1382 lethal, 1392–1395, 1395f sonographic appearance of, 1380f Hypophosphatasia congenita, 1392 Hypopituitarism, primary, pediatric, 1891 Hypoplasia. See also Pulmonary hypoplasia, fetal cerebellar, 1190 of femur, fetal, in caudal regression, 1237–1238 of kidneys, 317 of middle phalanx in trisomy 21, 1101 midface, 1148, 1149f–1150f pontocerebellar, 1190 pulmonary, 1245–1246 of thyroid gland, 694, 694f of uterus, 538 vermis, 1190–1192, 1192f inferior, arachnoid cysts diferentiated from, 1192–1193 Hypoplastic let heart syndrome, 1287, 1287f, 1292 Hypoplastic let ventricle, 1292 Hypoplastic right ventricle, 1287, 1287f Hypoplastic scapulae, in campomelic dysplasia, 1381–1382, 1395, 1396f Hypospadias, fetal, 1367 Hypotelorism conditions associated with, 1140, 1140b, 1142f–1144f craniosynostosis and, 1136–1138 Hypothalamus, in menstrual cycle, 1050f Hypothyroidism congenital, 694 pediatric, 1642–1643 pediatric ovarian cysts and, 1875 fetal fetal goiter in, 1163 wormian bones in, 1139 goitrous, 694 Hypoventilation, arterial velocities and, 1595 Hypoxic ischemic injury (HII), 1580, 1581f–1582f Hypoxic-ischemic events, neonatal/infant brain and, 1541–1557 arterial watershed and, 1541, 1541t cerebral edema and, 1550–1556 difuse, 1553–1555, 1554f cerebral infarction and, 1550–1556 focal, 1555–1556, 1556b, 1556f hemorrhage and cerebellar, 1548–1550, 1549f germinal matrix, 1541–1543, 1542f, 1543b, 1543t intraparenchymal, 1547–1548, 1547f– 1549f intraventricular, 1544–1545, 1544f–1546f, 1545b intraventricular, with hydrocephalus, 1545–1547, 1546f–1547f subarachnoid, 1550, 1550f subependymal, 1543–1544, 1543f–1544f hyperechoic caudate nuclei and, 1557, 1557f injury patterns from, 1541t lenticulostriate vasculopathy and, 1556–1557 PVL and, 1541, 1550–1553, 1551f–1553f I IBD. See Inlammatory bowel disease Identical twins. See Monozygotic twins Idiopathic disorders, fetal hydrops from, 1432 Idiopathic varicocele, 837–838 IEA. See Inferior epigastric artery IgG4. See Immunoglobulin G4 IJV. See Internal jugular vein

I-31

Ileal conduits, evaluation of, 375, 375f Ileal obstruction, fetal, 1310 Ileitis, terminal, 288 Ileus meconium, 1310 paralytic, 294f, 295 Iliac, angle of, in trisomy 21, 1101 Iliac artery, 966 stenosis of, 971f Iliac veins, 455–464 anatomy of, 456–457 external, ultrasound examination of, 982 thrombosis of, 459–460, 459f–461f detection diiculties with, 988, 988f Ilioinguinal nerve entrapment of, ater herniorrhaphy, 496 Iliopsoas tendon, injection for, 905, 906f Illicit drugs, fetal gastroschisis and, 1322–1323 Image display, 9–13, 9f–11f Image quality key determinants of, 16–19 spatial resolution in, 16–19, 18f–19f Image storage, 12–13 Imaging. See also speciic techniques amplitude and phase modulation, 64, 65f for drainage, ultrasound-guided, 610, 610f keepsake, 49b, 50 pancreatitis approach of acute, 221–222, 221b chronic, 231 parathyroid adenomas and accuracy in, 746–749 percutaneous needle biopsy methods for, 599 pitfalls in, 19–21 plane-wave contrast, 64 pulse inversion, 62–63, 62f–63f renal cell carcinoma approach for, 341, 341f special modes of, 13–16 elastography, 15–16, 16b, 17f–18f spatial compounding, 13–15, 14f–15f 3-D ultrasound, 15, 16f tissue harmonic imaging, 13, 13f–14f, 61–62 split-screen, for breast assessment, 769, 769f temporal maximum intensity projection, 64, 65f triggered, 65 volume, in obstetric sonography, 1030 Immunocompromised patients acute typhlitis and, 287–288, 289f hepatic candidiasis in, 86–87, 88f Immunoglobulin A nephropathy, CKD and, 1796–1798 Immunoglobulin G4 (IgG4) associated disease, 1635 cholangitis related to, 182–184, 185f Immunosuppression, adrenal glands and, 423 Impedance high-resistance waveform in brachial artery, 27f low-resistance waveform in peripheral vascular bed, 27f Imperforate anus, 1310–1311 block vertebrae with, 1689, 1692f high, pediatric, risk of spinal dysraphism with, 1689 pediatric, 1847–1848, 1850f Imperforate hymen, hematometrocolpos form, 546–547, 546f Implantation, 1051, 1052f Implants, breast abnormal capsule in, 804 extracapsular rupture of, 805–807, 806f ill valve causing palpable abnormalities in, 804, 804f intracapsular rupture of, 804–805, 805f radial folds causing palpable abnormalities in, 804, 804f Volume I pp 1–1014 • Volume II pp 1015–1968

I-32

Index

Implants, breast (Continued) shell in, 804 silicon granulomas and, 805–807, 806f ultrasound evaluation of, 804–807, 804f–806f in vitro fertilization (IVF), CHD risk with, 1270–1273 Inborn errors of metabolism, fetal hydrops from, 1432 Incarcerated hernias, 496–497 Incisional hernias, 492–493, 494f Inclusion cysts amnion, 1061 epidermal, 779 peritoneal, 508–509, 509f, 573, 573f surface epithelial, 569, 573 vaginal, pediatric, 1883–1884 Incomplete subclavian steal, 952–953, 953b, 953f Incontinence, fecal, anal endosonography in, 305, 305f Indirect controls, 48–50, 49t Indistinct margins, in breast sonography, 787, 787f Indomethacin in fetal hydrops management, 1436 in utero exposure to, fetal hydrops from, 1432 Inertial cavitation, 40, 67–68 Infants. See Brain, neonatal/infant, imaging of Infarction(s) cerebral, neonatal/infant, 1550–1556 focal, 1555–1556, 1556b, 1556f luxury perfusion and, 1580–1581, 1584f epididymitis and, pediatric, 1896 grat, pediatric renal transplantation and, 1807–1809, 1808f hepatic, ater liver transplantation, 638–639, 646f maternal loor, 1473–1474, 1476f omental pediatric, appendicitis diferentiated from, 1858–1860, 1858f segmental, right-sided, 288, 289f periventricular hemorrhagic, in infants, 1547 placental, 1466, 1473–1474, 1476f–1477f ater renal transplantation global, 653 segmental, 653–655, 657f silent cerebral, SCD and, 1598 splenic, 156–157, 157f pediatric, 1770, 1771f testicular pediatric, 1895 segmental, 832, 832f Infection(s). See also Bacteria, pediatric infections from; Cytomegalovirus infection; Liver, infectious diseases of; Urinary tract, pediatric, infection of; Virus(es), pediatric infections from of biliary tree, 176–182 in breast cysts, 782–785, 785f breast ultrasound for, 803–804, 803f–804f fetal brain development and, 1203–1204, 1205f dural sinus thrombosis from, 1205–1206 echogenic bowel and, 1316 hydrops and, 1431–1432, 1431f liver calciications and, 1316–1318 of gastrointestinal tract, 295–300 AIDS patients and, 296 bezoars and, 300 celiac disease and, 300 congenital cysts and, 297, 298f cystic ibrosis and, 300 hematomas and, 299 intraluminal foreign bodies and, 300 ischemic bowel disease and, 297 mucocele of appendix and, 299, 299f peptic ulcer and, 299, 300f

Infection(s) (Continued) pneumatosis intestinalis and, 297–299, 299f pseudomembranous colitis and, 296–297, 298f of genitourinary tract, 323–333 AIDS and, 331–333, 332f–333f alkaline-encrusted pyelitis as, 324–325 Candida albicans as, 330–331, 331f cystitis as, 333 fungal, 330–331 papillary necrosis as, 328–329, 329b, 329f parasitic, 331 pyelonephritis as, 323–328 pyonephrosis as, 325, 326f schistosomiasis as, 331 tuberculosis as, 329–330, 330f of liver, 83–91 of neonatal/infant brain acquired, 1560, 1561f–1563f CMV, 1558–1560, 1559f congenital, 1557–1560, 1559f ater pancreas transplantation, 682 percutaneous needle biopsy complications with, 609 renal transplantation complications with, 651–653, 655f–657f sot tissue, 872–874, 873f–874f of spinal canal, pediatric, 1695 of urinary tract, pediatric jaundice in, 1738 lower, 1904–1905, 1908, 1910f–1911f of uterus, pediatric, 1885–1887 of vagina, pediatric, 1885–1887 Infectious cystitis, 333, 334f Infective peritonitis, 517, 519f Inferior epigastric artery (IEA) as landmark for inguinal hernias, 474–475, 476f relationship of indirect inguinal hernia to, 476–477, 478f Inferior thyroid artery, 693 Inferior thyroid vein, 693, 694f Inferior vas aberrans of Haller, 820–821 Inferior vena cava (IVC), 75–76, 75f, 455–464 anastomosis of, for liver transplantation, 624–625 anatomic variants of, 457, 458f anatomy of, 456–457 azygous continuation of, 457 Budd-Chiari syndrome and, 463 dilation of, 464 duplicated, 457, 458f ilters of, 464, 464f let, 457 neoplasms of, 463–464 nutcracker syndrome and, 460–461, 462f pancreatic head and, 211–212, 213f pelvic congestion syndrome and, 461–463, 463f stenosis of, ater liver transplantation, 636–637, 641f thrombosis of, 459–460 ater liver transplantation, 636–637, 642f, 1766, 1769f–1770f Inferior vesical artery, 384 Infertility cryptorchidism of testis and, 851 ectopic pregnancy and, 1070 TRUS for prostate and, 392–394, 393f Iniltrative metastases, of liver, 125–128, 126f Inlammation in acute pancreatitis, 222–225, 224f–228f of appendix, 282–285 in breast cysts, 782–785, 785f in Crohn disease creeping fat and, 269, 271f masses and, 275–276, 278f–279f perianal inlammation and, 276, 281f, 305–306

Inlammation (Continued) of epididymis, 846 of musculoskeletal system, pediatric, 1936–1938, 1937f–1938f noninfectious, 1938 of prostate, 389, 390f of salivary glands, pediatric, 1632–1635 acute, 1632–1634, 1632f–1633f chronic, 1634–1635, 1634f–1636f of tendons, 861–862, 862f Inlammatory abdominal aortic aneurysm, 439–440, 443f Inlammatory bowel disease (IBD), 266–269. See also Crohn disease Inlammatory disease pediatric, neck and, 1658–1664 lymph nodes and, 1658–1663, 1661f–1663f pediatric, thyroid gland and, 1643–1646, 1645f–1646f perianal, transanal sonography in, 305–307, 306b, 307f Inlammatory myoibroblastic tumor, pediatric, 1812 Inlammatory pseudotumors gastric mucosa thickening in, 1839–1840 pediatric cystitis and, 1794, 1797f splenic, 153–156 Infrahyoid space, pediatric, 1628–1629. See also Parathyroid glands, pediatric; hyroid gland, pediatric anatomy of, 1640, 1642f cystic lesions of, diferential diagnosis of, 1644b cysts of, 1650 laryngoceles of, 1650 visceral space of, 1640–1650 Infraspinatus tendon anatomy of, normal, 879, 879f ultrasound evaluation of, 883–884, 885f Infundibulopelvic (suspensory) ligament, 564–565 Infundibulum, 565 Inguinal canal, testis in, 851, 851f Inguinal hernias. See Hernia(s), inguinal Inguinal wall insuiciency, posterior, sports hernia and, 486, 488f Inionschisis, deinition of, 1225t Injections. See Musculoskeletal injection(s) Inner cell mass, 1051 Innominate artery, 916, 938 Inspissated cysts, 779, 781f Instrumentation. See also Transducer(s) basic components of, 7–12 for Doppler ultrasound, 24–25, 25b, 25f–26f image display in, 9–11, 9f–11f mechanical sector scanners, 11 receiver in, 8–9, 8f–9f transducer arrays in, 11–12, 12f transducer in, 7–8 transmitter in, 7 Insula, fetal, normal sonographic appearance of, 1168 Insulin, NTDs from, 1218 Insulinomas, pediatric, 1865 Intellectual functioning, in spina biida, 1233 Intensity of sound, 5 of ultrasonic power, 35 Interdigital neuromas, injection for, 904, 904f Interhemispheric issure, fetal, normal sonographic appearance of, 1168, 1169f Intermittent harmonic power Doppler imaging, 66, 66f Intermittent imaging, with contrast agents, 64–67, 66f Internal echoes, in renal cysts, 357, 357b Internal inguinal ring, as landmark for inguinal hernias, 474–475, 476f

Index Internal jugular vein (IJV) acute DVT of, 994f anatomy of, 990–991, 990f as cerebral blood vessel, 955–956 monophasic venous waveforms of, stenosis and, 1006, 1009f phlebectasia of, 1658, 1660f sonographic technique for, 955, 955f thrombosis of, 955–956, 956f–957f central line placement causing, 1658, 1661f ultrasound examination for, 991, 991f Internal oblique aponeurosis, torn, in spigelian hernia, 483–484, 487f Internal urethral sphincter, 384 International Society for Ultrasound in Obstetrics and Gynecology (ISUOG), 1041 Interphalangeal joint, injection of, short-axis approach to, 901 Intersegmental laminar fusion, pediatric, 1688 Interstitial ectopic pregnancy, 1073, 1074f Interstitial line sign, 1073 Interventional sonography, pediatric for abscess drainage, 1953 appendiceal, 1956, 1960f transrectal, 1953–1954, 1954f anatomy for, 1950 colon or bowel and, 1950 diaphragm and, 1950, 1950f antibiotics for, 1951 for biopsy devices for, 1950 mediastinal mass, 1956, 1959f targeted organ lesion, 1961, 1961f–1962f central venous access for, 1954 Chiba needle for, 1948 color Doppler ultrasound and, 1945 CT and, 1943, 1943t for deep foreign body removal, 1961, 1965f drainage catheters for, 1948 equipment for, 1943 freehand, 1945–1947 correcting needle angle in, 1947, 1949f correcting of-target needle in, 1947 initial needle placement and localization in, 1945–1946, 1945f–1946f locating needle ater insertion in, 1946–1947, 1947f–1948f mechanical guides compared to, 1945 training aids for, 1947 guidance methods in, 1943, 1943t for head lesions, 1961, 1966f initial puncture device for, 1949–1950 local anesthetic technique for, 1951, 1952f multimodality interventional suites for, 1943, 1944f for musculoskeletal procedures, 1961, 1963f–1964f for neck lesions, 1961, 1967f one compared to two operators for, 1943–1945 patient and, 1942–1943 for percutaneous cholangiography and drainage, 1956, 1959f for peritoneal drainage, 1954–1956, 1958f personnel for, 1943 for PICC, 1954, 1955f–1957f for pleural drainage, 1954–1956, 1958f principles of, 1942–1943 sedation for, 1950–1951 for steroid injection, 1961, 1964f transducers in, 1943 locating needle ater insertion and, 1946– 1947, 1947f typical procedures for, 1951–1953 aims and expectations in, 1952–1953 coagulation studies in, 1952

Interventional sonography, pediatric (Continued) diicult catheter ixation for, in infants, 1953 initial ultrasound in, before sedation, 1953 postprocedural care and follow-up in, 1953 prior consultation and studies in, 1951–1952 Interventricular septum, viewed from right ventricle, 1283f Intervillous spaces, 1465–1466 blood low in, 1467–1468, 1468f Intestinal hematomas, small bowel obstruction from, 1843 Intestinal inlammatory disease, pediatric, 1848–1862. See also Appendicitis, pediatric appendicitis as, 1855–1860, 1857b, 1858f–1862f ascariasis and, 1853, 1853f Crohn disease and, 1853, 1854f grat-versus-host disease and, 1853–1854, 1855f Henoch-Schönlein purpura and, 1853, 1855f HUS and, 1851f, 1853–1854 mucosal, 1851, 1851f NEC and, 1854–1855, 1855b, 1856f transmural, 1851, 1852f Intestinal malrotation with midgut volvulus, 1841–1842, 1843f–1844f midline stomach and, 1307 Intestinal wall thickening, pediatric, causes of, 1851, 1851b, 1851f–1852f, 1853–1854, 1855f Intestine(s), acoustic cavitation in, 43. See also Bowel; Gastrointestinal tract Intima-media complex, in carotid wall, 918–919, 919f Intima-media thickness, atherosclerotic disease and, 918–919 Intraamniotic bleeding, fetal echogenic bowel and, 1316 Intraatrial septum, embryologic development of, 1282f Intracardiac focus, echogenic, in trisomy 21, 1100f, 1101 Intracranial hemorrhage fetal, 1206, 1207f neonatal/infant brain and, duplex Doppler sonography of, 1580–1581, 1584f Intracranial pressure, increased, vasospasm diferentiated from, 1609–1610 Intracranial tumors, neonatal/infant brain and, duplex Doppler sonography of, 1585, 1587f Intradecidual sac sign, 1054, 1055f Intraductal intrahepatic cholangiocarcinoma, 185, 186f–187f Intraductal papillary mucinous neoplasm (IPMN), 245–247, 245f–246f Intradural lipomas, pediatric, 1686, 1687f Intrahepatic cholangiocarcinoma, 184–185, 186f intraductal, 185, 186f–187f Intrahepatic stones, in biliary tree, 173, 173f Intramedullary lipoma, 1686 Intramural sinus tract, in Crohn disease, 269, 274f Intraoperative ultrasound for adrenal glands, 429 for liver, 133 Intraparenchymal hematomas, 638 Intraparenchymal hemorrhage IUFD and, 1124f neonatal/infant brain and, 1547–1548, 1547f–1549f Intraperitoneal gas, free, in acute abdomen, 277–281, 282f Intraperitoneal stomach, 218–219, 220f Intrasubstance rotator cuf tears, 888, 890f Intratesticular artery, 821, 821f

I-33

Intratesticular cysts, 829, 830f Intratesticular variocele, pediatric, 1891–1892 Intratesticular vessels, pediatric, 1888 Intrauterine devices (IUDs), 529 PID and, 587 uterine sonographic techniques and, 552–554, 553f Intrauterine fetal death (IUFD), 1123–1125, 1124f Intrauterine growth restriction (IUGR), 1062 from CMV, 1204 diagnosis of, 1455 fetal monitoring in, 1455 in Miller-Dieker syndrome, 1195 multifetal pregnancy morbidity and mortality and, 1119–1123 ossiication delayed in, 1091 risk factors for, 1455–1460 fetal and placental, 1456b maternal, 1456b with spina biida, 1233 in triploidy, 1105f in trisomy 18, 1077 Intrauterine pregnancy, 1052–1053 Intravaginal torsion, 844, 844f Intravascular ultrasound, in plaque characterization, 943 Intravenous Doppler contrast agents, 1749–1750 Intravenous ultrasound contrast agents, 1746 Intraventricular hemorrhage from germinal matrix hemorrhage, 1541 neonatal/infant brain and, 1544–1545, 1544f–1546f, 1545b with hydrocephalus, 1545–1547, 1546f–1547f signs of, 1545b Intussusception MBO from, 293, 296f pediatric, 1843–1847 Doppler ultrasound for, 1849f false-positive, 1843, 1846f Henoch-Schönlein purpura complicated with, 1853 ileocolic, 1847f–1848f small bowel, 1844–1845, 1849f sonographic signs of, 1843b Invasive ibrous thyroiditis, 727–728, 728f Invasive mole persistent trophoblastic neoplasia, 1080, 1081f Iodine, deiciency of, thyroid hyperplasia from, 695 IPMN. See Intraductal papillary mucinous neoplasm Irradiation, microcephaly from, 1194 Ischemic bowel disease, 297 Ischemic stricture, renal transplantation and, 1811 Ischemic-thrombotic damage, thick placenta in, 1466 Ischium, in sonogram of hip from transverse/ lexion view, 1927, 1928f Isolated ventriculomegaly (IVM), 1176 Isomerism, let atrial, AVSD and, 1284 Isthmus, 565, 692 ISUOG. See International Society for Ultrasound in Obstetrics and Gynecology IUDs. See Intrauterine devices IUFD. See Intrauterine fetal death IUGR. See Intrauterine growth restriction IVC. See Inferior vena cava Ivemark syndrome, 1292 IVF. See in vitro fertilization IVM. See Isolated ventriculomegaly J Jaundice neonatal, 1734–1740 Alagille syndrome and, 1737 Volume I pp 1–1014 • Volume II pp 1015–1968

I-34

Index

Jaundice (Continued) bile duct spontaneous rupture and, 1734, 1737 biliary atresia and, 1734–1735, 1737, 1738f causes of, 1734, 1735b choledochal cysts and, 1735–1737, 1735f–1736f inborn errors of metabolism and, 1738–1740, 1739b, 1740f interlobular bile duct paucity and, 1737 neonatal hepatitis and, 1734, 1737–1738, 1739f urinary tract infection/sepsis and, 1738 in periampullary neoplasms, 236 Jejunal obstruction, fetal, 1310 Jejunoileal atresia, small bowel obstruction with, 1310, 1311f Jeune syndrome, 1395, 1398 Joint assessment, ultrasound techniques for, 866–869, 867f–869f Joint efusion, rheumatoid arthritis and, 867, 867f Joint(s) fetal, multiple contractures of, in arthrogryposis multiplex congenita, 1401, 1405f injections of, 901–902, 901f–902f Joubert syndrome, 1182, 1190 Dandy-Walker malformation diferentiated from, 1532 vermian hypoplasia with, 1191 Jugular vein, internal. See Internal jugular vein Junctional parenchymal defect, 313, 314f renal, 1781, 1781f Juvenile cystic adenomyoma, 541 Juxtaglomerular tumors, 355–356 Juxtaphrenic paravertebral masses, pediatric, 1723 K Kaposi sarcoma, liver in, 129 Kasabach-Merritt sequence, fetal hydrops from, 1430–1431 Kasabach-Merritt syndrome, 108 Kawasaki disease acute, pediatric, 1741 cervical adenopathy in children with, 1660–1663 Keepsake imaging, of fetus, 49b, 50 Keyhole sign, from posterior urethral valves in fetus, 1361, 1361f Kidney(s). See also End-stage renal disease; Renal artery(ies); Renal vein(s); Ureteral bud abscesses of acute pyelonephritis and, 325, 325f drainage of, 617, 618f transplantation complications with, 651, 656f acute cortical necrosis of, 370, 372f acute interstitial nephritis and, 370 acute tubular necrosis of, 370 agenesis of, 318–319 anatomy of, 311–314, 313f–315f older child and adult, 1781–1783 angiomyolipoma of, 351–352, 351f–352f ascent of, congenital anomalies related to, 318, 318f–319f cadaveric, paired, in transplantation, 643–644, 648f calculi in, 334–336, 336f–337f entities that mimic, 336, 337b, 337f capsule of, 314 carcinoid tumor of, 355–356 compensatory hypertrophy of, 317–318 congenital anomalies of, 1336 cysts of, 356–365 in acquired cystic kidney disease, 340, 364, 364f calciications of, 358, 358f complex, 357, 357b, 358f cortical, 356–359 hydatid, 331, 332f internal echoes in, 357, 357b

Kidney(s) (Continued) lithium nephropathy and, 361, 363f in localized cystic disease, 362–364, 363f malignant potential of, 359 medullary, 359 in multicystic dysplastic kidney, 361, 362f in multilocular cystic nephroma, 361–362, 363f parapelvic, 359, 360f percutaneous management of, 617–618, 619f in polycystic kidney disease, 359–361, 361f–362f septations in, 357–358, 357b, 358f simple, 356–357, 357f in TSC, 364–365, 365f in von Hippel-Lindau disease, 364, 364f development of, 311, 312f disease of acquired cystic, 340, 364, 364f cystic, 356–365 end-stage, relux nephropathy and, 327, 327f localized, 362–364, 363f medullary, 359 neoplasm-related, 364–365 polycystic, 359–361, 361f–362f renal cell carcinoma and acquired cystic, 340 ectopia and, 318, 318f failure of, chronic, transplantation for, 641 glomerulonephritis of, 370, 371f growth of, congenital anomalies related to, 317–318 hemangiopericytoma of, 356 hematomas of, 365–366 horseshoe, 159–160, 318, 319f fetal, 1345–1346, 1345f, 1362 pediatric, 1784, 1785f hypoplasia of, 317 intrathoracic, pediatric, 1716 lacerations of, 365–366, 366f leiomyomas of, 355–356 leukemia involving, 353–354 lymphomas of, 333, 352–353, 353b maternal, IUGR and, 1455 medullary sponge, 339, 340f, 359 pediatric, 1799 metastases to, 354, 355f multicystic dysplastic, 361, 362f multilocular cystic nephroma and, 361–362, 363f oncocytoma of, 348–351 parenchyma of, calciication of, 339–340, 340f pelvic, 318, 318f identiication of, 592 percutaneous needle biopsy of, 605–606, 606f–607f “putty”, 330 sarcomas of, 356 shattered, 365–366 sonographic technique for, 314 squamous cell carcinoma of, 348 supernumerary, 319 thoracic, 318 transitional cell carcinoma of, 346–347, 346f–349f trauma to, 365–366, 366f tumors of, rare, 355–356 vascular abnormalities of, 366–369 renal vascular Doppler ultrasound and, 366 Kidneys, fetal agenesis of bilateral, 1342–1344, 1343f–1344f, 1344b unilateral, 1344 VUR with, 1360 cystic disease of, 1346–1352 ADPKD and, 1350, 1350f ARPKD and, 1348–1350, 1349f

Kidneys, fetal (Continued) bilateral reniform enlargement of, 1348, 1349f HNF1β mutations in, 1350–1351 MCDK as, 1346–1347, 1346f–1347f Meckel-Gruber syndrome and, 1351, 1351f obstructive cystic renal dysplasia as, 1347–1348, 1347f–1348f syndromes associated with, 1350–1351, 1351f duplex, VUR with, 1360 ectopic, 1344–1345, 1344f–1345f embryology of, 1336–1338, 1337f horseshoe, 1345–1346, 1345f megalourethra and, 1362 hyperechogenic, 1351–1352, 1352f length of, at 14-42 weeks’ gestation, 1338–1339, 1339t lobation in, 317, 1781, 1781f lobes of, formation of, 1781, 1781f normal sonographic appearance of, 1342f pelvic, 1344–1345, 1344f postnatal function of fetal urinalysis in prediction of, 1365, 1365t poor, antenatal predictors of, 1364b routine sonographic view of, 1026f sonographic appearance of, 1338–1339, 1338f tumors of, 1352–1353, 1353f Kidneys, pediatric. See also Hydronephrosis, pediatric, causes of; Nephrocalcinosis; Urinary tract, pediatric abscess of, complicating acute pyelonephritis, 1792–1793 absence of, 1784, 1784f biopsies of, Doppler assessment of, 1809, 1810f–1811f “cake”, 1785 crossed-fused ectopia, 1784–1785, 1785f cystic disease of, 1812–1818 ADPKD and, 1814–1815, 1815f ARPKD and, 1812–1813, 1814f MCDK and, 1815, 1816f medullary cystic kidney disease and, 1816, 1817f nephronophthisis and, 1815–1816, 1816f cysts of, congenital, 1816–1818 dialysis and acquired, 1816–1818, 1817f ater liver transplantation, 1816–1818 in TSC, 1816, 1817f in VHL disease, 1816 Doppler ultrasound for, 1778 dysplastic, 1798, 1798f focal scarring of, from acute pyelonephritis, 1792, 1793f horseshoe, 1784, 1785f hydronephrosis and, 1785–1791 length of age, height, weight compared to, 1776–1778, 1777f by age, with single functioning kidney, 1779t birth weight and gestational age compared to, 1776–1778, 1780f normal measurements of, 1776–1778, 1777f position for visualizing, 1776f reference values for, according to age and gender, 1776–1778, 1778t medical diseases of, 1794–1798 acute kidney injury as, 1795–1796, 1796b, 1797f chronic kidney disease as, 1796–1798, 1797t, 1798f normal anatomy of, 1781–1783, 1781f–1782f normal term, 1781–1783 “pancake”, 1785 pelvic, 1908 premature, normal, 1781–1783 renal duplication and, 1783–1784, 1784f

Index Kidneys, pediatric (Continued) sonographic technique for, 1776–1781 patient preparation for, 1776, 1776t transplantation of Doppler ultrasound in, 1807–1812 parenchymal abnormalities and, 1809–1810, 1812f perinephric luid collections in, 1809, 1811f tumors of, 1812, 1813f urologic complications and, 1810–1812 vascular complications in, 1807–1809, 1808f, 1810f–1811f trauma to, 1801, 1802f tumors of, 1818–1820 angiomyolipoma as, 1820, 1822f mesoblastic nephroma as, 1818–1820, 1821f MLCN as, 1820, 1822f RCC as, 1820, 1821f renal lymphoma as, 1820, 1823f Wilms, 1818, 1818f–1820f vascular disease of, Doppler assessment of, 1801–1805 acute renal vein thrombosis and, 1804–1805, 1804b, 1804f clinical applications of, 1803–1805 HUS and, 1805, 1807f increased resistance to intrarenal low and, 1802–1803, 1803b, 1803f normal anatomy and low patterns and, 1801–1802, 1803f renal artery stenosis and, 1805, 1805t, 1806f in renal transplantation, 1807–1809, 1808f, 1810f–1811f technique for, 1801 vessel patency and, 1803–1804 volume of by age, with single functioning kidney, 1779t determination of, 1776, 1776f mean total, 1779t reference values for, according to age and gender, 1776–1778, 1778t Kimura disease, 1635 Klebsiella, 846 Kleihauer-Betke test, 1421 Klinefelter syndrome, 826 pediatric, 1891 testicular microlithiasis and, 1904 Klippel-Trénaunay-Weber syndrome, hemimegalencephaly associated with, 1195 Knee, dislocations of, pediatric, 1933–1934, 1934f Kniest dysplasia, achondrogenesis type 2 diferentiated from, 1391 Krukenberg tumor, 585 Küttner tumor, 1635 Kyphoscoliosis body stalk anomaly and, 1329 fetal, 1404 in skeletal dysplasias, 1382 Kyphosis, fetal, 1235–1237, 1236f, 1237b cervical, in campomelic dysplasia, 1381–1382 L Labor, preterm, 1495–1496. See also Preterm birth Labrum, of acetabulum, 1923 Lacerations pediatric pregnancy and, 1884 renal, 365–366, 366f Lactobezoars, 1840, 1841f Laminae in posterior angled transaxial scan plane, 1224f in posterior transaxial scan plane, 1222f in spina biida, 1228, 1229f–1230f

Laminectomy, spinal sonography ater, 1697 Langerhans cell histiocytosis in infant, 1751f metastasis of, to teste, 1901 Langer-Saldino form of achondrogenesis, 1391 Laparoscopy, for ectopic pregnancy, 1076 Large bowel, dilated loops of, 1311–1312 Large-for-gestational age (LGA) fetus, 1453–1454 diabetic mothers and, 1454, 1455t incidence of, 1453–1454 sonographic criteria for, 1454t–1455t Larsen syndrome elbow and knee dislocation and, 1933–1934 teratologic hip dislocation and, 1932 Laryngeal webs, fetal, CHAOS and, 1253 Laryngoceles, pediatric, 1650 Laryngotracheomalacia, 1395 Larynx, fetal, CHAOS and, 1253 Lateral nasal prominence, 1134, 1134f Lateral resolution, 19, 19f Lehman syndrome, spina biida and, 1226 Leiomyoma(s) adenomyosis coexisting with, 541 bladder, 356 gastric, 265f gastrointestinal, endosonographic identiication of, 301 paratesticular, 1903–1904 renal, 355–356 spermatic cord, 840–841, 840f uterine, 538–540, 539f, 540b Leiomyomatosis peritonealis disseminata, 523–524, 525f Leiomyosarcoma(s) bladder, 356 gastric, 265f paratesticular, 1903–1904 uterine, 540, 541f Lemierre syndrome, 1658, 1661f Lemon sign, in Chiari II malformation, 1183–1185, 1184f spina biida screening and, 1221, 1232–1233 Lemon-shaped skull, 1136, 1137f Lenticulostriate vasculopathy, 1203, 1204f, 1585, 1588f neonatal/infant, 1556–1557 Leptomeningeal collaterals, MCA occlusion, 1610 Leriche syndrome, 441–442 Lesser omentum, portal hypertension and thickened, 1756, 1756f Lesser peritoneal sac, 218–219, 220f Leukemia acute lymphocytic, AKI and, 1796 liver metastases from, pediatric, 1746 lymphadenopathy from, 1724 ovarian iniltration by, pediatric, 1880 in pancreas, pediatric, 1865 renal involvement in, 353–354 salivary gland iniltration by, pediatric, 1639 testicular, 827, 828f pediatric, 1901, 1901f Leukodystrophy, megalencephaly associated with, 1194–1195 Leukomalacia, periventricular. See Periventricular leukomalacia Levocardia, 1273 Levotransposition, of great arteries, 1289–1290 Levovist, 55–56, 107, 111f Leydig cells testosterone secretion and, 819 tumors of, 826, 827f pediatric, testicular, 1900, 1900f LGA. See Large-for-gestational age fetus LHBT. See Long head biceps tendon

I-35

LHR. See Lung-to-head circumference ratio Li-Fraumeni syndrome adrenocortical neoplasms and, 1827 prenatal intracranial tumors in, 1208 Ligament(s) anatomy of, normal, 862–863, 863f falciform, 77, 79f pediatric, 1731, 1731f–1732f injuries to, 862–863, 863f–864f diagnosing, 864, 864f of liver, 77, 79f–80f ultrasound techniques for, 862–864 Ligamentum teres, 77, 80f Ligamentum venosum, 77 pediatric, 1731, 1731f Limb deformities, congenital pediatric, 1933 PFFD and, 1933, 1934f tibial hemimelia and, 1933 Limb enlargement, asymmetrical, 1403 Limb pterygium, 1403 Limb reduction defects, 1399–1404 amniotic band sequence as, 1401, 1403f arthrogryposis multiplex congenita as, 1401–1404, 1405f caudal regression syndrome as, 1401, 1404f deformations as, 1399 disruptions as, 1399 isolated, 1400 malformations as, 1399 nomenclature of, 1400t proximal focal femoral deiciency as, 1400, 1400f radial ray, 1400–1401, 1401f–1402f sirenomelia as, 1401, 1404f terminal transverse, 1400 Limb shortening, patterns of, 1381, 1381b, 1382f Limb-body wall complex, 1182–1183, 1329 OEIS diferentiated from, 1328–1329 Limb–body wall complex, 1401 Limey bile, 194, 195f Lindegaard ratio, 1596, 1609–1610 Linea alba, appearance of, 489, 489f Linea alba hernias, 488–491. See also Hernia(s), linea alba Linear array transducers beam steering in, 10–11, 11f use and operation of, 11–12 Lingual thyroid, pediatric, 1639 Lipid cysts, in breast, 775–779, 779f Lipoadenomas, parathyroid, 735 Lipoleiomyomas, 539f, 540 Lipoma(s) corpus callosum, 1529, 1533f ilum terminale, 1674 closed spinal dysraphism and, 1684–1685, 1686f intracranial, fetal, 1209–1210, 1210f intradural, pediatric, 1686, 1687f intramedullary, 1686 intramuscular, simulating anterior abdominal wall hernias, 500, 502f of liver, 117–118, 119f midline, in corpus callosum agenesis, 1201 pancreatic, 249–251, 250f paratesticular, 1903–1904 parotid gland, pediatric, 1639 simulating groin hernias, 500, 501f spermatic cord, 840–841, 840f spina biida occulta with, 1226 subcutaneous simulating anterior abdominal wall hernias, 500, 502f tethered cord and, 1679 ultrasound techniques for, 870, 871f, 871t Volume I pp 1–1014 • Volume II pp 1015–1968

I-36

Index

Lipomyelocele, closed spinal dysraphism and, pediatric, 1682, 1684f Lipomyelomeningoceles closed spinal dysraphism and, pediatric, 1682, 1685f spine embryology and diferentiation of, 1674 Liposarcomas, scrotal, 840f, 841 Lips, fetal, normal sonographic appearance of, 1135f. See also Clet lip/palate Lissencephaly classical (type 1), 1195, 1196f cobblestone (type 2), 1195, 1197f fetal, 1195–1196, 1196f–1197f neonatal/infant, 1537 Lithium nephropathy, 361, 363f Lithium therapy, long-term, primary hyperparathyroidism and, 734 Lithotripters, acoustic cavitation evidence from, 42–43, 42f Littoral cell angioma, splenic, 153–156, 156f Liver abscesses of drainage of pyogenic, 612–613, 614f–615f ater liver transplantation, 638–639, 646f from pyogenic bacteria, 85–86, 87f agenesis of, 80 anatomy of Couinaud, 76–77, 77t, 78f echogenicity of, 80, 81f hepatic venous, 76, 76f, 77t ligaments, 77, 79f–80f normal, 75–80, 75f–76f, 77t size of, 80 anomalies of congenital, 82–83 developmental, 80–82 vascular, 80–82 bare area of, 77 benign neoplasms of, 108–118 adenoma as, 115–117, 116f–118f angiomyolipomas as, 117–118, 119f cavernous hemangioma as, 108–112, 112f–113f, 603–604, 604f FNH as, 112–115, 114f–115f lipomas as, 117–118, 119f biopsy of percutaneous, 132–133 percutaneous needle, 603–604, 603f–604f circulation in, 78–80 hepatic artery and, 78 hepatic veins and, 80 portal veins and, 78 cirrhosis of, 92–96 Doppler ultrasound characteristics of, 95, 95f HCC and, 122, 122t intrahepatic portal hypertension from, 96 morphologic patterns of, 92–95, 94f pseudocirrhosis of, 125–128, 129f sonographic features of, 95b SWE and, 95–96 cysts of, 82, 82f–83f autosomal dominant polycystic kidney disease and, 83 percutaneous management of, 618 peribiliary, 82–83 fatty, 91–92, 92f–93f fetal, 1316–1318 calciications of, 1316–1318, 1317f, 1318b cysts and, 1318, 1318f hemangioma of, 1319f hepatomegaly and, 1316, 1317f ibrosis of, periportal, Caroli disease with, 171 issures of, 75–76 accessory, 80, 81f luid collection in, ater transplantation, 638–639, 645f–646f

Liver (Continued) glycogen storage disease afecting, 92 herniation of, 80 infectious diseases of, 83–91 bacterial, 85–86, 87f fungal, 86–87, 88f parasitic, 87–90, 89f–90f Pneumocystis carinii and opportunistic, 91, 91f viral hepatitis, 83–85 intraoperative ultrasound for, 133 in Kaposi sarcoma, 129 lobes of, 75–76, 75f–76f lymphoma of, 125, 129f malignant neoplasms of, 118–124 EHE as, 123–124 HCC as, 118–123, 120f–121f, 122t, 123f hemangiosarcoma as, 123 masses of, 105–107 characterization of, 105–106, 106f–107f, 108t, 109f–110f detection of, 106–107, 111f microbubble contrast agents in characterization of, 105–106, 106f–107f, 108t, 109f–110f neoplasms in, 107–129 metabolic disorders of, 91–96 metastatic disease of, 124–129, 126f–130f portosystemic shunts and, 130–132 transjugular intrahepatic, 131–132, 132b, 132f–133f scalloping of, in pseudomyxoma peritonei, 514, 518f schistosomiasis of, 90 situs inversus totalis of, 80 sonographic technique for, 75, 75f trauma to, 129–132, 131f vascular abnormalities in, 96–104 Budd-Chiari syndrome as, 98–103, 100f–103f hepatic artery pseudoaneurysm as, 104 hereditary hemorrhagic telangiectasia as, 104 intrahepatic portosystemic venous shunts as, 104 peliosis hepatis as, 104, 104f portal hypertension as, 96–98, 96f–97f portal vein aneurysms as, 103–104 portal vein thrombosis as, 98, 99f–100f veno-occlusive disease of, 103 volumetric imaging of, 75 as window to pleural space, 1702, 1707f Liver, pediatric. See also Jaundice, neonatal; Liver transplantation, pediatric; Portal hypertension, pediatric abscess of, 1746–1748, 1751f parasitic, 1747–1748 pyogenic, 1746–1747, 1751f adenomas of, 1746 inborn errors of metabolism and, 1738 anatomy of, 1730–1734 hepatic vein, 1733–1734, 1734f portal vein, 1731–1734, 1732f segmental, external, 1730–1731, 1731f biliary rhabdomyosarcoma in, 1746, 1749f biopsy of, targeted, 1962f cholelithiasis and, 1741, 1741b, 1743f cirrhosis and, 1741, 1742f congenital ibrosis of, prehepatic portal hypertension from, 1757–1759, 1762f Doppler assessment of, 1748–1764 basic principles of, 1748–1750 of normal low patterns in splanchnic vessels, 1750 for portal hypertension, 1752–1754, 1754f–1755f possibilities and pitfalls of, 1750

Liver, pediatric (Continued) sonographic technique for, 1750–1752 surgical portosystemic shunts and, 1764 Echinococcosis in, 1748 fatty degeneration/iniltration of, 1740, 1740f FNH and, 1746 granulomas of, 1748 HCC of, 1746 hemangiomas and, 1742–1743, 1744f hepatoblastomas of, 1746, 1747f infantile hemangioendotheliomas and, 1743–1744, 1745f jaundice and, 1734–1740 let lobe of, 1731–1733 masses in, 1743b mesenchymal hamartomas and, 1744 metastases to, 1746, 1750f quadrate lobe of, 1731–1733 right lobe of, 1733, 1733f schistosomiasis in, 1748 steatosis and, 1740, 1740f, 1741b SWE and, 1764, 1765f tumor angiogenesis detection in, 1746 tumors of, 1741–1746 benign, 1742–1746 identiication of, 1741–1742 malignant, 1746 undiferentiated embryonal sarcoma and, 1746, 1748f Liver lukes, biliary tree and, 176–179, 177f–179f Liver transplantation, 624–641 abscess ater, 638–639, 646f adrenal hemorrhage ater, 638, 645f arterial complications of, 629–635 celiac artery stenosis as, 634–635, 637f hepatic artery pseudoaneurysms as, 634, 636f hepatic artery resistive index elevation as, 634 hepatic artery stenosis as, 631–634, 634f–635f hepatic artery thrombosis as, 627, 628f, 631, 633f biliary tree complications with, 625–629 bile leakage as, 627–629, 629f biliary sludge as, 629, 631f biliary stones as, 629, 632f biliary strictures as, 626–627, 627f–628f pneumobilia as, 625, 1767–1768, 1769f–1770f recurrent sclerosing cholangitis as, 629, 630f sphincter of Oddi dysfunction as, 629 biloma ater, 638 choledochojejunostomy for, 625 common bile duct anastomosis for, 625 contraindications for, 624 Doppler studies of recipient of, pediatric, 1764–1769 with multiorgan transplants, 1768–1769 for posttransplantation evaluation, 1766–1768, 1768f–1770f for pretransplantation evaluation, 1764–1766 rejection in, 1767 luid collection ater extrahepatic, 638, 644f–645f intrahepatic, 638–639, 645f–646f hematomas ater, 638, 644f hepatic artery anastomosis for, 624 infarction ater, 638–639, 646f intrahepatic solid masses complicating, 639–641, 646f IVC anastomosis for, 624–625 living related donor, 625 normal appearance of, 625, 626f, 1767f patient selection for, 624 pediatric Doppler studies of recipient of, 1764–1769 renal cysts ater, 1816–1818 portal vein anastomosis for, 624

Index Liver transplantation (Continued) PTLD ater, 683–688, 687f split liver grat and, from deceased donor, 625 surgical technique for, 624–625, 624f venous complications of hepatic artery aneurysms as, 1768, 1769f–1770f hepatic vein stenosis as, 637, 643f IVC stenosis as, 636–637, 641f IVC thrombosis as, 636–637, 642f, 1766, 1769f–1770f portal vein aneurysms as, 1768, 1769f–1770f portal vein stenosis as, 635–636, 638f, 1766, 1768f portal vein thrombosis as, 635–636, 639f–640f, 1766 Lobar emphysema, congenital, 1251, 1253f “Lobster claw” deformity, 1406–1407, 1406f Localized cystic disease, 362–364, 363f Long head biceps tendon (LHBT), 879, 880f–881f longitudinal split tear of, 893, 894f pathology of, 892–893 tenosynovitis and, 892–893, 893f Longitudinal split tear, of long head of biceps, 893, 894f Longitudinal waves, 2–3 Longus colli muscle, parathyroid adenomas confused with, 745 Lower face abnormalities, 1153–1154 macroglossia as, 1153, 1153b, 1158f micrognathia as, 1153–1154, 1158f retrognathia as, 1153–1154 Lower limb anomalies, pediatric, 1689 Lower urinary tract symptoms (LUTS), 387–388 Lumbar arteries, 446, 446f Lumbar spine deiciency, in caudal regression, 1237–1238 LUMBAR syndrome, tethered cord and, 1679 Lumbosacral area, spina biida in, 1228 Lumbosacral hypogenesis, spinal cord embryology and, 1674 Lung(s). See also Pulmonary hypoplasia, fetal acoustic cavitation in, 43 CHAOS and, 1253–1255, 1254f congenital malformations of BPS as, 1250–1251, 1251f CLO as, 1251–1252, 1253f CPAM as, 1246–1252 pediatric abscess in, 1711, 1713f atelectatic, 1714, 1716f consolidated, 1711, 1714f–1715f disease of, pleural disease diferentiated from, sonography in, 1709, 1710f parenchyma, 1711–1716 sequestrations in, 1715–1716, 1717f percutaneous needle biopsy of, 607–608, 609f pleuropulmonary blastoma and, 1252–1253 Lung(s), fetal development of, 1243 stages of, 1245b hypoplasia of campomelic dysplasia and, 1384f in lethal skeletal dysplasia, 1386, 1386b lethality of skeletal dysplasia and, 1382, 1384f masses in, hydrops from, 1426 size of, evaluation of, 1244 space-occupying lesions and, 1243 Lung-to-head circumference ratio (LHR), 1262 Luteal phase defect, early pregnancy failure from, 1062–1063 Luteoma of pregnancy, 572 LUTS. See Lower urinary tract symptoms

Luxury perfusion, cerebral infarction with, 1580–1581, 1584f “Lying down” adrenal sign in bilateral renal agenesis, 1342, 1343f in neonate with absence of let kidney, 1784, 1784f Lyme disease, pediatric, 1936 Lymph node(s) breast cancer and assessment of, 807–810, 808f–810f cortex of, 807 eccentric cortical thickening of, 807–808, 809f hilum of, 807 masses of, in carotid region, 948, 949f normal appearance of, 807, 808f pathologic, near carotid bifurcation, 948, 949f pediatric, inlammatory disease of, 1658–1663, 1661f–1663f Rotter, 762, 808–810, 810f Lymphadenitis, pediatric, 1658–1663, 1662f–1663f Lymphadenopathy in Crohn disease, 269, 272f Doppler ultrasound assessment of, 771–772, 772f pediatric age and causes of, 1660, 1662t cervical, 1658, 1660–1663 mediastinal masses and, 1724 site of node and causes of, 1660, 1662t supraclavicular, 1658 retroperitoneal, 464 in tuberculous peritonitis, 521 Lymphangiectasia, appearance of, 1412, 1413f Lymphangioma(s) abdominal, pediatric, 1862, 1864f fetal, neck, hydrops from, 1425 paratesticular, 1903–1904 pediatric pancreas and, 1865 pelvic, mesenteric cysts in, 509–510, 510f splenic, 148 Lymphatic dysplasia, congenital, hydrops from, 1428, 1436f Lymphatic malformations. See also Cystic hygroma(s) fetal neck abnormalities and, 1159, 1161f macroglossia in, 1153, 1153b, 1158f pediatric of chest, 1723 chest wall, macrocystic, ultrasound-guided sclerotherapy of, 1726, 1727f of neck, 1655–1657, 1657f parotid gland, 1636, 1637f submandibular space, 1639–1640 in Turner syndrome, 1159 Lymphedema, hereditary, fetal, 1403–1404, 1405f Lymphocele(s) pelvic, 591 ater renal transplantation, 665–666, 673f–674f pediatric, 1809, 1811f Lymphocytic leukemia, acute, 1796 Lymphoma(s) adrenal, 426–427, 427f AIDS-related, 266, 266f B-cell, AKI and, 1796 bladder, 353, 354f Burkitt, pediatric, 1860 gastric, endosonographic identiication of, 301 gastrointestinal, 264–266, 266f pediatric, 1862 genitourinary tract tumors and, 352–353 Hodgkin, pediatric, neck, 1665, 1665f

I-37

Lymphoma(s) (Continued) of liver, 125, 129f lymphadenopathy from, 1724 mediastinal, pediatric, biopsy of, 1956 non-Hodgkin, 125, 264–266 pediatric, neck, 1665 splenic lesions in, 152–153, 154f ovarian, 585 pediatric, 1880 pediatric liver metastases from, 1746 neck, 1665, 1665f paratesticular, 1903–1904 peritoneal, 513, 517f renal, 333, 352–353, 353b pediatric, 1820, 1823f retroperitoneal, 464 salivary gland, pediatric, 1639 of small bowel, 266, 266f splenic lesions in nodular, 152, 154f solid, 152–153 testicular, 826–827, 828f pediatric, 1901 of thyroid gland, 708–709, 709f pediatric, 1648 ureteral, 353 Lymphoplasmacytic sclerosing pancreatitis, 236 Lymphoproliferative disorder. See Posttransplant lymphoproliferative disorder Lysosomal disorders, fetal hydrops from, 1432 M Macrocephaly, 1135–1136 fetal brain and, 1194–1195 Macrocranium(ia) in skeletal dysplasia, 1382 in thanatophoric dysplasia, 1387 Macrocysts, ovarian, pediatric, 1873–1875 Macroglossia, 1153, 1153b, 1158f Macronodular cirrhosis, 92–93 Macrosomia, 1453 sonographic criteria for, 1454t–1455t Mafucci syndrome, in venous malformations of neck, 1657 Magnetic resonance angiography (MRA), in carotid stenosis diagnosis, 916 Magnetic resonance imaging (MRI), 32–33 breast ultrasound correlation with, 810–811, 811f–812f of CNS, 1166–1167 of fetal brain, 1166–1167, 1172f for fetal spine, 1216 for fetal urinary tract abnormalities, 1342, 1342f of fetus, 1031–1032, 1031f musculoskeletal system ultrasound compared to, 856 parathyroid adenomas and accuracy of, 748, 749f in pregnancy, 1031–1032, 1031f shoulder ultrasound compared to, 877–878 in skeletal dysplasia evaluation, 1385 Mainzer-Saldino syndrome, 1395 Majewski syndrome, 1396 Malacoplakia, 333, 333f Male pseudohermaphroditism, dysplastic gonads and, 1899 Malformations, deinition of, 1399 Malignancies, childhood, obstetric sonography and, 1041 Malignant melanoma, splenic lesions in, 153, 155f MALToma, pediatric, 1639 Volume I pp 1–1014 • Volume II pp 1015–1968

I-38

Index

Mammary ducts normal sonographic appearance of, 762, 764f subareolar and intranipple, scanning of, 762, 765f Mammary fascia, 761, 762f Mammary zone, of breast, 761, 761f, 763f Mandible, fetal, normal sonographic appearance of, 1135f Mandibular nasal prominence, 1134, 1134f MAP (minimal-access parathyroidectomy), 749, 750f Marfan syndrome, 946 Marginal placental cord insertion, 1484–1485, 1487f multifetal pregnancy and, 1119 Massa intermedia, enlarged, in Chiari II malformation, 1526, 1527f Masseter muscle, pediatric, chloroma of, 1641f Massive splenomegaly, 145, 146t Masticator space, pediatric, pathology of, 1640, 1641f Mastitis granulomatous, 803–804 periductal, 771, 771f sonography for, 803–804 Maternal age, chromosomal abnormalities risk and, 1088, 1089f Maternal loor infarction, 1473–1474, 1476f Mathias laterality sequence, spina biida and, 1226 Matrix metalloproteinases (MMPs), 434 Maxilla, fetal, normal sonographic appearance of, 1135f Maxillary nasal prominence, 1134, 1134f Maximum vertical pocket, 1339 Maximum-intensity projection (MIP), 105–106 Mayer-Rokitansky-Küster-Hauser syndrome, 1881–1883, 1882f May-hurner syndrome, 456–457 MBO. See Mechanical bowel obstruction MCA. See Middle cerebral artery McCune-Albright syndrome, pediatric ovarian cysts and, 1875 MCDA. See Monochorionic diamniotic twins MCDK. See Multicystic dysplastic kidney MCMA. See Monochorionic monoamniotic twins MDCT. See Multidetector computed tomography Mean sac diameter (MSD) in gestational age estimation, 1061, 1061f, 1444–1445, 1445t of gestational sac for gestational age estimation, 1444–1445, 1445t small, in relationship to CRL, early pregnancy failure and, 1066, 1067f yolk sac and, 1057 Mechanical beam steering, 10–11 Mechanical bowel obstruction (MBO) aferent loop, 293 closed-loop, 293, 295f gastrointestinal tract and, 293 intussusception causing, 293, 296f midgut malrotation predisposing to, 293 sonographic assessment of, 293, 294f Mechanical index (MI) for acoustic cavitation, 44–45, 45f deinition of, 58 microbubbles as contrast agents and, 58, 58b, 105 in obstetric sonography, 1035 Mechanical sector scanners, 11 Mechanical ventilation, in neonatal/infant brain, 1578, 1579f Meckel diverticulum intussusception and, 1844–1845, 1849f pediatric appendicitis diferentiated from, 1858–1860, 1862f

Meckel-Gruber syndrome Dandy-Walker malformation diferentiated from, 1532 fetal brain dorsal induction errors and, 1182 fetal cystic kidneys and, 1351, 1351f spina biida and, 1226 Meconium ileus, 1310 fetal CF and, 1316 Meconium periorchitis, focal calciications from, 1904, 1904f Meconium peritonitis fetal CF and, 1316 hydrops from, 1428, 1428f liver calciications and, 1316–1318 massive ascites in, 1418–1419, 1421f small bowel and, 1313, 1313t, 1314f pediatric cystic, 1842–1843, 1846f testicular torsion and, 1892–1893 Medial ibroplasia, renal artery stenosis and, 447 Medial gastrocnemius muscle, tear of, 858, 859f Medial nasal prominence, 1134, 1134f Median arcuate ligament syndrome, 453, 453f Mediastinal shit, in unilateral pulmonary hypoplasia, 1246, 1247f Mediastinum fetal, masses in, hydrops from, 1425 pediatric, assessment of, 1702, 1703f–1704f pediatric, masses of, 1723–1724 abnormal thymus location mimicking, 1723 anterior, 1723–1724 biopsy of, 1956, 1959f lymphadenopathy and, 1724 posterior, 1724 thymic index and, 1723, 1724t, 1725f, 1726t Mediastinum testis, 819, 820f pediatric, 1888 Medical renal disease. See Kidneys, pediatric, medical diseases of Medulla adrenal, functions of, 417 cerebral, as foramen magnum approach landmark, 1592, 1595f Medullary carcinoma, of thyroid gland, 701–707, 707f–708f pediatric, 1648 Medullary cystic kidney disease, 359 pediatric, 1816, 1817f Medullary nephrocalcinosis, 339, 340f pediatric, 1798–1799, 1799f Medullary sponge kidney, 339, 340f, 359 pediatric, 1799 Megacalices, congenital, 321 Mega-cisterna magna fetal, 1189 arachnoid cysts diferentiated from, 1192–1193 normal sonographic appearance of, 1168–1169 neonatal/infant, Dandy-Walker malformation diferentiated from, 1531, 1534f Megacystis, fetal, 1360, 1360b, 1360f megalourethra and, 1362f Megacystis-microcolon-intestinal hypoperistalsis syndrome (MMIHS), 1362–1363 pediatric hydronephrosis and, 1788–1791 Megacystitis, fetal, thickened NT and, 1096f Megahertz, deinition of, 2 Megalencephaly, 1194–1195 Megalourethra, fetal, urinary tract obstruction in, 1362, 1362f Megaureter(s) congenital, 321, 322f fetal, 1358–1359 primary, pediatric hydronephrosis and, 1786–1788, 1787f

Meigs syndrome, 585 Membranous glomerulonephritis, 369 Membranous VSDs, 1281 MEN. See Multiple endocrine neoplasia Ménétrier disease, gastric mucosa thickening in, 1839–1840 Meningeal layer, in myelocystocele, 1233 Meningitis, neonatal/infant, 1560, 1561f–1562f Meningocele atretic, tethered cord and, 1679 fetal cranial, 1179 deinition of, 1225t pathogenesis of, 1226 sonographic indings in, 1218 spina biida occulta and, 1226 posterior, closed spinal dysraphism and pediatric, 1682–1683 Meningoencephalocele, 1218 Meningomyelocele, fetal cloacal exstrophy and, 1328 Menopause endometrial abnormalities ater bleeding and, 545–546 luid and, 546–547, 546b, 547f hormone use and, 544–545, 544b, 545f ovaries ater, 569 cysts in, 569–570, 571f Menstrual age deinition of, 1443–1444 usage of term, 1167 Menstrual cycle, interrelationships in, 1050f Menstruating females, ovarian volume in, 1873, 1875t Mesencephalon, formation of, 1077 Mesenchymal dysplasia, of placenta, 1479, 1479f Mesenchymal tumors, intracranial, fetal, 1208 Mesenchyme, formation of, 1053 Mesenteric, adenopathy, in acute abdomen, 282 Mesenteric adenitis pediatric, 1858–1860, 1862f right lower quadrant pain in acute abdomen from, 288 Mesenteric adenopathy, in acute abdomen, 282 Mesenteric artery(ies), 451–455. See also Celiac artery anatomy of, 451, 452f celiac artery as, 451 duplex Doppler sonography of, 453–455, 455f interpretation of, 454–455, 456f–458f inferior anatomy of, 451, 452f connections of, with superior mesenteric artery, 451 duplex Doppler sonography of, 454 ischemia of, 451–453 in median arcuate ligament syndrome, 453, 453f stenosis of, turbulence ater, 454, 456f superior anatomy of, 451, 452f connections of, with inferior mesenteric artery, 451 duplex Doppler sonography of, 454 occluded, 454–455, 458f stenosis of, 457f Mesenteric cyst(s) fetal, ovarian cysts diferentiated from, 1369 gastrointestinal cysts diferentiated from, 1860, 1863f pediatric, ovarian cysts diferentiated from, 1875 peritoneal, 509–510, 510f Mesenteric vein(s) clots in, in acute pancreatitis, 224–225, 227f pediatric Doppler studies of, best approaches for, 1752 low direction in, in portal hypertension, 1752

Index Mesentery, small bowel, 505, 505f Mesoblastic nephroma congenital, 1352–1353, 1353f pediatric, 1818–1820, 1821f Mesocardia, 1273 Mesocolon, transverse, inlammation of, in acute pancreatitis, 224–225, 226f Mesoderm layer, of trilaminar embryonic disc, 1216–1217, 1217f Mesomelia, 1381, 1381b, 1382f Mesonephric (wolian) duct, 820–821 Mesonephros, 311, 312f, 1336–1338 Mesorchium, torsion of, pediatric, 1325 Mesosalpinx, 564–565 Mesothelioma(s) cardiac, in infants, 1293 multicystic, 508–509 pediatric, 1712f peritoneal, primary, 513, 516f Mesovarium, 564–565 Metabolic disorders fetal hydrops from, 1432 of liver, 91–96 neonatal jaundice caused by, 1734 neonatal/infant brain abnormalities from, 1538 Metabolic syndrome, fatty liver in, 91 Metabolism, inborn errors of, jaundice and, 1738–1740, 1739b, 1740f Metacarpophalangeal joint, injection of, short-axis approach to, 901 Metanephrogenic blastema, in kidney development, 311, 312f Metanephros, 311, 312f, 1053–1054, 1336–1338 Metastasis(es) adrenal, 425–426, 426f–427f to biliary tree, 188, 192f bladder, 354–355, 355f of breast cancer, lymph node assessment for, 807–810, 808f–810f characterization of, with microbubble contrast agents, 106f drop, 266, 267f gastrointestinal, 266, 267f genitourinary tract tumors and, 354–355 of liver, 124–129, 126f–130f bulls-eye pattern of, 125, 127f calciied, 125, 128f CEUS diagnosis of, 128–129, 130f cystic, 125, 128f echogenic, 125, 128f hypoechoic, 125, 127f–128f iniltrative, 125–128, 126f pediatric, 1746, 1750f target pattern of, 125, 127f neuroblastoma, paratesticular, 1903–1904 ovarian, 585, 586f pancreatic, 251, 251f pediatric, neck, 1666–1667, 1667f peritoneal, 510 renal, 354, 355f retroperitoneal, 464, 465f salivary gland, pediatric, 1639 to spleen, cystic, 148 splenic nodular lesions in, 152, 154f percutaneous needle biopsy of, 608f solid lesions in, 153, 155f testicular, 822b, 826–829, 826b hamartomas as, 829, 829f leukemia as, 827, 828f lymphoma as, 826–827, 828f myeloma as, 827–829 pediatric, 1901

Metastasis(es) (Continued) of thyroid gland, 709, 710f ureteral, 354 Metastatic nodal disease, pediatric, neck, 1666–1667, 1667f Metatarsophalangeal joints, injection of, short-axis approach to, 900f, 901 Methotrexate, in ectopic pregnancy management, 1076, 1076f Metopic craniosynostosis, 1137f MI. See Mechanical index Micrencephaly, 1194 Microabscesses, splenic, 150–152, 154f Microbubbles acoustic behavior of, regimens of, 57t, 58–59, 59f as contrast agents, 53–54, 54f behavior of, incident pressure and, 56–58, 57t disruption of, 64–67, 66f FNH characterization with, 106, 106f, 108t, 109f future of technology for, 68–69, 69f–70f HCC characterization with, 106, 106f hemangioma characterization with, 106, 106f–107f, 108t inertial cavitation and, 67–68 lesional enhancement with, 105, 106f–107f, 109f liver mass characterization with, 105–106, 106f–107f, 108t, 109f–110f MI and, 58, 58b, 105 need for, 56–58, 57f regulation of, 68 safety of, 67–68 resonance of, in ultrasound ield, 58, 59f Microcalciications, in thyroid nodules, papillary carcinoma and, 699, 702f Microcephaly, 1135–1136 fetal brain and, 1194, 1195f sloped forehead in, 1139, 1141f Microcolon, fetal, in MMIHS, 1362–1363, 1788–1791 Microcysts, in breast, 782, 784f Microemboli, cerebral, in pediatric procedures, 1622 Microembolization, intraoperative, TCD detection of, 950 Microencephaly, temperature increase in utero and, 1037 Microgallbladder, in biliary atresia, 1737, 1738f Micrognathia, 1153–1154, 1158f campomelic dysplasia and, 1395 Microlithiasis, 194–195 acute pancreatitis and, 221 testicular, pediatric, 1904, 1904f Microlithiasis, testicular, 833, 833b, 834f Microlobulations, in breast sonography, 789, 791f Micromelia, fetal, 1381, 1381b, 1382f in achondrogenesis, 1391, 1391f in lethal skeletal dysplasia, 1386 in osteogenesis imperfecta type II, 1391–1392, 1392f severe with decreased thoracic circumference, 1387t in hypophosphatasia, 1392 in thanatophoric dysplasia, 1387 Micromelic dysplasia, features of, 1397t Micronodular cirrhosis, 92–93 Micropenis, fetal, 1367 Microphthalmia midface hypoplasia with, 1149f sonographic evaluation of, 1140, 1145f, 1147b temperature increase in utero and, 1037 microRNAs, ibrous cap thinning and, 920 Microstomia, 1154

I-39

Microtia hypotelorism and, 1142f incidence of, 1148 Midaortic syndrome, renal artery stenosis and, 447 Middle cerebral artery (MCA) cerebroplacental ratio and, 1458, 1460f cerebrovascular disease indicators with SCD and, 1600f, 1604f–1605f Doppler ultrasound of in fetal alloimmunization detection, 1421, 1422f in fetal assessment, 1458–1460, 1460f neonatal/infant, in coronal imaging, 1514 occlusion of, leptomeningeal collaterals and, 1610 PSV of blood low in, 1421–1423, 1421b, 1422t as transtemporal approach landmark, 1592, 1593f–1594f Midface abnormalities, 1148–1153. See also Clet lip/palate absent nasal bone as, 1133–1134, 1150f clet lip and palate as, 1151–1153 hypoplasia as, 1148, 1149f–1150f Midface hypoplasia, craniosynostosis and, 1136–1138 Midgut, 1304–1305 physiologic herniation of, 1077, 1077f, 1322, 1323f omphalocele confused with, 1325, 1327f volvulus intestinal malrotation with, 1841–1842, 1843f–1844f “whirlpool” sign of, 1841–1842, 1843f Midline, in sagittal imaging of neonatal/infant brain, 1515, 1516f Midline falx, fetal, sonographic view of, 1024f Migrational abnormalities, corpus callosum agenesis and, 1526–1528 Mikulicz disease, 1635 Milk allergy, gastric mucosa thickening and, 1839–1840 Milk of calcium bile, 194, 195f breast cysts and, 775, 776f–777f cysts, as renal transplantation complication, 653, 657f renal, calyceal diverticula and, 1799, 1800f Miller-Dieker syndrome, 1195 Mineralization abnormal, in achondrogenesis, 1391, 1391f decreased in hypophosphatasia, 1392, 1395f in osteogenesis imperfecta type II, 1392, 1393f of thalamostriate vessels, 1203, 1204f Minimal-access parathyroidectomy (MAP), 749, 750f MIP. See Maximum-intensity projection Mirizzi syndrome, 174, 174f Mirror syndrome, fetal hydrops prognosis and, 1436 Misregistration, of structure, 5, 6f Misregistration artifacts, 3f, 420–421 Mitral regurgitation, fetal, hydrops from, 1423–1424 Mitral stenosis, fetal, hydrops from, 1423–1424 MLCN. See Multilocular cystic nephroma MMIHS. See Megacystis-microcolon-intestinal hypoperistalsis syndrome M-mode echocardiography, fetal, 1275, 1280f–1281f M-mode ultrasound, 9, 9f MMPs. See Matrix metalloproteinases Volume I pp 1–1014 • Volume II pp 1015–1968

I-40

Index

Molar pregnancy. See Hydatidiform molar pregnancy Molar tooth, Joubert syndrome and, 1182 Mole, Breus, 1471 Mondor disease, 768 Monochorionic diamniotic (MCDA) twins, 1019f, 1058f, 1115–1116, 1116f CHD and, 1270–1273 complications of, 1125–1129 TAPS and, 1126–1127 TRAP and, 1127–1129, 1127f–1128f TTTS and, 1125–1126, 1125t, 1126f growth discrepancy in, 1123f IUFD and, 1124f sonographic indings of, chorionicity and, 1119, 1121f Monochorionic monoamniotic (MCMA) twins, 1057, 1115–1116, 1116f complications of, 1125–1129, 1129f TAPS and, 1126–1127 TRAP and, 1127–1129, 1127f–1128f TTTS and, 1125–1126, 1125t, 1126f conjoined twins as, 1130f IUFD and, 1124f sonographic indings of, chorionicity and, 1119, 1121f Mononucleosis of parotid gland, pediatric, 1632f splenic enlargement and, pediatric, 1769 Monorchidism, 1890 Monosomy X. See Turner syndrome Monozygotic (identical) twins, 1115, 1116f Morgagni hernia, 1258, 1718f Morton neuromas, injection for, 904, 904f Morula, 1051, 1051f Motor function, impaired, in spina biida, 1233 Moyamoya angiopathy, SCD and, 1598, 1600f, 1602f, 1608f, 1610 mpMRI. See Multiparametric magnetic resonance imaging MRA. See Magnetic resonance angiography MRI. See Magnetic resonance imaging MSD. See Mean sac diameter Mucinous cystadenocarcinoma, ovarian, 580f, 581 Mucinous cystadenoma, ovarian, 580f–581f, 581 Mucinous cystic neoplasm, 247–248, 247f Mucocele, of appendix, 299, 299f Mucoepidermoid carcinoma, salivary gland, pediatric, 1638 Müllerian ducts cysts of, pediatric, 1908, 1910f duplication of, 1881 uterus and anomalies of, 529, 533–538, 537f categories of, 534, 536f Multicystic dysplastic kidney (MCDK), 361, 362f fetal, 1346–1347, 1346f–1347f pediatric, 1815, 1816f Multicystic mesotheliomas, 508–509 Multidetector computed tomography (MDCT), 238, 241, 241b Multifetal pregnancy amniocentesis in, 1125–1126 amnionicity in, 1115–1116, 1116f determining, 1057, 1058f sonographic determination of, 1117, 1119t triplets and, 1122f aneuploidy screening in, 1091 birth weight discordance in, 1123 cervical assessment in, 1504–1505 chorionicity in, 1115–1116, 1116f sonographic determination of, 1117–1119, 1118f, 1119t, 1120f–1121f triplets and, 1122f congenital malformation in, 1123 irst-trimester scans in, 1017, 1019f general issues with, 1119–1123

Multifetal pregnancy (Continued) growth discordance in, 1123, 1123f hydrops in, 1429, 1429f identiication of, routine ultrasound screening in, 1029 incidence of, 1115 maternal serum alpha-fetoprotein elevation in, 1228 morbidity and mortality in IUFD and, 1123–1125, 1124f IUGR and, 1119–1123 prematurity and, 1119–1123 placental cord insertion and, 1119, 1122f placentation and, 1115–1116, 1116f zygosity in, 1115–1116, 1116f Multilocular cystic nephroma (MLCN), 361–362, 363f pediatric, 1820, 1822f Multinodular goiter, 711, 711f parathyroid adenomas detection and, 746 sonographic appearance of, 727 Multiparametric magnetic resonance imaging (mpMRI), 381–382 prostate cancer, TRUS fusion with, 406–407, 410–411 Multipath artifact, 19–21, 21f Multiple endocrine neoplasia (MEN), 421 pheochromocytomas with, 1826, 1910–1912 type I, 734 type II, 701 type IIA, 734 Multiple gland disease, parathyroid adenomas in, 735, 738f Mumps EF from, 1294 orchitis, 1896 parotitis from, pediatric, 1632 Mural nodules, PAM causing, 782, 783f–784f Murphy sign, 198–199, 199f, 201f Muscle-eye-brain disease, cobblestone lissencephaly in, 1195 Muscle(s) anatomy of, 857–858, 858f atrophy, 859, 860f rotator cuf, 888–889, 891f ultrasound for, 877–878 injuries to, 858–859, 858f–859f medial gastrocnemius, tear of, 858, 859f myofascial defects and, 858–859, 859f ultrasound techniques for, 857–859 Muscular dystrophy, congenital, cobblestone lissencephaly in, 1195 Muscular VSDs, 1281, 1284f Musculoskeletal injection(s) anesthetics for, 901 of Baker cyst, 907–909, 908f bursal, 907–909, 908f for calciic tendinitis, 909, 911f corticosteroids for, 900 of deep tendons, 904–907 abductor, 905–907, 907f biceps, 904–905, 905f–906f hamstring, 905–907, 907f–908f iliopsoas, 905, 906f of ganglion cyst, 907–909, 909f intratendinous, 909–910, 912f of joints, 901–902, 901f–902f materials for, 900–901 pain as indication for, 898 of paralabral cysts, 907–909, 910f–911f perineural, 910–912, 913f supericial peritendinous and periarticular, 902–904 for foot and ankle, 902–904, 903f–904f for hand and wrist, 904, 905f

Musculoskeletal injection(s) (Continued) technique for, 899–900 long-axis approach in, 900–901, 900f–901f short-axis approach in, 900–901, 900f Musculoskeletal system. See also Bone(s); Ligament(s); Muscle(s); Tendon(s) fetal, development of, movements and, 1378 interventions for contrast agents in, 898 technical considerations for, 898–899, 899f pediatric congenital deformities of, 1933 congenital nonhip dislocations of, 1933–1936 inlammation of, 1936–1938, 1937f–1938f inlammation of, noninfectious, 1938 interventional sonography for, 1961, 1963f–1964f trauma to, 1938–1939, 1939f ultrasound techniques for Doppler imaging in, 857, 857f elastography in, 857 extended ield of view in, 857 general considerations in, 856–857 MRI compared to, 856 Mycobacterial infections, pediatric, lymphadenitis diferentiated from, 1660–1663 Mycobacterium avium-intracellulare, 91 Mycobacterium tuberculosis, 329–330, 1852–1853 Myelination development of, 1167 in organogenesis, 1524–1525 Myelocele, open spinal dysraphism and, pediatric, 1681, 1683f Myelocystocele fetal, 1233–1234, 1234f–1235f pediatric, 1683–1684, 1686f Myelodysplasia, 1382 Myelolipomas, adrenal, 420–421, 420b, 420f Myeloma, testicular, 827–829 Myelomeningocele(s), 1218 deinition of, 1225t fetal surgery for, 1233 no Chiari II malformation and search for, 1526, 1529f open compared to closed, 1226 open spinal dysraphism and, pediatric, 1681, 1683f pathogenesis of, 1226 pediatric, neurogenic bladder in, 1907 spine embryology and, 1674 Myeloschisis, 1218, 1226 deinition of, 1225t sonographic indings in, 1218 Myocardium, fetal, hydrops from decreased function of, 1425 Myofascial defects, 858–859, 859f Myoibroblastic tumor, inlammatory, pediatric, 1812 Myoibromatosis, congenital infantile, 1664, 1665f Myometrium abnormalities of, 538–541 adenomyosis as, 540–541, 540b, 542f leiomyoma as, 538–540, 539f, 540b leiomyosarcomas as, 540, 541f calciications of, 531–533, 533f–534f layers of, 531 veins of, 531–532, 533f Myopathy, congenital, atypical hips and, 1932 Myositis, complicated lymphadenitis with, 1662f N Nabothian cysts, 533, 535f, 1499 Nanodroplets, therapeutic use of, 68 Nasal bone, fetal absent, 1133–1134, 1150f in aneuploidy screening, 1093–1095, 1094b, 1094f

Index Nasal bone, fetal (Continued) NT in, 1094 in trisomy 21, 1099–1100, 1099f Nasal placodes, 1134 NASCET. See North American Symptomatic Carotid Endarterectomy Trial Nasolacrimal ducts, obstruction of, dacryocystocele from, 1143, 1147f National Council on Radiation Protection and Measurements (NCRP), 38–39 Near ield, of beam, 8 Near-ield structures, neonatal/infant brain and, duplex Doppler sonography of, 1585, 1588f NEC. See Necrotizing enterocolitis Neck, fetal. See also Face, fetal abnormalities of, 1154–1163 cervical teratoma as, 1159, 1161f goiter as, 1159–1163, 1162f lymphatic malformations as, 1159, 1161f NT and, thickening of, 1154–1159 thyromegaly as, 1159–1163 embryology and development of, 1134 hydrops from, 1425, 1426f normal, sonography of, 1135, 1136f Neck, pediatric. See also Infrahyoid space, pediatric; Suprahyoid space, pediatric carotid space of, 1650 congenital abnormalities of, 1651–1654 branchial, 1651, 1651f–1653f cervical teratomas and, 1654, 1654f dermoid cysts and, 1652–1654, 1654f ectopic thymus and, 1652, 1653f epidermoid cysts and, 1652–1654 danger space of, 1650 deep cervical fascia of, 1628, 1629f iatrogenic lesions and, 1658, 1661f inlammatory disease of, 1658–1664 ibromatosis coli and, 1663–1664, 1663f lymph nodes and, 1658–1663, 1661f–1663f lesions of, 1961, 1967f neoplasms of, 1664–1667 congenital infantile myoibromatosis as, 1664, 1665f granulocytic sarcomas as, 1666, 1667f lymphoma as, 1665, 1665f malignant, 1664–1667 metastases and, 1666–1667, 1667f neuroblastoma as, 1665–1666, 1666f pilomatricoma as, 1664, 1664f rhabdomyosarcoma as, 1665, 1666f normal anatomy of, 1628–1629 prevertebral space of, 1650 retropharyngeal space of, 1650 supericial fascia of, 1628, 1629f vascular anomalies of, 1654–1655 malformations, 1655–1658, 1655b, 1657f, 1659f tumors, 1655, 1655b, 1656f Neck masses of, in carotid region, 947–948, 949f–950f Necrotizing enterocolitis (NEC), 1854–1855, 1855b, 1856f Necrotizing fasciitis, of perineum, 846–847 Needle(s). See also Biopsy(ies), percutaneous needle large-caliber, uses of, 600 for musculoskeletal interventions, technique for, 898–899, 899f for percutaneous needle biopsies guidance systems for, 600, 601f selection of, 599–600 visualization in, 601–603, 602f small-caliber, uses of, 599–600

Neisseria gonorrhoeae, 846 Neonatal brain sonography. See Brain, neonatal/ infant, imaging of Neonatal resuscitation, in fetal hydrops, 1437 Nephrectomy, evaluation ater, 374–375 Nephritis, acute interstitial, 370 Nephroblastoma, pediatric, 1818 Nephroblastomatosis, pediatric, 1818 Nephrocalcinosis, 339–340, 340f, 359 cortical, 339 pediatric, 1798, 1798b, 1798f medullary, 339, 340f pediatric, 1798–1799, 1799f Nephroma cystic, multilocular, 361–362, 363f, 1820, 1822f mesoblastic congenital, 1352–1353, 1353f pediatric, 1818–1820, 1821f Nephronophthisis familial juvenile, 359 pediatric, 1815–1816, 1816f Nephropathy HIV-associated, 332–333, 333f lithium, 361, 363f relux, 327, 327f Nephrosis, congenital, maternal serum alphafetoprotein elevation in, 1228 Nephrotoxic drugs, AKI and, 1796 Nerve sheath tumors, 871, 872f Nerve(s) anatomy of, normal, 864–865, 865f dysfunction of, 865–866, 866f ilioinguinal, entrapment of, ater herniorrhaphy, 496 subluxation of, 865–866 ultrasound techniques for, 864–866 Nesidioblastosis, pediatric pancreatic enlargement and, 1865, 1865f Neural arch, ossiication of, 1218 Neural canal, in spine embryology, 1217 Neural crest cells, 1133–1134, 1672–1673 Neural plate, in spine embryology, 1217 Neural process, ossiication of, 1218, 1219f Neural tube closure of, 1524, 1525b abnormalities of, 1218 brain disorders of, neonatal/infant, 1526– 1532 Chiari malformations and neonatal/infant disorders of, 1526, 1526b, 1527f–1529f corpus callosum agenesis and neonatal/infant disorders of, 1526–1528, 1529b, 1530f–1533f corpus callosum lipoma and neonatal/infant disorders of, 1529, 1533f Dandy-Walker malformation and neonatal/ infant disorders of, 1529–1532, 1530b, 1533f–1534f formation of, 1524, 1672–1673, 1673f in spine embryology, 1217, 1218t Neural tube defects (NTDs), 1183. See also Spina biida CDH and, 1263 descriptions of, 1218 risk factors for, 1225b spina biida and, 1223 teratogens inducing, 1218 ultrasound screening of, 1226–1228 X-linked, 1226 Neurenteric cysts fetal, 1256 pediatric, 1686–1688 Neurenteric istula, 1674

I-41

Neuroblastoma(s) adrenal, 427–428 fetal, 1353–1354, 1353f pediatric, 1825–1826, 1826f metastatic, paratesticular, 1903–1904 pediatric intraspinal, 1689–1691, 1693f liver metastases from, 1746, 1750f metastasis of, to teste, 1901 neck, 1665–1666, 1666f ovarian, 1880 presacral, 1914, 1915f Wilms tumor mistaken for, 1818 Neuroepithelial tumors, intracranial, fetal, 1208 Neuroibroma(s) bladder, 356 paratesticular, 1903–1904 plexiform, in intraoperative procedures, 1621f Neuroibromatosis hemimegalencephaly associated with, 1195 prenatal intracranial tumors in, 1208 renal artery stenosis and, 447 rhabdomyosarcoma associated with, 1908 type 1 megalencephaly associated with, 1194–1195 neuroblastoma with, pediatric, 1825 pheochromocytomas with, 1826 Neurogenic bladder, 372–374, 373f pediatric, hydronephrosis and, 1788 Neurogenic tumors, pediatric, 1724 Neurologic development, obstetric sonography and, 1040–1041 Neuroma, interdigital, injection for, 904, 904f Neuronal proliferation, in organogenesis, 1524–1525 Neurons development of, 1167 neonatal/infant, injury to, difuse, duplex Doppler sonography and, 1580 Neurulation, 1053, 1179 in spine embryology, 1217, 1672, 1673f Nevus, giant pigmented, choroid plexus papillomas in, 1209 Nipple discharge, ultrasound examination for, 798–799, 799f–801f Nitric oxide, inhaled, 1578 Nodular lesions. See also hyroid gland, nodular disease of splenic, 148–152, 151f–154f thyroid, 694–723 Nonarthrosclerotic carotid disease, 944–948. See also Carotid artery(ies), nonarthrosclerotic diseases of ultrasound examination of, 916 Noncommunicating rudimentary uterine horn, 546 Non-Hodgkin lymphoma, 125, 264–266 pediatric, neck, 1665 of peritoneum, 513, 517f splenic lesions in, 152–153, 154f Nonlinear echoes, contrast agents and, 58–64 amplitude and phase modulation imaging and, 64, 65f harmonic B-mode imaging and, 60 harmonic spectral and power Doppler and, 60–61, 60f–62f plane-wave contrast imaging and, 64 pulse inversion Doppler imaging and, 63–64 pulse inversion imaging and, 62–63, 62f–63f temporal maximum intensity projection imaging and, 64, 65f tissue harmonic imaging and, 61–62 Nonne-Milroy lymphedema, 1403–1404, 1405f Nonobstructive cardiomyopathy, 1294–1295 Volume I pp 1–1014 • Volume II pp 1015–1968

I-42

Index

Nonrhizomelic chondrodysplasia punctata, 1399 Nonright-handedness, obstetric sonography and, 1040 Nonseminomatous germ cell tumors (NSGCTs), 822b, 823–824, 825f Noonan syndrome characteristics of, 1887 low-set ears in, 1148 pulmonic stenosis and, 1292 Norepinephrine, secretion of, 417 North American Symptomatic Carotid Endarterectomy Trial (NASCET), 916, 929 Nose, fetal abnormalities of, 1151 bones of absent, 1133–1134, 1150f in aneuploidy screening, 1093–1095, 1094b, 1094f NT in, 1094 in trisomy 21, 1099–1100, 1099f normal sonographic appearance of, 1135f saddle, in skeletal dysplasia, 1382 Notochord disorders of midline formation, 1689 integration, 1686–1689 in spine embryology, 1216–1217, 1217f, 1218t Notochordal process, in spine embryology, 1217, 1217f, 1218t Notochordal remnants, in spine embryology, 1217, 1217f, 1218t NSGCTs. See Nonseminomatous germ cell tumors NT. See Nuchal translucency NTDs. See Neural tube defects Nuchal cord, 1483–1484 Nuchal fold, in trisomy 21, 1097–1099, 1099f, 1154–1159 Nuchal translucency (NT) in aneuploidy risk assessment, 1018–1019, 1019f, 1049 CRL compared to, 1089, 1090f echogenic material in yolk sac and, 1067–1068 in fetal nasal bone assessment, 1094 HPE and thickened, 1096f measurement technique for, standardization of, 1091–1093, 1092b with normal karyotype, 1095–1097, 1096f screening of, human studies on, 1039–1040 thickened abdominal wall defects and, 1095–1096 anencephaly and, 1096f congenital heart defects and, 1095–1097, 1096f in cystic hygroma, hydrops and, 1425 cystic hygroma and, 1096f diaphragmatic hernia and, 1095–1096 fetal neck conditions and, 1154–1159 megacystitis and, 1096f omphalocele and, 1096f in trisomy 13, 1093 in trisomy 18, 1093 in trisomy 21, 1089, 1090f Nutcracker syndrome (nutcracker phenomenon), 460–461, 462f, 838, 839f Nutrients, yolk sac in transfer of, 1057 Nyquist limit, 29–30, 32f O Obesity fatty liver in, 91 renal artery duplex Doppler sonography in, 447 Observed-to-expected lung-to-head ratio (o/e LHR), 1262

Obstetric sonography. See also Pregnancy, irst trimester of auditory response in, 1038 bioefects of animal research and, 1038–1039 behavioral changes and, 1040–1041 birth weight and, 1040 childhood malignancies and, 1041 congenital malformations and, 1041 delayed speech and, 1040 Doppler ultrasound and, 1041 dwell time and, 1036 dyslexia and, 1040 human studies on, 1039–1041 instrument outputs and, 1035–1036 mechanical, 1038 neurologic development and, 1040–1041 nonright-handedness and, 1040 scanning mode and, 1035 system setup and, 1035–1036, 1035f–1037f thermal, 1036–1038 cell aggregation in, 1038 cell membrane alteration from, 1038 contrast agent avoidance in, 1038 default output power for, 1035 Doppler mode, sample volume and velocity range in, 1036 duration of, as function of TI in, 1035–1036, 1036f, 1042t equipment for, 1015–1016 ield of view in, 1036, 1036f focal depth in, 1036, 1036f frame rate in, 1036 guidelines for, 1016–1022 in irst trimester, 1016–1019, 1016b, 1017f–1020f level I examination in, 1019–1020, 1021f–1029f level II examination in, 1019–1022, 1023b in second and third trimesters, 1019–1022, 1020b hemolysis from, 1038 in hydrops diagnosis, 1432–1433 MI in, 1035 personnel for, 1015–1016 receiver gain in, 1036 for routine screening, 1022–1031 beneits of, 1030b for fetal malformations, diagnostic accuracy of, 1030 in gestational age estimation, 1022–1029 perinatal outcomes and, 1029–1030 prudent use of, 1030–1031 three- and four-dimensional ultrasound in, 1030, 1042, 1043f in twin/multiple pregnancy identiication, 1029 safety of, 1034–1035 guidelines for, 1041–1042, 1042t, 1043f tactile sensation in, 1038 training for, 1015–1016 transducer heating in, 1038 transducer selection for, 1035 volume imaging in, 1030 Obstructed hernias, 496–497 Obstructive cystic renal dysplasia, 1347–1348, 1347f–1348f Obstructive uropathy, CKD and, 1796–1798 Occipital issure, neonatal/infant, development of, 1520–1521 Occipital horn(s) atrium of fetal, transverse measurement in, 1178 neonatal/infant in coronal imaging, 1515 in corpus callosum agenesis, 1528, 1530f–1531f

Occipital horn(s) (Continued) in posterior fontanelle imaging, 1517, 1518f Occipital lobe cortex, neonatal/infant, in coronal imaging, 1514f, 1515 Occipitofrontal diameter, in gestational age determination, 1446, 1447f Occlusion, 27 o/e LHR. See Observed-to-expected lung-to-head ratio OEIS complex, 1328–1329, 1329f, 1365–1366, 1689 OHS. See Ovarian hyperstimulation syndrome Oligodactyly deinition of, 1399 fetal, 1406f Oligohydramnios deinition of, 1340 diagnostic signiicance of, 1340–1341 early, 1066, 1067f fetal lung size and, 1244 in sirenomelia, 1238 Oligospermia, prostate and, 393 Omental cakes, 266, 267f Omentum cysts of, pediatric ovarian cysts diferentiated from, 1875 greater, 505, 505f herniated, 1902 infarction of pediatric, appendicitis diferentiated from, 1858–1860, 1858f right-sided segmental, 288, 289f, 521, 523f lesser, 505 Omohyoid muscle, 692f, 694 Omphalocele detection of, early, 1018–1019, 1020f fetal, 1325–1326, 1326f associated conditions with, 1325, 1327f cloacal exstrophy and, 1328 epidemiology of, 1325 management of, 1325–1326 pentalogy of Cantrell and, 1329 prenatal diagnosis of, 1325, 1327f liver herniation in, 80 maternal serum alpha-fetoprotein elevation in, 1228 in Miller-Dieker syndrome, 1195 with spina biida, 1233 thickened NT and, 1096f in triploidy, 1105f in trisomy 18, 1103, 1103f fetal, 1325 Omphalomesenteric duct, 1059 Oncocytoma, renal, 348–351 Oncotype DX test, 396 One-Stop Clinic to Assess Risk (OSCAR), 1090 Oocyte, transport of, 1049 Ophthalmic artery cerebrovascular disease indicators with SCD and low in, 1599f evaluation of, orbital approach to, 1592, 1596f Opisthorchiasis, biliary tree and, 178–179 Opportunistic infection, Pneumocystis carinii and, 91, 91f Optison, 56 harmonic emission from, 58–59, 59f Oral contraceptives, hepatic adenomas and, 1746 Oral-facial-digital syndrome 4, 1395 Orbital window, for TCD sonography, 1592, 1596f Orbits, fetal abnormalities of, 1140–1143 anophthalmia as, 1140, 1145f coloboma as, 1143, 1146f congenital cataracts as, 1143, 1147b dacryocystocele as, 1143, 1147f exorbitism as, 1140

Index Orbits, fetal (Continued) hypertelorism as, 1140, 1141b, 1144f–1145f, 1149f hypotelorism as, 1140, 1140b, 1142f–1144f microphthalmia as, 1140, 1145f, 1147b proptosis as, 1140 normal sonographic appearance of, 1135f Orchitis, 845–846 isolated, 1896 pediatric, 1896 sonographic appearance of, 846, 847f–849f Organ of Giraldés, 820–821 Organ transplantation, 623–624. See also Liver transplantation; Pancreas transplantation; Posttransplant lymphoproliferative disorder; Renal transplantation Organogenesis deinition of, 1524 stages of, 1524, 1525b, 1525f Oriental cholangiohepatitis, 179 Oropharynx, teratomas of, 1159 Ortolani test, for hip stability, 1923 OSCAR. See One-Stop Clinic to Assess Risk Osler-Weber-Rendu disease, 104 Ossiication centers primary, 1091 secondary, 1091, 1378f Osteitis pubis, sports hernia and, 486–487, 489f Osteoarthritis, 869, 869f acromioclavicular joint, 893, 894f Osteogenesis, normal, 1091 Osteogenesis imperfecta, 1391–1392 anencephaly diferentiated from, 1179 bowing of long bones in, 1381–1382 classiication of, by type, 1394t facial proile in, 1394f fractures in, 1392, 1393f sonographic appearance of, 1380f 3-D reconstruction of, 1385f type I, 1391–1392, 1393f, 1394t, 1399 bowing of femur in, 1380f type II, 1391–1392, 1392f–1394f, 1394t calvarial compressibility in, 1382, 1392, 1393f diagnosis of, 1376–1377 hypophosphatasia diferentiated from, 1392–1395 type III, 1391–1392, 1393f, 1394t, 1399 type IV, 1391–1392, 1394t, 1399 type V, 1391–1392 wormian bones in, 1139 Osteomyelitis, pediatric, 1936–1938, 1938f of costochondral junction, aspiration and drainage of, 1963f Ostium primum, 1279 Ostium primum ASD, 1279–1280, 1283f Ostium secundum, 1279 Ostium secundum ASD, 1279–1280, 1282f Otocephaly, 1148 Outlow tracts, fetal, routine sonographic view of, 1025f Ovarian artery(ies), 565–566, 565f pediatric, 1875 Ovarian crescent sign, 581 Ovarian cycle, 1051, 1051f Ovarian follicles, 1049 Ovarian hyperstimulation syndrome (OHS), 572, 572f Ovarian remnant syndrome, 571 Ovarian vein(s) thrombophlebitis, 589–590, 589f thrombosis of, 369, 589–590, 589f Ovary(ies) anatomy of, 564–570, 565f calciication in, 566–568

Ovary(ies) (Continued) cystadenocarcinoma of mucinous, 580f, 581 serous, 580–581, 580f cystadenoma of mucinous, 580f–581f, 581 serous, 580–581, 580f cysts in dermoid, 582–584, 583f fetal, 1369, 1369f functional, 570–571, 571f hemorrhagic, 570–571, 571f, 575 menstrual cycle and follicular, 568 neonatal, 1876f paratubal, 573 parovarian, 573 percutaneous management of, 618–619 peritoneal inclusion, 573, 573f postmenopausal, 569–570, 571f surface epithelial inclusion, 569, 573 in triploidy, 1105f edema of, massive, 578 endometriosis in, 574–576, 575f–576f fetal, cysts in, 1369, 1369f hyperstimulation of, 572, 572f lymphomas of, 585 in menstrual cycle, 1050f menstrual cycle changes to, 568–569, 569f neoplasms of, 578–585 borderline, 580f, 581 clear cell, 581, 582f cystadenocarcinomas as, 580–581, 580f cystadenomas as, 580–581, 580f–581f cystic teratomas as, 582–584, 582b, 583f dysgerminomas as, 584, 584f endodermal sinus, 585 endometrioid, 581 ibromas as, 585, 586f germ cell, 582–585 granulosa cell, 585 metastatic, 585, 586f ovarian cancer as, 578–579 Sertoli-Leydig cell, 585 sex cord-stromal, 585 surface epithelial-stromal, 579–582, 580f–582f thecomas as, 585 transitional cell, 581–582, 582f types of, 579t nonneoplastic lesions of, 570–578 cysts as, functional, 570–571, 571f endometriosis as, 574–576, 575f–576f ovarian remnant syndrome as, 571 polycystic ovarian syndrome as, 573–574, 574f pregnancy-associated, 572, 572f polycystic ovarian syndrome and, 573–574, 574f postmenopausal, 569 cysts in, 569–570, 571f pregnancy-associated lesions of, 572, 572f punctate echogenic foci in, 566–568, 568f shape of, 565–566 sonography for normal appearance in, 566–568, 567f technique in, 566 torsion of, 576–578, 577f volume of, 566 Ovary(ies), pediatric, 1873 abnormalities of, 1875–1881 cysts of, 1873–1877 hemorrhagic, 1877, 1878f–1879f in polycystic ovarian disease, 1877–1878, 1879f torsion and, 1875–1876, 1876b, 1877f ectopic, 1874f edema of, massive, 1878–1879, 1879f

I-43

Ovary(ies), pediatric (Continued) macrocysts of, 1873–1875 neoplasms of, 1879–1881, 1880b, 1880f normal, 1874f torsion of, 1875–1876, 1876b, 1877f volume measurements for, 1873, 1875t Ovotestis, pediatric, 1891, 1891f Ovulation, 1049 Oxygenation, extracorporeal membrane. See Extracorporeal membrane oxygenation P Pacchionian, 1177 Pachygyria, in lissencephaly, 1195 PACs. See Premature atrial contractions PACS. See Picture archiving and communications system Paget-Schroetter syndrome, pediatric, 1721, 1723f Painless (silent) thyroiditis, 725–727 Palate. See also Clet lip/palate clet, 1151–1153 secondary fetal, 1135, 1135f isolated clet of, 1153 Palmar arch, 977–978, 980f PAM. See Papillary apocrine metaplasia Pampiniform plexus, 565–566, 565f “Pancake” kidneys, pediatric, 1785 Pancreas abscesses of, 230 anatomy of, 210–219 surrounding structures and, 218–219, 220f variants of, 218 annular, small bowel obstruction and, 1308 body of, 211, 211f–212f carcinoma of, 236–238, 238b color Doppler ultrasound for, 241, 241b, 241f–243f, 241t detection of, 238–241 resectability imaging in, 241 ultrasound indings for, 238–241, 239f–240f CEUS for, 251 cystic neoplasms of, 243–248, 243t intraductal papillary mucinous, 245–247, 245f–246f mucinous, 247–248, 247f rare, 248, 248b serous, 243, 244f–245f solid-pseudopapillary tumor, 248, 248f cysts of, 242–248, 243f congenital, 1865 fetal, 1320 high-risk features of, 243b simple, 243, 244f VHL disease and, 243, 244f embryology of, 215–218, 218f endocrine tumors of, 248–249, 249f–250f, 249t enlarged, in acute pancreatitis, 222, 223f fatty, 215, 216f–217f fetal, 1319–1320 annular, 1320, 1321f cysts of, 1320 head of, 211–213, 213f–214f lipoma of, 249–251, 250f metastases of, 251, 251f neoplasms of, 236–241 periampullary, 236 unusual and rare, 249–251 parenchyma of, 213–215, 215f–217f pediatric, 1862–1865 neoplasms of, 1865, 1865f normal anatomy of, 1862 pancreatitis and, 1862–1865, 1864f–1865f sonographic technique for, 1862 Volume I pp 1–1014 • Volume II pp 1015–1968

I-44

Index

Pancreas (Continued) percutaneous needle biopsy of, 604–605, 605f pseudoaneurysms of, 230, 230f pseudocysts of acute pancreatitis complications with, 228–229, 229f chronic pancreatitis complications with, 232, 233f–234f drainage of, 230, 615–617, 617f pediatric pancreatitis and, 1864–1865, 1865f pseudomass of, 214–215, 217f shape of, 214–215, 217f size of, 214, 216f sonographic technique for, 210–219, 211f tail of, 213, 214f Pancreas divisum, 218, 220f pediatric pancreatitis and, 1862–1864, 1864f Pancreas transplantation, 666–682 abnormal, 676–682 AVF as, 678, 680f luid collections as, 682, 683f pancreatitis as, 679–682, 681f pseudoaneurysms as, 678, 680f rejection as, 678–679, 681f thrombosis as, 677–678, 678f–679f alloimmune arteritis ater, 677 bladder drainage in, 668–672, 675f CEUS for, 676 duodenal leaks ater, 682 endocrine drainage in, 672, 675f enteric drainage in, 672 infection ater, 682 normal appearance ater, 676, 676f surgical techniques for, 668–676, 673t, 675f venous drainage in, 672–676 Pancreatic duct, 215–218, 219f–220f Pancreaticoduodenectomy, 233 Pancreatitis acute, 219–230 abscess complications of, 230 biliary sludge and, 221 causes of, 221, 221t clinical spectrum of, 220–221 common bile duct stones and, 221 complications of, 225–230, 225b enlarged pancreas from, 222, 223f luid collection complications in, 228, 228f gallstones and, 221 imaging approach for, 221–222, 221b necrosis complications of, 230 pseudocyst complications in, 228–230, 229f treatment for complications of, 230 ultrasound indings in, 222–225, 222t, 223f–228f vascular complications of, 230, 230f–231f autoimmune, 236, 237f chronic, 230–236 imaging approach for, 231 masses associated with, 233–236, 235f–237f portal vein thrombosis in, 232–233, 235f pseudocysts in, 232, 233f–234f sclerosing, 236 splenic vein thrombosis in, 232–233, 234f–235f tumefactive, 236 ultrasound indings on, 231–233, 231f–235f lymphoplasmacytic sclerosing, 236 ater pancreas transplantation, 679–682, 681f pediatric, 1862–1865, 1864f–1865f Pancreatoblastoma, pediatric, 1865 Pancytopenia, Fanconi, 1400, 1402f Panovarian cysts, 573 Pantaloon hernias, 493–494, 495f Papillary apocrine metaplasia (PAM), 778f, 779, 780f–781f mural nodules caused by, 782, 783f–784f

Papillary carcinoma ethanol ablation of cervical nodal metastasis from, 720, 721f of thyroid gland, 698–701, 701f–705f cystic, sonographic features of, 705f, 713 pediatric, 1648, 1649f Papillary cystadenomas, of epididymis, 840–841 Papillary microcarcinoma, of thyroid, 701, 706f Papillary necrosis, 328–329, 329b, 329f Papillary process, 75–76 Papilloma(s) breast, 769–771, 770f intracystic, 782, 783f intraductal, 799, 799f–800f peripheral, 799, 800f choroid plexus Aicardi syndrome and giant pigmented nevi in, 1209 neonatal/infant, 1562, 1565f in neonatal/infant brain, duplex Doppler sonography of, 1588f VM with, 1177–1178 transitional cell, lower urinary tract, pediatric, 1910–1912 VM with, 1177–1178 PAPP-A. See Pregnancy-associated plasma protein A Paracentesis, 610, 610f Paracoccidiomycosis, 423 Paradidymis, 820–821 Paragangliomas, carotid body tumors and, 947–948, 949f Paralabral cysts, injection for, 907–909, 910f–911f Parallel orientation, in breast sonography not (taller-than-wide), 789–790, 792f wider-than-tall, 797, 797f Paralytic ileus, 294f, 295 Parameniscal cysts, 907–909 Paramesonephric duct cysts, pediatric. See Müllerian ducts Parapelvic cysts, 359, 360f Paraplegia, traumatic, neurogenic bladder in, 1907 Parapneumonic collections, in pediatric chest, 1710–1711 Pararenal spaces, inlammation in, in acute pancreatitis, 224–225, 225f Parasagittal infarction, from hypoxic-ischemic injury in full-term infant, 1541 Parasites, fetal brain and, 1203–1204 Parasitic diseases of genitourinary tract, 331 of liver, 87–90, 89f–90f Paratenon, 859 Parathyroid glands. See also Hyperparathyroidism adenomas of carcinomas diferentiated from, 735–736, 738f carotid sheath/undescended, 740, 742f combined modalities for accuracy with, 748 compression for detection of, 739 CT accuracy for, 748, 748f echogenicity of, 735, 736f ectopic locations of, 739–741 false-negative examination for, 745b, 746 false-positive examination for, 745–746, 745b ine-needle aspiration biopsy accuracy for, 746 hypoechoic, 735 imaging accuracy with, 746–749 inferior, 738–739, 739f internal architecture of, 735, 736f intrathyroid, 740, 742f localization of, 736–741 mediastinal, 740, 741f, 748 MRI accuracy in, 748, 749f multiple gland disease in, 735, 738f percutaneous needle biopsy of, 750–751, 753f pitfalls in examination of, 745–746, 745b

Parathyroid glands (Continued) retrotracheal/retroesophageal, 739–740, 740f scintigraphy accuracy for, 747, 747f shape of, 735, 735f size of, 735, 737f sonographic appearance of, 735–736 sonographic examination and typical locations in, 736–739, 739f superior, 738–739, 739f surgical removal of, 749, 750f ultrasound accuracy for, 746–747, 748f vascularity of, 735, 737f anatomy of, 732–733, 733f autotransplantation of tissue of, recurrent hyperparathyroidism from, 742–744, 743f carcinoma of adenomas diferentiated from, 735–736, 738f primary hyperparathyroidism from, 734 ectopic, 733, 739–741 embryology of, 732–733 enlarged, in secondary hyperparathyroidism, 745 eutopic, 733 inferior, 733 pediatric, 1650, 1650f supernumerary, 733 Parathyroid hormone, chief cells in production of, 733 Parathyroidectomy, minimal-access, for primary hyperparathyroidism, 749, 750f Parathyromatosis, in persistent hyperparathyroidism, 744, 744f Paratubal cysts, 573 Paraumbilical hernias, 492 Paraumbilical veins, pediatric low direction in, in portal hypertension, 1752, 1757, 1758f in intrahepatic portal hypertension, 1761 Paraurethral cysts, pediatric, 1883–1884 Parenchymal abscess, pediatric renal transplantation and, 1812 Parenchymal calciication, renal, 339–340, 340f Parenchymal junctional defects, 313, 314f Parietal peritoneal line, 510–511 Parinaud oculoglandular syndrome, 1633–1634 Parotid glands, pediatric accessory, 1630 acinic cell carcinoma of, 1638, 1639f anatomy of, 1630, 1630f bacterial infections in, 1632–1633, 1632f deep lobe of, 1630 hemangiomas of, 1636, 1637f lipomas of, 1639 lymphatic malformation of, 1636, 1637f nodal enlargement in, 1633–1634 peripheral nerve sheath tumors of, 1639 Parotid space, pediatric, 1629, 1630f cystic lesions of, 1639, 1640b Parotitis HIV and, 1635, 1636f juvenile, recurrent, 1634, 1634f from mumps, 1632 Parovarian cysts, pediatric, 1875, 1876f Paroxysmal supraventricular tachycardia, fetal, 1296, 1296f Partial molar pregnancy, 1078, 1080f Partial subclavian steal, 952–953, 953b, 953f Partial-thickness rotator cuf tears, 887–888, 889f–890f Particulate ascites, 507 Parvovirus infection, fetal hydrops from, 1431–1432, 1431f massive ascites in, 1418–1419 Pascals, 16

Index Patau syndrome. See Trisomy 13 Patellar dislocation, congenital, pediatric, 1934, 1935f Patent ductus arteriosus, intracranial RI and, 1576 Patent urachus, 322 pediatric, 1791 PCA. See Posterior cerebral artery PCA3 score, 396 PCOS. See Polycystic ovarian syndrome Peak end diastolic ICA/CCA ratio, in assessing degree of carotid stenosis, 930 Peak systolic ICA/CCA ratio in assessing degree of carotid stenosis, 930 in internal carotid artery stenosis evaluation, 937 Peak systolic velocity (PSV), 450 arterial stenosis and, 969, 971f bypass grat dysfunction and, 974–975 in determining carotid stenosis, 929–930 of MCA blood low, 1421–1423, 1421b, 1422t Pectoralis minor muscle, 878–879 Pediatric patients. See also Adrenal gland(s), pediatric; Bladder, pediatric; Hip(s), pediatric; Liver, pediatric; Neck, pediatric; Spinal canal, pediatric; Transcranial Doppler sonography, pediatric; Urinary tract, pediatric adrenal sonography for, 1820–1827 female anatomy in, normal, 1872–1875 pelvic sonographic technique for, 1870–1872 renal artery stenosis and, 447 spleen of, 1769–1772 Pedicles in lateral longitudinal scan plane, 1223f in lateral transaxial scan plane, 1222f in posterior angled transaxial scan plane, 1224f spina biida in, 1228, 1229f–1230f Peliosis, splenic, 147 Peliosis hepatis, 104, 104f Pelvic abscesses, 283 drainage of, 612, 613f Pelvic adnexa. See Adnexa Pelvic congestion syndrome, 461–463, 463f as adnexal vascular abnormality, 590, 590f Pelvic inlammatory disease (PID), 566 fallopian tubes and, 587–589, 588f IUDs and, 587 pediatric, 1885–1887, 1886b, 1886f sonographic indings of, 587t tubo-ovarian complex and abscess in, 588–589, 588f, 1886–1887, 1886f Pelvic kidney, 318, 318f fetal, 1344–1345, 1344f pediatric, 1908 Pelvic masses in adult women, sonographic evaluation of, 590–591, 591t gastrointestinal tract, 592 nongynecologic, 591–592 postoperative, 591 urinary tract, 592 Pelvic sonographic technique, pediatric, 1870– 1872. See also speciic organs Pelvic varices, pediatric hemorrhagic ovarian cyst diferentiated from, 1877, 1879f in portal hypertension, 1760f Pelvis fetal, routine sonographic views of, 1021, 1026f free luid of, ectopic pregnancy and, 1072, 1073f pediatric, sonographic technique for, 1870–1872 TAS for, 564 Pelvoinfundibular atresia, with MCDK, 1346 Penile chordee, fetal, 1367

Pentalogy of Cantrell, 1295 fetal abdominal wall and, 1329 OEIS diferentiated from, 1328–1329 Peptic ulcer, 299, 300f Percent free PSA (%fPSA), 395 Percutaneous cholangiography and drainage, pediatric, 1956, 1959f Percutaneous needle biopsy. See Biopsy(ies), percutaneous needle Percutaneous umbilical cord blood sampling (PUBS), 1434–1435, 1434f–1435f Perluorocarbons, in contrast agents, 56, 107, 111f Perforation, of bowel, in Crohn disease, 274–275, 277f Perfusion disruption-replenishment imaging measuring, 66–67, 67f luxury, cerebral infarction with, 1580–1581, 1584f Perianal inlammation, in Crohn disease, 276, 281f, 305–306 Perianal inlammatory disease, transanal sonography in, 305–307, 306b, 307f Periaortitis, chronic, 439–440, 464, 465f Peribiliary cysts, liver and, 82–83 Pericardial efusion, fetal, 1258, 1258f in hydrops, 1416, 1418f Pericardial hernias, 1258, 1262 Pericholecystic luid collection, in perforated gallbladder, 200 Pericholecystic hyperechogenicity, NEC and, 1854–1855 Periductal mastitis, of breast, 771, 771f Perienteric sot tissues, in acute abdomen, 281–282 Perihepatitis, gonococcal or chlamydial, PID and, 1887 Perimembranous VSDs, 1281 Perinephric abscesses acute pyelonephritis and, 325 pediatric renal transplantation and, 1812 ater renal transplantation, 664–665 Perinephric luid collections, pediatric renal transplantation and, 1809, 1811f Perineum, necrotizing fasciitis of, 846–847 Period, of sound wave, 2, 2f Peripheral arteries, 965–978 aneurysms of, lower extremity, 971–972, 972f AVF of, 973–974, 974f lower extremity, 966–975 aneurysm of, 971–972, 972f AVF of, 973–974, 974f AVMs of, 973 bypass grats of, 974–975, 975f normal anatomy of, 966 occlusion of, 967–968, 967f–969f pseudoaneurysm of, 972–973, 973f stenosis of, 968–971, 969f–971f ultrasound examination and protocol for, 966–967, 967f occlusion of, lower extremity, 967–968, 967f–969f pseudoaneurysms of, lower extremity, 972–973, 973f sonographic examination technique for, 965 stenosis of evaluation of, 965–966, 966f lower extremity, 968–971, 969f–971f tardus-parvus waveforms in, 965–966 upper extremity, 975–978 aneurysm of, 976 normal anatomy of, 975–976, 976f occlusion of, 976 radial artery evaluation for coronary bypass grat and, 977–978, 980f

I-45

Peripheral arteries (Continued) stenosis of, 976, 978f–979f thoracic outlet syndrome in, 976–977, 980f ultrasound examination and protocol for, 976 Peripheral cholangiocarcinoma. See Intrahepatic cholangiocarcinoma Peripheral nerves normal anatomy of, 864–865, 865f sheath tumors, parotid gland, pediatric, 1639 Peripheral sexual precocity, pediatric ovarian cysts and, 1875 Peripheral veins, 978–996. See also Deep venous thrombosis lower extremity, 980–990 acute DVT of, 983–984, 983f–985f chronic DVT of, 984, 986f–987f complete venous Doppler for, 989 deep venous system of, 980–981, 981f DVT follow-up recommendations for, 989 normal anatomy of, 980–982 potential pitfalls with, 984–989, 988f supericial venous system of, 981–982, 981f ultrasound examination and protocol for, 982–983, 982f vein mapping of, 989–990 venous insuiciency in, deep, 989, 990f sonographic examination technique for, 979–980 upper extremity, 990–996 acute DVT of, 992–994, 994f–995f chronic DVT of, 994–995, 995f–996f hemodialysis and ultrasound examination of, 1000 normal anatomy of, 990–991, 990f potential pitfalls with, 995–996 ultrasound examination and protocol for, 991–992, 991f–993f vein mapping of, before hemodialysis, 996–998, 998f–1000f Peripherally inserted central catheter (PICC), 993f interventional sonography for, pediatric, 1954, 1955f–1957f Periportal cuing, in acute hepatitis, 85, 85f–86f Periportal hepatic ibrosis, Caroli disease with, 171 Periprocedural antithrombotics, percutaneous needle biopsy and, 598–599 Perirenal space, inlammation in, in acute pancreatitis, 224–225, 225f Perirenal urinoma, from UPJ obstruction, 1358, 1358f Peristalsis, 257 Peritoneal bands, obstruction from, 1841–1842 Peritoneal cavity, 504 luid in, free compared to loculated, 508, 509f localized inlammatory process of, 521, 523f Peritoneum anatomy of, 504 ascites and, 506–508, 507f–509f carcinomatosis of, 510–511, 510f–515f cysts in inclusion, 508–509, 509f, 573, 573f mesenteric, 509–510, 510f endometriosis and, 521–523, 524f inlammatory disease of, 514–521 leiomyomatosis peritonealis disseminata and, 523–524, 525f metastases of, 510 Non-Hodgkin lymphoma of, 513, 517f parietal, 504 pneumoperitoneum and, 524–526, 525f pseudomyxoma peritonei and, 513–514, 518f sonographic technique for, 505–506, 506f–507f Volume I pp 1–1014 • Volume II pp 1015–1968

I-46

Index

Peritoneum (Continued) tumors of, 510–514 carcinomatosis as, 510–511, 510f–515f primary, 511–513, 515f–517f pseudomyxoma peritonei as, 513–514, 518f visceral, 504 Peritonitis abscesses and, 517, 520f chemical, 514 deinition of, 514 ibrinous, 509f granulomatous, 514 Histoplasma, 520f infective, 517, 519f meconium CF and, 1316 cystic, pediatric, 1842–1843, 1846f hydrops from, 1428, 1428f liver calciications and, 1316–1318 massive ascites in, 1418–1419, 1421f small bowel and, 1313, 1313t, 1314f primary, 517 sclerosing, 514, 521, 523f tuberculous, 517–521, 522f Peritrigonal blush, in sagittal imaging of neonatal/ infant brain, 1517 Periumbilical hernias, 492, 494f, 500f Perivascular inlammation, in acute pancreatitis, 224–225, 226f–227f Periventricular cysts, of neonatal/infant brain, 1566, 1566f Periventricular hemorrhagic infarction, in infants, 1547 Periventricular leukomalacia (PVL) cystic, 1551–1552, 1552f from hypoxic-ischemic injury in premature infant, 1541, 1550–1553, 1551f–1553f IUFD and, 1124f in neonatal/infant brain, 1541, 1550–1553, 1551f–1553f, 1566 Periventricular leukomalacia, IUFD and, 1124f Periventricular nodular heterotopia, 1196, 1199f Perlman syndrome CDH and, 1263 hyperechogenic kidneys and, 1351 Peroneal arteries, 966 Peroneal tendons, posterior, injection of, 902, 903f Peroneal veins, 981 Persistent terminal ventricle, pediatric, 1685 Persistent trophoblastic neoplasia (PTN), 1078, 1080–1084, 1082f choriocarcinoma and, 1080–1082, 1083f diagnosis and treatment of, 1083–1084 Doppler ultrasound for, 1083 ater hydatidiform molar pregnancy, 1080, 1081f invasive mole, 1080, 1081f PSTT and, 1082 sonographic features of, 1082–1083 Perthes disease, 1930 Peutz-Jeghers syndrome, 544, 826 Pfeifer syndrome bilateral complete clet lip/palate in, 1156f craniosynostosis in, 1136–1138 hypertelorism with exorbitism in, 1145f midface hypoplasia in, 1148 PFFD. See Proximal focal femoral deiciency PHACES syndrome, pediatric, 1655 Phalanx, middle, hypoplasia of, in trisomy 21, 1101 Pharyngeal pouches, 1651 Phase aberration, 13 Phase inversion, 62–63 Phase modulation imaging, 64, 65f Phased array transducers beam steering in, 10–11, 11f use and operation of, 12 Phenylketonuria, microcephaly from, 1194

Pheochromocytomas adrenal, 421, 422f pediatric, 1826–1827, 1827f percutaneous needle biopsy of, 607 bladder, 356 deinition of, 1826 lower urinary tract, pediatric, 1910–1912 PHI. See Prostate Health Index Phlebectasia, IJV, 1658, 1660f Phleboliths, in venous malformations of neck, 1657 Phlegmonous change, in Crohn’s disease, 274–275, 277f Phocomelia, deinition of, 1399 Phrygian cap, 194 Physics of ultrasound, 1. See also Acoustics; Doppler ultrasound; Instrumentation acoustics in, 2–7 Doppler ultrasound in, 21–30 HIFU in, 31–33, 33f image display and storage in, 12–13 image quality in, 16–19 imaging pitfalls in, 19–21 instrumentation in, 7–12, 24–25, 25b, 25f–26f operating modes and clinical implications in, 30–31 special imaging modes in, 13–16 Phytobezoars, 300 PI. See Pulsatility index PICC. See Peripherally inserted central catheter Picture archiving and communications system (PACS), 12–13 PID. See Pelvic inlammatory disease Pierre-Robin sequence campomelic dysplasia and, 1395 clets of secondary palate in, 1153 micrognathia with, 1153, 1158f Piezoelectricity, 7 Pilomatricoma, pediatric, neck and, 1664, 1664f Pineal cyst, cavum veli interpositi cysts diferentiated from, 1170 Pinworms, 1853 Pituitary gland, in menstrual cycle, 1050f PKD1 gene, mutation in, in ADPKD, 1350 PKD2 gene, mutation in, in ADPKD, 1350 PKHD1 gene, mutation in, in ARPKD, 1348–1350 Placenta abruption of, 1471–1473, 1474f–1475f fetal hydrops and, 1436 pediatric pregnancy and, 1884 accessory lobes of, 1480–1481, 1481f battledore, 1484 bilobed, 1481, 1482f circumvallate, 1479–1480, 1480f–1481f cysts of, subchorionic, 1474, 1477f development of, 1465–1469, 1466f hydropic degeneration of, 1078 infarctions of, 1466, 1473–1474, 1476f–1477f insertion of umbilical cord into, 1484, 1485f low, 1469, 1470f marginal sinus of, 1466, 1467f masses of, 1474–1476 chorioangioma as, 1476, 1478f–1479f malignant, 1476 mesenchymal dysplasia of, 1479, 1479f in molar gestations, 1479, 1480f morphologic abnormalities of, 1479–1481 in multifetal pregnancy, chorionicity and, 1119, 1120f position of, sonographic determination of, 1469, 1470f postpartum, 1487–1489, 1490f RPOC and, 1487–1489, 1490f size of, 1466–1467, 1467f–1468f sonographic appearance of, 1466, 1467f subamniotic hematomas of, 1474 subchorionic hematomas of, 1474

Placenta (Continued) succenturiate lobes of, 1480–1481, 1481f thickness of, 1466, 1467f in third stage of labor, 1487 vascularity of, 1468f Doppler ultrasound and, 1467–1469 vascularization of, 1052–1053 volume of in irst trimester, in early pregnancy evaluation, 1466–1467 second trimester, assessment of, 1466, 1468f Placenta accreta, 1470–1471, 1472f–1473f Placenta increta, 1470–1471 Placenta percreta, 1470–1471, 1473f Placenta previa, 1469–1470 complete, 1469, 1470f marginal, 1469, 1470f placenta accreta with, 1471 Placental bed, subinvolution of, 556 Placental cord insertion, multifetal pregnancy and, 1119, 1122f Placental lakes, 1466, 1467f Placental shelf, 1479–1480 Placental villi, hydropic degeneration of, 1078, 1080f Placental volume quotient, 1466–1467 Placental-site trophoblastic tumor (PSTT), 530–531, 1082 Placentation, multifetal pregnancy and, 1115–1116, 1116f Placentomegaly, fetal, hydrops and, 1418, 1420f Placodes nasal, 1134 spinal dysraphism and, pediatric, 1680 Plagiocephalic heads, 1136–1138 Plane-wave contrast imaging, 64 Plantar fasciitis, injection for, 902, 904f Plaque(s) in atherosclerosis, 433 carotid atheromatous, 919 atherosclerotic rupture of, 919–920 calciied, 920–921, 921f carotid artery dissection and, 946 characterization of, 919–922, 920f–922f, 922b heterogenous, 920–921, 922f homogenous, 920–921, 920f–921f, 936–937, 938f intraplaque hemorrhage and, 920–921 morphology of, ultrasound types of, 921, 922b nonstenotic, 936–937, 938f qualitative assessment of, in carotid stenosis, 924 tandem, in carotid stenosis, 923–924 types 1-4, 921, 922b ulceration of, 923, 923b, 923f–924f vulnerable, identiication of, treatment decisions and, 943 Plasma protein A, pregnancy-associated, 1089–1090 Plasmacytoma, 827–829 Platelet-rich plasma, intratendinous injection of, 909–910 Platyspondyly in skeletal dysplasias, 1382 in thanatophoric dysplasia, 1388–1389, 1390f Plavix (clopidogrel), 598 PLCO (Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial), 397 Pleomorphic adenomas, salivary gland, pediatric, 1636–1638, 1638f Pleural disease, pediatric, pulmonary disease diferentiated from, sonography in, 1709, 1710f Pleural drainage, fetal, hydrops from, 1426–1427

Index Pleural efusions fetal, 1256–1258, 1257f hydrops and, 1413–1416, 1417f, 1425 lung size and, 1244 primary, 1256 secondary, 1256 pediatric drainage of, ultrasound-guided, 1724–1725 sonographic signs of, 1702–1711, 1704f–1708f Pleural luid, pediatric aspiration of, ultrasound-guided, 1724–1725, 1726f through hepatic window, 1707f pneumonia with small amount of, 1706f septated, 1702, 1708f sonogram compared to CT scan for, 1709, 1711f sonographic signs of bare area sign in, 1709, 1709f color Doppler ultrasound signal in, 1709, 1710f diaphragm sign in, 1709 displaced-crus sign in, 1709 free movement in, with respiration, 1709, 1709f septations in, 1709 sonographic signs of, 1709, 1709b through splenic window, 1707f Pleuropulmonary blastoma, 1252–1253 Plexiform neuroibroma, in intraoperative procedures, 1621f Plicae palmatae, 533, 535f PMPI. See Power modulation pulse inversion Pneumatosis intestinalis in acute abdomen, 277–281 in gastrointestinal tract, 297–299, 299f pediatric, sonography for, 1854–1855 Pneumobilia biliary tree and, 175–176, 176f ater liver transplantation, 625, 1767–1768, 1769f–1770f Pneumocystis carinii, hepatic opportunistic infection by, 91, 91f Pneumonia, pediatric, 1711–1714 air bronchograms from, 1702, 1703f, 1708f chest radiograph compared to ultrasound for, 1712–1714, 1715f on chest ultrasound, 1703f empyema from, 1707f round, 1711–1712, 1715f with small amount of pleural luid, 1706f Pneumoperitoneum, 524–526, 525f Pneumothoraces, sonographic detection of, 1725–1726 Poland syndrome, ribs in, 1382–1384 Polar arteries, 445–446 Polycystic kidney disease, 359–361 autosomal dominant, 83, 243, 361, 362f pediatric, 1814–1815, 1815f autosomal recessive, 359, 361f, 1799 pediatric, 1812–1813, 1814f congenital hepatic ibrosis and, 1757–1759, 1762f fetal pancreatic cysts and, 1320 Polycystic ovarian disease, pediatric, 1877–1878, 1879f Polycystic ovarian syndrome (PCOS), 573–574, 574f Polycythemia, dural sinus thrombosis from, 1205–1206 Polydactyly deinition of, 1399 fetal, 1405–1406 postaxial, in trisomy 13, 1104, 1105f

Polydactyly (Continued) short-rib, syndromes associated with, 1382, 1383f, 1395–1396, 1397f toe, fetal, 1406f Polyhydramnios anorectal malformations and, 1311–1312 cervical assessment in, 1505 diagnostic signiicance of, 1340–1341 esophageal atresia and, 1305–1306 fetal hydrops and, 1418, 1420f, 1432–1433 jejunoileal atresia and, 1310 in lethal skeletal dysplasias, 1386 meconium peritonitis and, 1313 with mesoblastic nephroma, 1352–1353 in trisomy 18, 1104 Polymicrogyria, 1196, 1198f Polyorchidism, 838–839, 841f pediatric, 1891 Polypoid intraluminal tumors, 261–264, 263f Polyps endometrial, 544, 548, 549f tamoxifen and, 544–545 intussusception and, 1844–1845 urethral, posterior, pediatric, bladder outlet obstruction from, 1906, 1906f Polysplenia, 159–161 in cardiosplenic syndrome, 1292, 1293b fetal, 1320 univentricular heart with, 1287–1288 Polysplenia syndrome biliary atresia in, 1737, 1738f Doppler evaluation of liver transplant recipient with, 1764–1766 Polyvinyl chloride, 123 Pontocerebellar hypoplasia, 1190 Pontocerebellar syndrome, vermian dysplasia with, 1191 Popliteal artery, 966 aneurysms of, 972f normal appearance of, 966–967 occlusion of, 968f Popliteal cysts, pediatric, 1939 Popliteal vein normal anatomy of, 980–981, 981f ultrasound examination of, 982–983 Porcelain gallbladder, 202, 202f Porencephalic cysts, neonatal/infant brain and, 1537, 1565 Porencephaly from germinal matrix hemorrhage, 1541 HPE diferentiated from, 1189 from intraparenchymal hemorrhage, 1547, 1548f Porta hepatis, 77, 79f Portal hypertension duplex Doppler sonography in, 98 intrahepatic, from cirrhosis, 96 let sided, splenic vein thrombosis from, in chronic pancreatitis, 232–233, 234f–235f liver vascular abnormalities and, 96–98, 96f–97f portosystemic venous collaterals in, 96–98, 96f presinusoidal, 96 splenomegaly and, 145, 147f Portal hypertension, pediatric, 1756–1757 backward-low theory of, 1760–1761 Doppler assessment of abnormal low patterns in, 1754–1756 abnormal hepatic arterial Doppler patterns in, 1755–1756 absent Doppler signal in, 1754, 1754b arterialized low patterns in, 1754 hepatofugal low in, 1757 intrahepatic portal hypertension and, 1759–1762 in liver disease, 1752–1754, 1754f–1755f

I-47

Portal hypertension, pediatric (Continued) of normal low patterns in splanchnic vessels, 1750 paraumbilical veins low direction in, 1757, 1758f pelvic varices in, 1760f possibilities and pitfalls of, 1750 in prehepatic portal hypertension, 1757–1759 reversed low in, 1754–1755 sonographic technique for, 1750–1752 splenorenal shunts in, 1757, 1759f in suprahepatic (posthepatic) portal hypertension, 1762–1764, 1763f surgical portosystemic shunts and, 1764 to-and-fro low in, 1754–1755, 1755f Doppler ultrasound assessment of, 1748–1764 basic principles of, 1748–1750 forward-low theory of, 1760–1761 thickened lesser omentum and, 1756, 1756f Portal triad, 78 Portal vein(s) anastomosis of, for liver transplantation, 624 aneurysms of, 103–104 ater liver transplantation, 1768, 1769f–1770f anomalies of, 81 cavernous transformation of, 98, 99f clots in, in acute pancreatitis, 224–225, 228f fetal liver calciications and, 1316–1318 let, Doppler studies of, best approach for, 1752 liver circulation and, 78 main, Doppler studies of, best approach for, 1752 normal, 76, 77t, 78f pediatric anatomy of, 1731–1734, 1732f cavernous transformation of, in prehepatic portal hypertension, 1757, 1761f low direction through, meals and, 1750 let, branches of, 1734 let, Doppler studies of, 1750 right, branches of, 1733f, 1734 thrombosis of, 1757, 1757b pseudostenosis of, 636 stenosis of, ater liver transplantation, 635–636, 638f, 1766, 1768f thrombosis of, 98, 99f–100f chronic pancreatitis and, 232–233, 235f from HCC, 120, 121f ater liver transplantation, 635–636, 639f–640f, 1766 malignant, 98, 99f pediatric, 1757, 1757b Portosystemic shunts intrahepatic, 104, 1761–1762 liver and, 130–132 in portal hypertension, 1757 portocaval, patency of, Doppler assessment of, 1764 surgical, 1764 total or partial, 1764 transjugular intrahepatic, 131–132, 132b, 132f–133f, 1764 Portosystemic venous collaterals, in portal hypertension, 96–98, 96f spontaneous routes of, 1752, 1754f Port-wine stains, 1679 Postablation tubal sterilization syndrome, 551–552 Postaxial polydactyly, fetal, 1405–1406 Posterior cerebral artery (PCA), as transtemporal approach landmark, 1592, 1593f–1594f Posterior fossa. See also Cerebellum abnormalities of, 1192 hemorrhage of, 1548–1550 Volume I pp 1–1014 • Volume II pp 1015–1968

I-48

Index

Posterior fossa (Continued) subarachnoid cysts of, Dandy-Walker malformation diferentiated from, 1190, 1531, 1531b ventral induction errors in, 1189–1192 Posterior inguinal wall insuiciency, sports hernia and, 486, 488f Postmeningitis hydrocephalus, 1887 Posttransplant lymphoproliferative disorder (PTLD), 682–688 Epstein-Barr virus and, 682 ater liver transplantation, 683–688, 687f patterns of, 688 pediatric, 1812, 1813f ater renal transplantation, 683–688, 684f–686f treatment options for, 688 Posttraumatic aortic stenosis, 444 Posttraumatic pseudoaneurysms, of common carotid artery, 948, 950f Pouch of Douglas, 566 endometrioma in, 524f Power Doppler ultrasound, 25, 25b, 26f amplitude evaluation in, 935 for carotid stenosis evaluation, 935–939, 935b pitfalls and adjustments in, 935f–939f, 936–939, 937b color streaking in, breast cysts with, 775, 776f harmonic imaging and, 60–61, 60f–62f intermittent harmonic, 66, 66f for neonatal/infant brain, 1573–1574 for prostate cancer, 404f–405f, 406 for prostate examination, 387 Power modulation pulse inversion (PMPI), 64 Power settings, 505–506 Preaxial polydactyly, fetal, 1405–1406 Precocious pseudopuberty, pediatric ovarian cysts and, 1875 Precocious puberty, 1746, 1887–1888 Predelivery aspiration procedure, in fetal hydrops, 1437 Preeclampsia fetal hydrops prognosis and, 1436 pediatric pregnancy and, 1884 placental infarction in, 1477f Preexisting cavitation nuclei, 41 Pregnancy. See also Ectopic pregnancy; Hydatidiform molar pregnancy; Multifetal pregnancy adnexal cysts in, 1020 “cornual”, 1073 early failure of, 1062–1069 hydronephrosis in, 316 iliac vein compression in, 459, 460f keepsake imaging in, 49b, 50 luteoma of, 572 MRI in, 1031–1032, 1031f ovarian lesions associated with, 572, 572f pediatric, 1884–1885 second trimester of indications for ultrasound in, 1015, 1016b ultrasound guidelines for, 1019–1022, 1020b teen, fetal gastroschisis and, 1322–1323 thermal index for bone in late, 1039 thermal index for sot tissue in early, 1039 third trimester of indications for ultrasound in, 1015, 1016b ultrasound guidelines for, 1019–1022, 1020b of unknown location, 1075 uterus size in, 531 Pregnancy, irst trimester of. See also Aneuploidy, screening for, irst-trimester; Ectopic pregnancy; Gestational trophoblastic disease aneuploidy screening for, 1089–1097 change during, 1048 early failure of, 1062–1069

Pregnancy, irst trimester of (Continued) amnion size in, 1066, 1067f–1068f arrhythmia and, 1069 chromosomal anomaly causing, 1062 CRL and no heartbeat in, 1063, 1064f diagnostic indings of, 1063–1064, 1063b embryonic bradycardia and, 1068–1069, 1068f embryos with CRL less than 7mm and no heartbeat in, 1064 gestational sac appearance concerns in, 1065, 1066f gestational sac with no embryo in, 1063–1065, 1065f gestational sac with small MSD in relationship to CRL, 1066, 1067f luteal phase defect causing, 1062–1063 spontaneous abortion rate and, 1062, 1062t subchorionic hemorrhage and, 1069, 1069f worrisome indings of, 1064–1069, 1065t yolk sac size and shape in, 1067–1068, 1068f ectopic, 1069–1076 embryo evaluation during, 1076–1077 embryology in, 1049–1054 gestational age estimation in, 1061–1062 gestational trophoblastic disease and, 1077–1084 indications for ultrasound in, 1015, 1016b maternal physiology in, 1049–1054 normal anatomy in, 1077, 1077f normal sonographic appearance of, 1054–1061 amnion in, 1057, 1059f–1060f β-hCG levels and, 1055–1057, 1057b embryo in, 1057, 1059f–1060f embryonic cardiac activity in, 1058–1059, 1060f gestational sac in, 1054–1055, 1055f–1056f umbilical cord cysts in, 1061, 1061f umbilical cord in, 1059–1061 yolk sac in, 1057, 1058f sonography in current trends in, 1049 goals of, 1049 transvaginal ultrasound safety in, 1049 ultrasound guidelines for, 1016–1019, 1016b, 1017f–1020f Pregnancy dating, 1022 Pregnancy of unknown location (PUL), 1075 Pregnancy-associated plasma protein A (PAPP-A), 1089–1090 Premammary zone, of breast, 761, 761f Premature atrial contractions (PACs), 1295–1296 Premature rupture of membranes, pulmonary hypoplasia and, 1246 Premature ventricular contractions (PVCs), 43 fetal arrhythmias and, 1295–1296 Premenarchal girls, ovarian volume in, 1873, 1875t Preplacental hematoma, 1471, 1475f Presacral mass(es) fetal, 1239, 1239b pediatric, 1913–1915, 1913b, 1914f–1915f solid, 1914–1915 Presteal waveform, 953b, 954, 954f Preterm birth (PTB) cervical length and, 1499–1500, 1499f short, 1500–1501, 1500f, 1501t deinition of, 1495 incidence of, 1495 multifetal pregnancy morbidity and mortality and, 1119–1123 prior, cervical assessment in, 1504 spontaneous, prediction of, 1495–1496, 1501–1503 cervical change rate in, 1501 cervical funneling in, 1501, 1502f dynamic cervical change in, 1501–1503, 1503f gestational age at cervical length measurement in, 1500–1501, 1501t

Preterm birth (PTB) (Continued) obstetric factors in, 1501 sonographic features in, 1503, 1504f PRF. See Pulse repetition frequency Primary peritoneal mesothelioma, 513, 516f Primary peritoneal serous papillary carcinoma, 511–513, 515f Primary peritonitis, 517 Primary sclerosing cholangitis, biliary tree and, 182, 183f, 184 Primitive neuroectodermal tumors, neonatal/infant brain and, 1562 Proboscis cyclopia with, 1140, 1144f in trisomy 13, 1104, 1105f Probst bundles, in corpus callosum agenesis, 1528 Process vaginalis, relationship of indirect inguinal hernia to, 476–477 Processus vaginalis, 819 pediatric, 1902 Profunda femoris artery, 966 nonocclusive thrombi in, missing, 988 Profunda femoris vein chronic DVT in, 987f normal anatomy of, 980–981, 981f Prominence, forming fetal face, 1134, 1134f Pronephros, 311, 312f, 1336–1338 Propagation speed, of transducer, 7 Propagation velocity artifact, 3, 3f, 420–421 of sound, 2–3, 3f in SWE, 16, 18f Proptosis, 1140 Prosencephalon, formation of, 1077 Prostaglandin-induced antral foveolar hyperplasia, 1839–1840 Prostate abscesses of, 389, 390f, 392 adenocarcinoma of, 395 anatomy of, 382–384 axial, 383f, 384 neural structures in, 384 sagittal, 383f, 384–386 vascular, 384, 386f zonal, 382–384, 382f–383f, 385f–386f azoospermia and, 393 benign conditions of, 387–392 benign ductal ectasia of, 387, 388f benign hyperplasia of, 384, 385f–386f, 387–388 biopsy of PSA-directed, 395 ultrasound-guided, 407–411, 408f calciications of, 387, 388f cancer of, 394–407 active surveillance for, 401 alternate biomarkers of, 396 brachytherapy for, 401, 402f CEUS for, 406 color Doppler ultrasound for, 404f, 406 elastography for, 407 epidemiology of, 395 external beam radiotherapy for, 400–401, 401f focal therapy for, 400 high-intensity focused ultrasound for, 400 histologic grading of, 399–400 key facts of, 395b mortality by age in, 397 mpMRI-TRUS fusion for, 406–407, 410–411 power mode Doppler ultrasound for, 404f–405f, 406 prostate-speciic antigen in, 395–396, 396b radical prostatectomy for, 400, 401f screening for, 396–397 sonographic appearance of, 403–407, 403f–405f, 406b staging, 397–400, 397f, 398t, 399f

Index Prostate (Continued) therapy for, 400–402, 401f–402f 3-D ultrasound for, 406–407 transrectal sonography of, 302, 302f, 403–406, 403f–405f, 406b watchful waiting for, 401 congenital abnormalities in, 392 corpora amylacea of, 387 cysts of, 388, 390–392, 391f hematospermia and, 394, 394b infertility and, 392–394, 393f inlammation of, 389, 390f normal variants of, 387, 388f oligospermia and, 393 pediatric, anatomy of, 1888, 1888f prostatitis and, 389–390, 390f transurethral resection of, 385f–386f, 388 ultrasound of appearance in, 383f, 384–386, 385f–386f equipment and technique for, 386–387, 386f history of, 381–382 power mode Doppler, 387 transrectal, 381–382 volume of, 387 weight of, 387 Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial (PLCO), 397 Prostate Health Index (PHI), 396 Prostatectomy, TRUS-guided biopsy ater radical, 411, 411f Prostate-speciic antigen (PSA), 381–382 density of, 395–396 in directing biopsy, 395 elevated levels of, 395 free/total ratio of, 395 velocity of, 396 Prostatic artery, 384 Prostatism. See Lower urinary tract symptoms Prostatitis, chronic, 389–390, 390f Proteus syndrome, hemimegalencephaly associated with, 1195 Proximal focal femoral deiciency (PFFD), 1400, 1400f pediatric, 1933, 1934f Prune belly syndrome fetal lower urinary tract obstruction from, 1361–1362 megalourethra and, 1362 pediatric hydronephrosis and, 1788 lower urinary tract obstruction and, 1906 PSA. See Prostate-speciic antigen Psammoma bodies, in papillary carcinoma of thyroid gland, 698 Psammomatous calciication, in peritoneal nodule, 510–511, 513f Pseudoacetabulum, in DDH, 1921 Pseudoaneurysm(s) abdominal aortic dilation from, 441 anastomotic, 438 in AVF for hemodialysis, 1003, 1005f common carotid artery posttraumatic, 948, 950f of common femoral artery, 973f hepatic artery, 104 ater liver transplantation, 634, 636f ater pancreas transplantation, 678, 680f pancreatic, 230, 230f of peripheral arteries lower extremity, 972–973, 973f upper extremity, 976, 977f radial artery, 977f renal biopsies and, Doppler assessment of, 1809, 1811f

Pseudoaneurysm(s) (Continued) ater renal transplantation, 664, 669f–670f in synthetic arteriovenous grat for hemodialysis, 1003, 1006f Pseudoascites, 1413, 1415f Pseudocirrhosis, of liver, 125–128, 129f Pseudocyst(s) gastrointestinal cysts diferentiated from, 1860, 1863f meconium, fetal, 1313, 1314f ovarian cysts diferentiated from, 1369 pancreatic acute pancreatitis complications with, 228–229, 229f chronic pancreatitis complications with, 232, 233f–234f drainage of, 230, 615–617, 617f pediatric pancreatitis and, 1864–1865, 1865f splenic, 146–147, 149f umbilical cord, 1483, 1484f Pseudoephedrine, fetal gastroschisis and, 1322–1323 Pseudohermaphroditism female, prenatal diagnosis of, 1368 male, dysplastic gonads and, 1899 Pseudokidney sign, in gut wall, 257, 260f Pseudomembranous colitis, 1850f gastrointestinal tract infections and, 296–297, 298f Pseudomonas, 846 Pseudomyxoma peritonei, 513–514, 518f, 581 Pseudopapillary tumor, of pancreas, pediatric, 1865, 1865f Pseudopolyps, cystitis and, 333, 333f Pseudoprecocious puberty, 1887–1888 Pseudopuberty, precocious, pediatric ovarian cysts and, 1875 Pseudospectral broadening, in carotid spectral analysis, 927 Pseudostenosis, of portal vein, 636 Pseudostring of low, on power Doppler, 935 Pseudosyndactyly, fetal, 1404 Pseudothalidomide syndrome, 1401 Pseudotumor(s) ibrous, 838, 840f inlammatory gastric mucosa thickening in, 1839–1840 pediatric cystitis and, 1794, 1797f splenic, 153–156 Pseudoulceration, of carotid artery, 923 Psoriatic arthritis, of hand and wrist, injections for, 904 PSTT. See Placental-site trophoblastic tumor PSV. See Peak systolic velocity PTB. See Preterm birth PTLD. See Posttransplant lymphoproliferative disorder PTN. See Persistent trophoblastic neoplasia Puberty, precocious, 1746, 1887–1888 PUBS. See Percutaneous umbilical cord blood sampling PUL. See Pregnancy of unknown location Pulmonary agenesis, 1245–1246 Pulmonary aplasia, 1245–1246 Pulmonary artery, fetal continuity of, 1278f diameter of, 1277f dilated, TOF and, 1288 Pulmonary atresia Ebstein anomaly with, 1286 fetal, hydrops from, 1423–1424 hypoplastic right ventricle secondary to, 1287 TOF and, 1288 Pulmonary development, fetal, 1243

I-49

Pulmonary embolism, DVT causing lower extremity, 979, 981f upper extremity, 994 Pulmonary hypertension, with CDH, 1264 Pulmonary hypoplasia fetal, 1245–1246 campomelic dysplasia and, 1384f causes of, 1246t hydrops and, 1413 in lethal skeletal dysplasia, 1386, 1386b lethality of skeletal dysplasia and, 1382, 1384f premature rupture of membranes and, 1246 primary, 1245 secondary, 1245, 1246f unilateral, 1246, 1247f pediatric, 1689 Pulmonary lymphangiectasia, 1258, 1259f Pulmonary sequestrations, pediatric, 1715–1716, 1717f Pulmonary veins anatomy of, normal, 1290, 1291f anomalous, 1290, 1291f Pulmonic stenosis, 1292 in TGA, 1289 Pulsatility index (PI), 27, 27f of intracranial vessels, 1595 Pulse average intensity, 36 Pulse inversion Doppler imaging, 63–64 Pulse inversion imaging, 62–63, 62f–63f Pulse length, 8 Pulse repetition frequency (PRF) in color Doppler, setting of, for low-low vessel evaluation, 933 in color Doppler ultrasound, 28, 29f, 30–31 increasing, to overcome aliasing, 939 output control and, 48–50 transmitter controlling, 7 Pulsed wave Doppler, 24, 25f testicular low, 1890 testicular hyperemia and, pediatric, 1896 Pulsed wave operating modes, 7 Pulsed wave ultrasound, 36 Pulse-echo principle, 36 Purkinje system, 1297 Pus, 1953 Push-and-pull maneuver, in dynamic examination of hip, 1926f, 1927 PVCs. See Premature ventricular contractions PVL. See Periventricular leukomalacia Pyelectasis deinition of, 1354 fetal, signiicance of, 1355 Pyelitis alkaline-encrusted, 324–325 emphysematous, 326–327, 327f Pyelonephritis acute, 323–325 gallbladder wall thickening signs in, 201f pediatric, 1792–1793, 1793f–1794f renal and perinephric abscess from, 325, 325f on sonography, 324, 324b, 324f chronic, 327, 327f–328f pediatric, 1794, 1795f emphysematous, 325–326, 326f renal transplantation complications with, 653, 657f as genitourinary tract infection, 323–328 transplant, 651, 655f xanthogranulomatous, 328, 329f Pyknodysostosis, wormian bones in, 1139 Pyloric atresia, dilated fetal stomach diferentiated from, 1307 Volume I pp 1–1014 • Volume II pp 1015–1968

I-50

Index

Pyloric muscle hypertrophy of minimal, in pylorospasm, 1836–1838, 1838f in pyloric stenosis, 1835–1838, 1835b, 1837f–1838f tangential imaging artifacts of, 1834–1835, 1836f Pyloric stenosis dilated fetal stomach diferentiated from, 1307, 1308f hypertrophic, 1835–1838, 1835b, 1837f–1838f pitfalls in diagnosis of, 1838, 1838b, 1839f pylorospasm and minimal muscular, 1836–1838, 1838f Pylorospasm, 1836–1838, 1838f Pyoceles, scrotal, 835f, 836 Pyogenic bacteria, liver abscesses from, 85–86, 87f pediatric, 1746–1747, 1751f Pyonephrosis genitourinary tract infections and, 325, 326f pediatric, complicating acute pyelonephritis, 1793, 1794f renal transplantation complication with, 651, 655f Pyosalpinx, 587–588 Q Quadrigeminal cistern, 1518 R Rachischisis, 1218 deinition of, 1225t Radial arteries, 531–532 calciication of, evaluation for, 998, 998f for coronary bypass grat, evaluation of, 977–978, 980f pseudoaneurysm of, 977f Radial ray anomalies, 1103f Radial ray defects, 1400–1401, 1401f–1402f Radial veins, normal anatomy of, 990–991 Radiation forces, 35 Radical prostatectomy for prostate cancer, 400, 401f TRUS-guided biopsy ater, 411, 411f Radiofrequency ablation, for autonomously functioning thyroid nodules, 720 Radiography, for skeletal dysplasia evaluation, 1384 Radiotherapy, external beam, for prostate cancer, 400–401, 401f Radius, aplastic or hypoplastic, in Fanconi pancytopenia, 1400, 1402f Ranula, pediatric, 1639–1640, 1640f Ranunculi, 313 in kidney development, 1781, 1781f Rapidly involuting congenital hemangiomas, cutaneous, 1742–1743 Rapunzel syndrome, trichobezoars and, 1840 RAR. See Renal aortic ratio Rarefaction, in sound wave, 2, 2f RCC. See Renal cell carcinoma Real-time B-mode ultrasound, 9–10, 10f Receiver, 8–9, 8f–9f Receiver gain, in obstetric sonography, 1036 Rectal cleansing, prior to TRUS, 387 Rectouterine recess, 528 Rectum, carcinoma of, 301–302, 301f–304f Red blood cell production, decreased, from fetal hydrops, 1431 Red cell alloimmunization, screening fetus with hydrops for risk of, 1421–1423, 1421b, 1422f, 1422t Relected sound, 3–4 Relection, in acoustics, 4, 5f Relection coeicient, 4 Relectors difuse, 4, 5f specular, 4, 4b, 5f

Relux nephropathy, CKD and, 1796–1798 Refraction, 5, 6f Rejection acute, renal transplantation abnormalities and, 1809–1810 chronic, renal transplantation abnormalities and, 1810, 1812f in liver transplantation, pediatric, 1767 in pancreas transplantation, 678–679, 681f in renal transplantation acute, 649–651, 653f chronic, 651, 654f Remapping, of amplitudes, 9 Renal agenesis, 318–319 Renal aortic ratio (RAR), 450 Renal artery(ies) accessory, 445–446 anatomy of, 445–446 aneurysms of, 369, 369f, 451 duplex Doppler sonography of, 447–450, 450f false-positive/false-negative results with, 450, 450f interpretation of, 450 fetal absent, 1344f normal, 1344f infarction of, 366, 367f occlusion of, 366 pediatric patency, Doppler assessment of, 1803–1804 stenosis of, Doppler assessment of, 1805, 1805t, 1806f polar, 445–446 stenosis of, 368–369, 368f causes of, 447 Doppler assessment of, pediatric, 1809 false-positive Doppler diagnosis of, 658, 661f intraparenchymal, 658 pediatric, Doppler assessment of, 1805, 1805t, 1806f in pediatric patients, 447 ater renal transplantation, 655–658, 656b, 658f–661f renovascular hypertension and, 446–447, 446b thrombosis of, ater renal transplantation, 653–655, 657f Doppler assessment of, pediatric, 1807–1809, 1808f Renal biopsies, pediatric, Doppler assessment of, 1809, 1810f–1811f Renal calculi, 334–336, 336f–337f entities that mimic, 336, 337b, 337f Renal cell carcinoma (RCC) acquired cystic kidney disease and, 340 biopsy of, 343–344, 345f classic diagnostic triad for, 340 cystic, 343, 343f Doppler ultrasound for detection of, 343, 344f genitourinary tumors and, 340–344 histologic subtypes of, 340 imaging approaches to, 341, 341f interpretation pitfalls with, 344, 345f necrotic, 343 papillary, 342 pediatric, 1820, 1821f prognosis of, 343–344 radiofrequency ablation of, 341, 341f sonographic appearance of, 341–343, 342f–344f treatment approaches to, 341 von Hippel-Lindau disease and, 340 Renal collecting system, pediatric. See also Hydronephrosis, pediatric, causes of dilation of, 1785 duplication of, 1783–1784, 1784f urolithiasis and, 1799–1801, 1799f Renal cortex, 313, 313f

Renal duplication, pediatric, 1783–1784, 1784f Renal dysgenesis, 361 Renal dysplasia, 361, 1689 obstructive cystic, 1347–1348, 1347f–1348f Renal hilum, 311–313 Renal junctional parenchymal defect, 1781, 1781f Renal medullary pyramids, 313, 313f Renal milk of calcium, calyceal diverticula and, 1799, 1800f Renal parenchyma, 313 Renal pelvic diameter (RPD), 1354, 1354f normal, 1355 Renal pelvic echo, 1339 Renal pelvis. See also Hydronephrosis adenocarcinoma of, 348 fetal diameter of, measurement of, 1354, 1354f dilation of, 1354 pediatric duplication of, 1784f wall thickening in, from acute pyelonephritis, 1792, 1793f Renal sinus, 311–313 Renal transplantation, 641–666 abnormal, 649 AVMs complicating, 661–664, 667f–670f twinkling artifacts mimicking, 662–664, 668f cadaveric kidneys in, paired, 643–644, 648f for chronic renal failure, 641 donor renal vein anastomosis in, 643 luid collections ater, 664–666, 671f–674f hematomas ater, 665, 671f infarctions ater global, 653 segmental, 653–655, 657f lymphoceles ater, 665–666, 673f–674f pediatric, 1809, 1811f normal appearance of, 644–648 Doppler ultrasound assessment in, 648, 651f–652f gray-scale assessment in, 644–648, 648f–650f parenchymal pathology complicating, 649–653 abscesses as, 651, 656f acute rejection as, 649–651, 653f acute tubular necrosis as, 649–651, 653f chronic rejection as, 651, 654f emphysematous pyelonephritis as, 653, 657f hyperacute rejection and, 651 infections as, 651–653, 655f–657f milk of calcium cysts as, 653, 657f pediatric, 1809–1810, 1812f pyonephrosis as, 651, 655f pediatric Doppler ultrasound for, 1807–1812 parenchymal abnormalities and, 1809–1810, 1812f perinephric luid collections in, 1809, 1811f tumors of, 1812, 1813f urologic complications and, 1810–1812 vascular complications in, 1807–1809, 1808f, 1810f–1811f perinephric abscesses ater, 664–665 postrenal collecting system obstruction complicating, 630f–633f, 659–661 prerenal vascular complications of, 653–659 arterial thrombosis as, 653–655, 657f renal artery stenosis as, 655–658, 656b, 658f–661f renal vein stenosis as, 658–659, 663f venous thrombosis as, 658, 662f pseudoaneurysms ater, 664, 669f–670f PTLD ater, 683–688, 684f–686f surgical technique for, 641–644, 648f ureter anastomosis of in, 643, 648f

Index Renal transplantation (Continued) ureteral obstruction complicating, 659–660, 663f–664f urinomas ater, 665, 672f pediatric, 1809 Renal tubular acidosis, medullary nephrocalcinosis and, 1798 Renal tubular disease, inborn errors of metabolism and, 1738 Renal vein(s) donor, anastomosis, in renal transplantation, 643 let, anatomic variants of, 457 pediatric acute thrombosis of, Doppler assessment of, 1804–1805, 1804b, 1804f patency of, Doppler assessment of, 1803–1804 stenosis of, ater renal transplantation, 658–659, 663f thrombosis of, 369, 370f Doppler assessment of, pediatric, 1809 hyperechogenic kidneys and, 1351 pediatric, acute, Doppler assessment of, 1804–1805, 1804b, 1804f ater renal transplantation, 658, 662f urinary tract calciications and, 1799, 1800f Renal/abdominal circumference ratio, 1338–1339 Renal-coloboma syndrome, MCDK and, 1815 Renovascular disease, 368 Renovascular hypertension clinical indings suggesting, 446b renal artery stenosis and, 446–447 Resistive index (RI), 27, 27f in ACA, in infants, 1576, 1577t in hepatic artery, elevation of, ater liver transplantation, 634 intracranial, 1595 in asphyxiated infants, 1580 factors changing, 1612t factors modifying, 1576, 1576f–1577f, 1576t hydrocephalus and, 1582, 1584f intrarenal, pediatric, causes of increased, 1802–1803, 1803b, 1803f in monitoring intracranial hemodynamics in infants, 1576, 1577t in renal artery duplex Doppler sonography, 450 in shunt malfunction and hydrocephalus, 1613, 1613f Resolution, spatial, 16–19, 18f–19f Resuscitation, neonatal, in fetal hydrops, 1437 Retained products of conception (RPOC), 554–555 pediatric, 1884, 1884f placenta and, 1487–1489, 1490f Rete testis, 819 tubular ectasia of, 829–830, 830f pediatric, 1891–1892, 1892f Retinoblastoma, metastasis of, to teste, 1901 Retinoic acid, NTDs from, 1218 Retrocalcaneal bursal injection, 902, 903f Retrocaval ureter, 322 Retrognathia, 1153–1154 Retrogressive diferentiation, in spine embryology, 1672, 1673f Retromammary zone, of breast, 761, 761f Retromandibular vein, pediatric, 1630, 1630f Retroperitoneum, 210. See also Abdominal aortic aneurysm abdominal aortic aneurysm and, 433–439 abdominal aortic dilation and, 439–441 atherosclerosis and, 432–433 ibrosis of, 464–465, 465f luid collections in, 464 masses in, 464 metastases of, 464, 465f nonvascular diseases of, 464–465

Retroperitoneum (Continued) prepancreatic, inlammation of, in acute pancreatitis, 224–225, 224f–225f stenotic disease of abdominal aorta and, 441–445, 445f Retrorenal spleen, 162 Reverberation artifacts, 19, 20f posterior, liver abscess and, 85–86, 87f Rh alloimmunization, screening fetus with hydrops for risk of, 1421–1423 Rh0(D) immune globulin (RhoGAM), in immune hydrops prevention, 1418 Rhabdoid tumors intraspinal, pediatric, 1689–1691 neonatal/infant brain and, 1562 Rhabdomyoma(s), cardiac fetal, 1293–1294, 1293f fetal hydrops from, 1424, 1424f in infants, 1293 tuberous sclerosis, 1424 Rhabdomyosarcoma(s) bladder, 356 pediatric, 1820, 1823f pediatric biliary, in liver, 1746, 1749f embryonal, paratesticular, 1903–1904, 1903f hydrosonovaginography and, 1871f lower urinary tract and, 1908–1912, 1912f metastasis of, to teste, 1901 neck, 1665, 1666f presacral, 1914–1915 salivary gland, 1638–1639 vaginal, 1883, 1883f scrotal, 840f, 841 in TSC, 1200f Rh(D) antibodies, immune hydrops and, 1419 Rheumatoid arthritis, 866 erosive, 867, 868f gout and, 867–869, 868f of hand and wrist, injections for, 904 joint efusion in, 867, 867f Rheumatoid nodules, in Achilles tendon, 867, 868f Rhizomelia, 1381, 1381b, 1382f Rhizomelic chondrodysplasia punctata, 1399 Rhizomelic dysplasia, features of, 1397t RhoGAM. See Rh0(D) immune globulin Rhombencephalic cavity, 1167 Rhombencephalic neural tube, 1167 Rhombencephalon, formation of, 1077, 1077f, 1167 Rhombencephalosynapsis, 1192 RI. See Resistive index Rib shadowing, in pediatric chest sonography, 1710 Rib(s) fractures of, pediatric, 1727 in skeletal dysplasias, 1382–1384 Riedel lobe, 80 Riedel struma, 727–728, 728f Right atrial isomerism, in total APVR, 1290 “Rim-rent” rotator cuf tears, 888, 890f “Ring of ire” sign, in pediatric ectopic pregnancy, 1884–1885 Ring-down artifacts, 266, 266f Roberts syndrome, 1401 Rocker-bottom foot, 1406f, 1407 Rokitansky-Aschof sinuses, 202, 203f Rolland-Desbuquois, 1399 Rostral neuropore, 1167 Rotator cable, 882, 884f Rotator cuf. See also Shoulder anatomy of, 879, 879f hydroxyapatite crystal deposition in, 891–892 muscle atrophy of, 888–889, 891f musculature evaluation of, 884–886, 885f postsurgical, 888, 891f

I-51

Rotator cuf (Continued) shoulder dysfunction and pathology of, 877 tears of, 886–892 background on, 886 calciic tendinitis and, 891–892, 892f full-thickness, 886–887, 887f–888f partial-thickness, 887–888, 889f–890f subacromial-subdeltoid bursa and, 888–889, 892f tendinosis as, 886, 886f Rotator interval, 879, 880f ultrasound evaluation of, 881–882 Rotter lymph nodes, 762, 808–810, 810f Round ligament(s), 528, 564–565 cysts of, simulating groin hernias, 500, 501f relationship of indirect inguinal hernia to, 476–479, 480f thrombosis of, simulating groin hernias, 500, 501f varices of, simulating groin hernias, 500, 501f Round pneumonia, pediatric, 1711–1712, 1715f RPD. See Renal pelvic diameter RPOC. See Retained products of conception Rubella congenital, neonatal/infant brain and, 1560 fetal hydrops from, 1432 maternal, pulmonic stenosis and, 1292 Rudimentary horn, 538 Rupture of membranes, preterm premature cervical assessment in, 1505 S SAAAVE Act. See Screening Abdominal Aortic Aneurysms Very Eiciently Act Sacral agenesis, 1689 fetal, 1237 in caudal regression, 1237–1238 in caudal regression syndrome, 1401 Sacral bone tumors, 1914–1915 Sacrococcygeal teratomas fetal, 1238–1239, 1238b, 1239f hydrops from, 1430–1431 pediatric, 1691, 1694f classiication of, 1691t cystic, 1694f intrapelvic, 1694f presacral, 1913, 1914f Saddle nose, in skeletal dysplasia, 1382 Safety. See also Bioefects AIUM on diagnostic ultrasound and general, 47, 47b hyperthermia and, 38, 38f of microbubble contrast agents, 67–68 of obstetric sonography, 1034–1035 guidelines for, 1041–1042, 1042t, 1043f of transvaginal ultrasound in irst trimester of pregnancy, 1049 Sagittal sinus, fetal, thrombosis of, 1206f Saldino-Noonan syndrome, 1396 Salivary glands, pediatric, 1629–1639. See also Parotid glands, pediatric; Submandibular glands, pediatric anatomy of, 1630–1631 inlammation of, 1632–1635 acute, 1632–1634, 1632f–1633f chronic, 1634–1635, 1634f–1636f masses of, 1636–1639 neoplasms of, 1636–1639, 1638f–1639f vascular masses of, 1636, 1637f viral infections of, 1632, 1632f Salmon patches, 1679 Salmonella, 1852–1853 Sample volume, in obstetric Doppler ultrasound, 1036 Volume I pp 1–1014 • Volume II pp 1015–1968

I-52

Index

Sample volume size, Doppler ultrasound and, 29b, 30 Sandal toes, fetal, 1406f, 1407 Saphenofemoral junction, as landmark for femoral hernias, 482, 485f Sappey plexus, 762 Sarcoid, chronic pediatric sialadenitis in, 1634–1635 Sarcoidosis, epididymis and, 841, 843f Sarcoma botryoides, pediatric, 1820, 1883, 1908 Sarcoma(s) embryonal, undiferentiated, in pediatric liver, 1746, 1748f endometrial, 551, 551f granulocytic, pediatric, neck, 1666, 1667f Kaposi, liver in, 129 masticator space, pediatric, 1640, 1641f renal, 356 sot tissue, 871–872, 872f uterine, 551 Sawtooth low disturbance, from temporal tap, 918, 918f Scanning mode, obstetric sonography and, 1035 Scapulae, 878–879, 878f hypoplastic, in campomelic dysplasia, 1381–1382 Scars from cesarean sections, 557, 558f exuberant, simulating anterior abdominal wall hernias, 500, 502f SCC. See Squamous cell carcinoma SCD. See Sickle cell disease Schistosomiasis bladder, 331, 331f liver, 90 pediatric, 1748 urinary tract, 331 Schizencephalic clets, hydranencephaly diferentiated from, 1208 Schizencephaly CMV infection and, 1536–1537, 1558 fetal, 1196, 1199f HPE diferentiated from, 1189 hydranencephaly diferentiated from, 1208 neonatal/infant, 1536–1537, 1537f Schneckenbecken dysplasia, 1396 Scintigraphy, in parathyroid adenomas of, 747, 747f Sclerosing cholangitis, recurrent, complicating liver transplantation, 629, 630f Sclerosing peritonitis, 514, 521, 523f Sclerosis of hemangioma, diagnostic challenges with, 112 Sclerotherapy ethanol, 719 ultrasound-guided, of macrocystic lymphatic malformation, pediatric, 1726, 1727f Sclerotome, in spine embryology, 1217–1218, 1217f, 1218t Scoliosis fetal, 1235–1237, 1237b campomelic dysplasia and, 1395 pediatric, 1688 Screening Abdominal Aortic Aneurysms Very Eiciently (SAAAVE) Act, 435 Scrotal pearls, 836–837, 837f Scrotal sac, torsion of, pediatric, 1325 Scrotoliths, 836–837, 837f, 1897 Scrotum. See also Epididymis; Testis(es) anatomy of, 819–822, 819f–821f biid, fetal, 1367 calciications of, 833–834, 833b, 834f calculi in, extratesticular, 836–837, 837f cysts of, extratesticular, 839, 842f edema of, idiopathic, 846 epididymal lesions and, 839–841

Scrotum (Continued) ibrous pseudotumor and, 838, 840f hematoceles of, 835f, 836 pediatric, 1902 hernia and, 836, 836f hydroceles of, 834–836, 835f fetal, 1367 pediatric, 1899, 1902, 1902f indirect inguinal hernias extending into, 478–479, 482f liposarcomas of, 840f, 841 masses in, 822–834 pain in, acute, 841–847 causes of, 843b from epididymitis, 846, 847f–848f, 1895–1896, 1896f from epididymo-orchitis, 846, 847f–849f from Fournier gangrene, 846–847 secondary to intraabdominal process, 1899 from testicular torsion, 844–846, 844f–845f from torsion of testicular appendage, 846 pathologic lesions of, extratesticular, 834–841, 836b pediatric acute pain or swelling in, 1892–1899, 1892b anatomy of, 1888 edema of, acute idiopathic, 1898–1899, 1898f hematoceles of, 1902 Henoch-Schönlein purpura and, 1899 hernia and, 1902 hydroceles of, 1899, 1902, 1902f masses of, 1899–1904 masses of, extratesticular causes of, 1902–1903 masses of, intratesticular causes of, 1899–1902 masses of, paratesticular, 1903–1904 trauma to, 1897–1898, 1898f polyorchidism and, 838–839, 841f pyoceles of, 835f, 836 rhabdomyosarcomas of, 840f, 841 sonography of current uses of, 819b technique for, 818–819 trauma to, 847–851, 850f tumors of, extratesticular, 840–841, 840f varicoceles of, 837–838, 838f–839f S/D ratio. See Systolic-to-diastolic ratio Sebaceous cysts, 779, 781f Second harmonic, transducers and, 105 Second-generation contrast agents, 56 Secretin injection, 218 Segmental spinal dysgenesis, 1674, 1689, 1691f Segmentation, in organogenesis, 1524, 1525f Seldinger technique, for drainage catheter placement, 611 Selective uptake contrast agents, 56, 57f Seminal vesicles, 382f–383f, 384 calciication of, 392 congenital abnormalities in, 392 cysts of, 392, 393f pediatric, 1908, 1910f pediatric, anatomy of, 1888, 1888f Seminiferous tubules, 819 Seminoma(s), 584 cryptorchidism and, 851 pediatric in dysplastic gonads, 1899 sonography of, 1899, 1900f testicular, 823, 823f–824f Sensenbrenner syndrome, 1395 Sepsis, pediatric, jaundice in, 1738 Septate uterus, 534–536, 536f–537f Septations, in renal cysts, 357–358, 357b, 358f Septi pellucidi, absence of, 1201–1203 Septic arthritis, pediatric, 1936, 1937f Septic shock, AKI and, 1796

Septo-optic dysplasia (SOD) fetal brain and, 1201–1203, 1203f HPE diferentiated from, 1187–1189 neonatal/infant brain and, 1532–1534, 1535f in rhombencephalosynapsis, 1192 Septula testis, 819, 820f Septum pellucidum absent, in rhombencephalosynapsis, 1192 cavum of, fetal, sonographic view of, 1024f Septum primum, 1279 Septum secundum, 1280 Seroma(s) pelvic, 591 retrosternal, 1726f spinal canal, pediatric, 1697, 1697f stitch, ater herniorrhaphy, 494–496, 495f Serous cystadenocarcinoma, ovarian, 580–581, 580f Serous cystadenoma, ovarian, 580–581, 580f Serous cystic neoplasm, 243, 244f–245f Sertoli cell tumors, 826, 827f pediatric, 1900 Sertoli-Leydig cell tumor, 585 Serum, Urine and Ultrasound Screening Study (SURUSS), 1090 Sex cord-stromal tumors ovarian, 585 testicular, 825–826, 827f Sex reversal, in campomelic dysplasia, 1395 SGA. See Small-for-gestational age fetus Shadowing acoustic, 786 breast sonography and, 791–792, 793f carcinoma causing, 791–792, 793f decreased/absent, in skeletal dysplasias, 1381–1382 malignant masses causes, diferential diagnosis for, 792 by rib, in pediatric chest sonography, 1710 as artifacts, 19–21, 22f in uterine ibroids, 539f, 540, 540b Shattered kidney, 365–366 Shear wave elastography (SWE), 16, 17f–18f, 772 cirrhosis of liver and, 95–96 for pediatric liver, 1764, 1765f Shear waves, in bone, 39 Shigella, 1852 Shockwave, 37, 37f Short umbilical cord, 1481 Short-rib polydactyly syndromes, 1382, 1383f, 1395–1396, 1397f Shoulder. See also Rotator cuf anatomy of, 878–879, 878f arthropathy and, 893–894 degenerative, 893, 894f inlammatory, 893–894, 894f clinical perspective on, 877–878 injection of, 901, 901f pediatric, brachial plexus injury and, 1934–1936, 1936f–1937f posterior, 884 rotator cuf pathology and dysfunction of, 877 subacromial impingement of, 877–879, 882–883 ultrasound techniques for anisotropy and, 895, 895f Crass position in, 881, 883f modiied Crass position in, 881, 883f–884f MRI compared to, 877–878 pitfalls in, 895, 895f protocol for, 879–886, 880t Shunt(s). See also Portosystemic shunts for hydrocephalus, in neonatal/infant brain, duplex Doppler sonography of, 1582, 1584f in hydrocephalus, malfunction of, RI in, 1613, 1613f

Index Shunt(s) (Continued) right-to-let, pediatric, TCD sonography evaluation of, 1614–1618 splenorenal, in portal hypertension, pediatric, 1757, 1759f ventriculoperitoneal, for Dandy-Walker malformation, 1530 vesicoamniotic, for lower urinary tract obstruction, 1363–1365, 1364f, 1365t Shwachman-Diamond syndrome, nesidioblastosis and, 1865, 1865f Sialadenitis, pediatric, chronic, 1634–1635, 1635f Sialoblastoma, salivary gland, pediatric, 1638–1639 Sialolithiasis, pediatric, of submandibular gland, 1633, 1633f Sickle cell disease (SCD) ACA stenosis with, 1607f bone marrow transplantation for, 1598 cerebrovascular disease indicators with, 1598, 1599b MCA and, 1600f, 1604f–1605f ophthalmic artery low as, 1599f stroke and, 1601f–1603f DICA stenosis and, 1606f moyamoya angiopathy and, 1598, 1600f, 1602f, 1608f, 1610 silent cerebral infarcts and, 1598 sleep-disordered breathing and, 1611 spleen in, 157 stroke and cerebrovascular disease indicators with, 1601f–1603f risk categories for, 1599–1604, 1605t, 1606–1607 screening for, 1598 velocity indications of, 1605–1607 TCD sonography for, 1591, 1598–1608, 1599b, 1599f–1608f Side lobe artifacts, 19, 20f Side lobes, 19, 20f Silent cerebral infarcts, SCD and, 1598 Silent (painless) thyroiditis, 725–727 Silicon granulomas, in extracapsular breast implant rupture, 805–807, 806f Silver-Handmaker, 1399 Simple cysts of breast, 774, 775f of pediatric testes, solitary, 1901–1902 Simpson-Golabi-Behmel syndrome CDH and, 1263 hyperechogenic kidneys in, 1351 Single-photon emission computed tomography (SPECT), 747, 747f Sinus bradycardia, fetal, 1297 Sinus venosus ASD, 1280, 1282f Sinus(es) dorsal dermal, pediatric, 1686, 1688f urachal, 322, 323f Sinusoidal obstruction syndrome, 1762–1763 Sirenomelia, fetal, 1238, 1238f, 1401, 1404f Sirenomelia sequence, sacral agenesis in, 1237 Site-speciic ovarian cancer syndrome, 578 Situs inversus totalis, of liver, 80 Sjögren syndrome, chronic pediatric sialadenitis in, 1634–1635 Skeletal deformities, fetal lung size and, 1244 Skeletal dysplasia, fetal categories of, 1377t diagnosis of, 1376–1377, 1377b femur/foot length ratio in, 1379 hydrops from, 1432 lethal, 1386–1396 achondrogenesis as, 1391 campomelic dysplasia as, 1395, 1396f

Skeletal dysplasia, fetal (Continued) features of, 1386b hypophosphatasia as, 1392–1395, 1395f osteogenesis imperfecta as, 1391–1392 short-rib polydactyly syndromes as, 1395–1396, 1397f thanatophoric dysplasia as, 1387–1390 lethality of, pulmonary hypoplasia and, 1382, 1384f nonlethal or variable prognosis, 1396–1399 asphyxiating thoracic dysplasia as, 1398 chondrodysplasia punctata as, 1399 diastrophic dysplasia as, 1398, 1398f dyssegmental dysplasia as, 1399 Ellis-van Creveld syndrome as, 1398–1399 heterozygous achondroplasia as, 1396–1398, 1398f micromelic dysplasia as, 1397t osteogenesis imperfecta types I, III, IV as, 1399 rhizomelic dysplasia as, 1397t prevalence of, 1376, 1377t sonographic evaluation of, 1379–1386, 1379b with abnormal bone length or appearance, 1380–1384, 1381b, 1382f–1384f additional imaging in, 1384–1386 molecular diagnosis in, 1385–1386 MRI in, 1385 with positive family history, 1379–1380 radiography in, 1384 3-D ultrasound in, 1384, 1385f three-dimensional CT in, 1384–1385 Skeletal dysplasia, pediatric, atypical hips and, 1932 Skeletal survey, in fetal hydrops diagnosis, 1435 Skeleton, fetal. See also Limb reduction defects aneuploidy indings in, 1407–1409 limb reduction defects and, 1399–1404 normal, 1089–1097 development of, 1089, 1378f extremity measurements of, 1089, 1379t, 1380f–1381f triploidy and, 1408–1409 trisomy 13 and, 1408, 1408b trisomy 18 and, 1408, 1408b trisomy 21 and, 1408, 1408b Skin folds, thickened, in lethal skeletal dysplasias, 1386 Skull, fetal cloverleaf-shaped, 1136 craniosynostosis with, 1137f–1138f in skeletal dysplasias, 1382 in thanatophoric dysplasia type 2, 1388–1389, 1389f lemon-shaped, 1136, 1137f strawberry-shaped, 1136, 1137f Sleep apnea, pediatric TCD sonography for, 1611 Sleep-disordered breathing, 1611 “Sliding organ sign”, 566 Slipped capital femoral epiphysis, 1931–1932 Sludge biliary acute pancreatitis and, 221 gallbladder and, 194–195, 196f gallbladder, pediatric, 1741, 1743f spontaneous PTB and, 1503 tumefactive, 195, 196f, 1741 SMA. See Superior mesenteric artery Small bowel. See also Bowel; Echogenic bowel fetal, 1308–1316 anorectal malformations and, 1310–1312, 1311f dilated loops of, 1311–1312

I-53

Small bowel (Continued) duodenal atresia and obstruction of, 1308–1309, 1310f echogenic, 1313–1316, 1315f enteric duplication cysts and, 1312–1313, 1313f Hirschsprung disease and, 1312, 1312f jejunoileal atresia obstructing, 1310, 1311f meconium ileus and, 1310 meconium peritonitis and, 1313, 1313t, 1314f meconium pseudocyst and, 1313, 1314f lymphoma of, 266, 266f pediatric, 1841–1847 anatomy of, 1841, 1842f intussusception and, 1844–1845, 1849f obstruction of, 1842–1843, 1846f sonographic technique for, 1841 Small bowel mesentery, 505, 505f Small saphenous vein, 981–982, 981f Small-for-gestational age (SGA) fetus, 1454–1455, 1454b SMI. See Superb microvascular imaging Smith-Lemli-Opitz syndrome ambiguous genitalia and, 1367 microcephaly in, 1194 SMV. See Superior mesenteric vein Snell law, 5 Society for Fetal Urology, grading system of, for hydronephrosis, 1354, 1355f SOD. See Septo-optic dysplasia Sot tissue(s) foreign bodies embedded in, 872, 873f ganglia, compression and, 865 heating of, 37–38, 37f infection of, 872–874, 873f–874f masses of, 869–872, 869f–872f, 871t perienteric, in acute abdomen, 281–282 sarcomas, 871–872, 872f thermal index for, in early, 1039 tumors of, fetal face and, 1154, 1160f Sot Tissue hermal Index (TIS), 39 Solid-pseudopapillary tumor, 248, 248f Soluble form, of injectable steroids, 900 Somites, in spine embryology, 1216–1217, 1217f, 1218t Sonazoid, 56 Sonochemistry, acoustic cavitation and, 42, 42f Sonographic air bronchograms. See Air bronchograms, sonographic Sonohysterography, uterine, 529 Sonoluminescence, 42 SonoVue, 56 Sotos syndrome, megalencephaly associated with, 1194–1195 Sound attenuation of sound energy, 5–7, 7f, 35 intensity of, 5 physical efects of, 35 propagation of, 2–3, 3f propagation velocity of, 2–3, 3f relected, 3–4 theoretical understanding of, 58–59 Sound waves, 2, 2f Spatial compounding, 13–15, 14f–15f Spatial focusing, tissue heating and, 35 Spatial peak temporal average (SPTA), 32 Spatial resolution, 16–19, 18f–19f Speckle, 4, 5f contrast efect of, 13–15, 14f spatial compounding and, 13–15 SPECT. See Single-photon emission computed tomography Volume I pp 1–1014 • Volume II pp 1015–1968

I-54

Index

Spectral broadening, in Doppler ultrasound, 24, 24f, 29, 29b, 31f in carotid artery stenosis, 927, 927f in peripheral arterial stenosis, 968, 969f Spectral window, 925, 925f Specular relectors, 4, 4b, 5f Speech, delayed, obstetric sonography and, 1040 Sperm, transport of, 1049–1051 Sperm granuloma, epididymis and, 841, 843f Spermatic cord anatomy of, 821–822, 821f leiomyomas of, 840–841, 840f lipomas of, 840–841, 840f pediatric cysts of, 1902–1903 torsion of, 1324–1325, 1369 relationship of indirect inguinal hernia to, 476–479, 479f, 481f torsion of, 841–843, 845f Spermatoceles, 839, 842f paratesticular, 1904 pediatric, 1902–1903 Sphincter, internal urethral, 384 Sphincter of Oddi, dysfunction of, complicating liver transplantation, 629 Spiculated breast carcinoma, 786 Spiculation, in breast sonography, 787–788, 788f Spigelian fascia anatomy of, 483–484 spigelian hernia location and, 483, 486f Spigelian hernias, 471, 483–484. See also Hernia(s), spigelian Spina biida, 1218, 1223–1233. See also Neural tube defects abnormalities associated with caudal regression as, 1237–1238, 1237f cranial, 1228–1233 noncranial, 1233 sacral agenesis as, 1237 anatomic landmarks establishing, 1228b closed, cranial changes in, 1183–1186, 1185f, 1185t–1186t deinition of, 1225t evaluation protocol for, with 3-D volume data, 1223b NTDs and, 1223 open, cranial changes in, 1183–1186, 1184f, 1185t–1186t pathogenesis and pathology in, 1226 prevention of, folic acid in, 1224–1225 prognosis of, 1228b screening for alpha-fetoprotein in, 1221, 1226–1228, 1226b, 1227f Chiari II malformation in, 1221, 1228, 1230–1233 ultrasound in, 1226–1228 sonographic indings in, 1228, 1229f–1232f sonographic signs of, 1233b terminology of, 1680 Spina biida occulta deinition of, 1225t pathology of, 1226 Spinal canal, pediatric. See also Spinal dysraphism, pediatric acoustic window for, 1672, 1673f, 1674, 1675f anomalies of, 1678–1679 arachnoid cysts of, 1695–1697, 1696f embryology of, 1672–1674, 1673f hemorrhage and, 1695, 1695f–1696f infection of, 1695 normal anatomy of, 1674–1678, 1675f–1680f seromas and, 1697, 1697f sonographic technique for, 1674–1678 intraoperative uses of, 1697 subcutaneous hemangioma and, 1697, 1697f

Spinal canal, pediatric (Continued) tethered cord and, 1678–1679, 1681f tumors of, 1689–1691, 1691t, 1693f–1694f Spinal column agenesis, 1689 Spinal cord fetal, normal position of, 1218–1221, 1221f pediatric, abnormally long, 1685 tumor of, pediatric, neurogenic bladder in, 1907 Spinal dysgenesis, segmental, 1674, 1689, 1691f Spinal dysraphism, fetal, 1218 cephalocele as, 1139–1140 deinition of, 1225t Spinal dysraphism, pediatric classiication of, 1680–1681, 1682t closed, with subcutaneous mass, 1682–1684, 1682t lipomyelocele and, 1682, 1684f lipomyelomeningocele and, 1682, 1685f meningocele and, 1682–1683 myelocystocele and, 1683–1684, 1686f closed, without subcutaneous mass, 1684–1689 abnormally long spinal cord and, 1685 anomalies at risk for, 1689, 1689b caudal agenesis and, 1689, 1690f complex states of, 1686–1689 diastematomyelia and, 1688–1689, 1688f dorsal dermal sinus and, 1686, 1688f dorsal enteric istulas and, 1686–1688 ilum terminale lipomas and, 1684–1685, 1686f intradural lipomas and, 1686, 1687f midline notochordal formation disorders, 1689 midline notochordal integration disorders, 1686–1689 persistent terminal ventricle and, 1685 segmental spinal dysgenesis and, 1689, 1691f simple states of, 1684–1686 deinition of, 1679–1680 open, 1681–1682, 1682t Chiari II malformation with, 1681–1682 myelomeningocele and, 1681, 1683f placodes and, 1680 terminology of, 1680 Spine, fetal. See also Spina biida abnormalities of deinition of terms for, 1225t diastematomyelia as, 1234–1235, 1236f kyphosis as, 1235–1237, 1236f, 1237b myelocystocele as, 1233–1234, 1234f–1235f presacral masses as, 1239, 1239b sacrococcygeal teratomas as, 1238–1239, 1238b, 1239f scoliosis as, 1235–1237, 1237b sirenomelia as, 1238, 1238f spina biida as, 1223–1233 assessment of, in skeletal dysplasia, 1382 developmental anatomy of, 1216–1221 embryology of, 1216–1218, 1217f, 1218t lower, cloacal exstrophy and, 1328 normal position of, 1218–1221, 1221f ossiication of, 1218, 1219f–1220f in lateral longitudinal scan plane, 1223f in posterior angled transaxial scan plane, 1224f in posterior longitudinal scan plane, 1224f timing and pattern of, 1220t routine sonographic views of, 1021, 1027f scanning techniques for, 1221–1223 MRI for, 1216 scan planes in, 1221, 1222f–1224f 3-D ultrasound in, 1216, 1221–1223 Spiral arteries, 531–532 Spiral clips, pain from, ater herniorrhaphy, 497, 498f

Spleen abscesses of, 148, 151f drainage of, 617 absence of, 142 accessory, 158–159, 160f, 1771f anatomy of, 139–142 bare area of, 139–141, 141f biopsy of percutaneous needle, 607, 608f ultrasound-guided, 161 congenital anomalies of, 158–161 cysts of, 146–148, 146b, 148f–151f fetal, 1320–1322, 1322f embryology of, 139–142, 140f fetal, 1320–1322, 1321f cysts of, 1320–1322, 1322f splenomegaly and, 1320 focal abnormalities of, 146–157 cysts as, 146–148, 146b, 148f–151f nodular lesions as, 148–152, 151f–154f solid lesions as, 152–157 focal solid lesions of, 152–157 benign, 153–157, 155b, 156f–157f malignant, 152–153, 154f–155f, 155b functions of, 141 Gamna-Gandy bodies in, 157 Gaucher disease in, 157, 158f hamartomas of, 153–156, 156f hemangiomas of, 148, 153–157, 156f hematomas of, 158, 159f infarctions of, 156–157, 157f interventional procedures for, 161 lymphangiomas of, 148 measurement of, sonographic approach to, 143–145, 145f metastases to, cystic, 148 nodular lesions of, 148–152 calciied, 150, 153f in candidiasis, 150–152, 154f causes of, 152b in lymphoma, 152, 154f metastatic, 152, 154f microabscesses as, 150–152, 154f in tuberculosis, 150, 151f–152f pathologic conditions of, 145–158 pediatric, 1769–1772 abscesses of, 1769 calciications in, 1769 contusion to, 1771f cysts of, 1769 enlargement of, 1769, 1770b, 1771f granulomas of, 1771f hematomas of, 1770, 1771f infarcts of, 1770, 1771f spontaneous rupture of, 1770 wandering, 1770–1772 peliosis of, 147 pitfalls in interpretation of, 161–162, 161f retrorenal, 162 rupture of, 158 in SCD, 157 sonographic appearance of, 142–158, 144f–145f sonographic technique for, 142, 142f–143f trauma to, 158, 159f–160f tuberculosis and, 150, 151f–152f wandering, 159, 161f weight of, 141 as window to pleural space, 1702, 1707f Splenic varices, in portal hypertension, 1759f Splenic vein pancreatic body and, 211, 211f pediatric Doppler studies of, best approach for, 1752 low direction in, in portal hypertension, 1752

Index Splenic vein (Continued) thrombosis of acute pancreatitis complicated by, 230, 231f chronic pancreatitis and, 232–233, 234f–235f Splenogonadal fusion, 833 paratesticular, 1904 Splenomegaly causes of, 145, 146t complications of, 146 diagnosis of, 145–146 fetal, 1320 massive, 145, 146t portal hypertension as cause of, 145, 147f in sickle cell disease, 157 sonographic appearance of, 143f–144f Splenorenal ligament, 139–141, 140f Splenorenal shunts, in portal hypertension, pediatric, 1757, 1759f Splenosis, posttraumatic, 160–161 Splenunculi, 158–159, 160f Split cord malformation fetal, 1234–1235 pediatric, 1688–1689, 1688f Split liver grat, from deceased donor, 625 Split-screen imaging, for breast assessment, 769, 769f Sports hernias, 484–488, 488f–489f SPTA. See Spatial peak temporal average Squamous cell carcinoma (SCC), 348 Staghorn calculus tyrosinemia and, 1799, 1800f in xanthogranulomatous pyelonephritis, 328, 329f Standard sonographic examination, 1019 Standof pad, in breast tumor imaging, 767, 767f Steatosis difuse, 91, 92f in inborn errors of metabolism, 1738 pediatric, 1740, 1740f, 1741b Stein-Leventhal syndrome, 573 pediatric, 1877–1878, 1879f Stener lesion, 864, 864f Stenotic disease, of abdominal aorta, 441–445, 445f Stensen duct, pediatric, 1630 Stent grat, 438 Stepladder sign, in intracapsular breast implant rupture, 804–805, 805f Sternocleidomastoid muscle, 692f, 694 Sternohyoid muscle, 692f, 694 Sternum, defect of, pentalogy of Cantrell and, 1329 Steroids anabolic, therapy with, hepatic adenomas and, 1746 injectable, for musculoskeletal interventions, 900–901 injection of, interventional sonography for, pediatric, 1961, 1964f Stickler syndrome, clets of secondary palate in, 1153 Stippled epiphyses, 1399 Stitch abscess, ater herniorrhaphy, 494–496, 495f Stomach, fetal, 1306–1308 absent or small, 1306, 1306b esophageal atresia and, 1305–1306, 1305f dilated, 1307, 1308f intraluminal gastric masses in, 1308, 1309f midline, 1307, 1308f–1309f normal, 1307f right-sided, 1307, 1308f–1309f Stomach, pediatric, 1833–1840 anatomy of, 1834–1835, 1835f–1836f antrum distention in, HPS pitfalls and, 1838, 1839f

Stomach, pediatric (Continued) artifact of empty, 1838, 1839f bezoars and, 1840, 1841f gastric diaphragm and, 1839, 1840f gastric ulcers and, 1839–1840, 1840f gastritis and, 1839–1840, 1840f HPS and, 1835–1838, 1835b, 1837f–1838f pitfalls in diagnosis of, 1838, 1838b, 1839f pylorospasm and minimal muscular, 1836–1838, 1838f optimal measurements of, 1834b sonographic technique for, 1833–1835 Stomodeum, 1133–1134 Strain elastography, 16, 17f, 772 Strain modulus, 15–16 Strangulated hernias. See Hernia(s), strangulated Strawberry-shaped skull, 1136, 1137f Streaming, 35 Streptococcal meningitis, group B, neonatal/infant, 1560, 1561f–1562f Stress maneuvers, for hip stability determination, 1923 Strictures in, in Crohn disease, 269–274, 275f–276f String sign, occluded carotid artery distinguished from, 939 Stroke cardioembolic, 915–916 from carotid artery stenosis, 915–916 in neonatal/infant brain, duplex Doppler sonography and, 1580–1581, 1584f SCD and cerebrovascular disease indicators with, 1601f–1603f risk categories for, 1599–1604, 1605t, 1606–1607 screening for, 1598 velocity indications of, 1605–1607 Stromal cell tumors, ovarian, pediatric, 1879 Stromal tumors, gastrointestinal, 264, 265f pediatric, 1862 Struma ovarii, 584 Sturge-Weber syndrome facial hemangiomas in, 1154 pheochromocytomas with, 1910–1912 TCD sonography assessing, 1614 Subacromial impingement, of shoulder, 877–879, 882–883 Subacromial spurs, 878–879 Subacromial-subdeltoid bursa, 879 appearance of, normal, 889, 891f rotator cuf tears and, 888–889, 892f thickening of, 889–891, 892f with ganglion, 889–891, 892f Subacute granulomatous thyroiditis, 724, 724f Subamniotic hematomas, of placenta, 1474 Subarachnoid hemorrhages, neonatal/infant brain and, 1550, 1550f Subarachnoid spaces, neonatal/infant development of, 1520–1521 luid collections in, duplex Doppler sonography of, 1585, 1588f Subchorionic cysts maternal loor infarction with, 1474, 1476f placental, 1474, 1477f Subchorionic hematoma, 1474 placental abruption diferentiated from, 1471, 1474f Subchorionic hemorrhage early pregnancy failure and, 1069, 1069f fetal echogenic bowel and, 1315f Subclavian artery, 975 stenosis of, 976, 978f–979f Subclavian steal phenomenon, 952–954, 953b, 953f–954f, 976, 979f

I-55

Subclavian vein anatomy of, 990–991, 990f stenosis of, sever, 1006, 1009f ultrasound examination for, 991, 991f Subcutaneous edema, fetal, in hydrops, 1417, 1419f–1420f Subdural efusions, neonatal/infant, duplex Doppler imaging of, 1585, 1588f Subdural hematomas, neonatal/infant, 1557, 1558f Subdural hemorrhage, fetal, bilateral, 1207f Subependymal cysts, 1543–1544 of neonatal/infant brain, 1566, 1567f Subependymal hemorrhage, neonatal/infant brain and, 1543–1544, 1543f–1544f Subfascial hematomas, cesarean sections and, 556–557, 557f Subglottic stenosis or atresia, CHAOS and, 1253 Sublingual gland, pediatric, anatomy of, 1631, 1631f Subluxation, 1923, 1927 Submandibular glands, pediatric anatomy of, 1630–1631, 1631f pleomorphic adenoma of, 1638f sialolithiasis of, 1633, 1633f Submandibular space, pediatric, 1630–1631, 1631f cystic lesions of, 1639–1640, 1640b Submandibular window, for TCD sonography, 1592–1593 Subphrenic abscess, 1716 Subplacental hematoma, 1471, 1474f Subscapular fossa, 878–879 Subscapularis tendon anatomy of, normal, 878–879, 879f ultrasound evaluation of, 880, 882f Subtrochanteric femur, absence of, 1400 Subvalvular aortic stenosis, 1292 Succenturiate lobes, of placenta, 1480–1481, 1481f “Sugar icing”, 868f Sulcation disorders, of neonatal/infant brain, 1536–1537 Sulcus(i), of brain development of, 1167 neonatal/infant development of, 1520–1521, 1520f–1521f efacement of, in difuse cerebral edema, 1553, 1554f normal sonographic appearance of, 1169, 1171f radial arrangement of, in corpus callosum agenesis, 1528, 1532f Sulfur colloid scanning, FNH and, 115 “Sunburst sign,” in corpus callosum agenesis, 1528, 1532f Superb microvascular imaging (SMI), 1746 basic technique of, 1749–1750, 1752f Supericial fascia, pediatric, 1628, 1629f Supericial peritendinous and periarticular injections, 902–904 for foot and ankle, 902–904, 903f–904f for hand and wrist, 904, 905f Supericial venous insuiciency, 981–982 Superior mesenteric artery (SMA) pancreatic body and, 211, 211f small bowel obstruction and, 1308 Superior mesenteric vein (SMV), 211, 211f Superior vena cava (SVC) anatomy of, 991 catheter position for, pediatric, 1716–1721, 1722f stenosis, with PICC line, 993f thrombosis of, pediatric, 1721, 1721b, 1722f ultrasound examination of, 991–992, 992f Supernumerary glands, 733 Supernumerary kidneys, 319 Supernumerary testes, 838–839, 841f Volume I pp 1–1014 • Volume II pp 1015–1968

I-56

Index

Superoanteromedial ridge, 416–417 Supraclavicular lymphadenopathy, pediatric, 1658 Suprahyoid space, pediatric anatomy of, 1628–1640, 1629f cystic lesions of, 1639–1640, 1640b, 1640f–1641f masticator space of, pathology of, 1640, 1641f salivary glands in, 1629–1639 anatomy of, 1630–1631 Supraspinatus fossa, 878–879 Supraspinatus tendon anatomy of, 878–879 calciic tendinitis of, 891–892, 892f postoperative, 888, 891f tendinosis of, 886f ultrasound evaluation of, 881–883, 883f–884f Supratentorial tumors, neonatal/infant brain and, 1562 Supraventricular tachycardia (SVTs) with Ebstein anomaly, 1286–1287 fetal, 1296–1297, 1296f hydrops from, 1424, 1425f Surface epithelial inclusion cysts, 569, 573 Surface epithelial-stromal tumors, 579–582, 580f–582f SURUSS. See Serum, Urine and Ultrasound Screening Study Surveillance of AAA, 435–437 CT in, 437 sonographic technique for, 436–437, 436f–437f active, for prostate cancer, 401 Suspensory (infundibulopelvic) ligament, 564–565 Sutures, cranial, premature fusion of, 1136–1139, 1138b, 1138f–1139f SVC. See Superior vena cava SVTs. See Supraventricular tachycardia SWE. See Shear wave elastography Swyer syndrome, 1887 Sylvian issure, neonatal/infant, development of, 1514f–1515f, 1520–1521 Syncytiotrophoblast, 1049, 1051–1052, 1052f, 1466f Syndactyly fetal, 1406, 1406f of ingers, in triploidy, 1105f, 1406 Synechia, amniotic band sequence and, 1401 Synovitis, 867, 869 hip joint, pediatric, 1931f Syntelencephaly, 1187, 1189, 1535–1536 Synthetic arteriovenous grat. See Arteriovenous grat, synthetic Syphilis, 1203–1204 fetal hydrops from, 1431–1432 Syringocele, 1683–1684 Syrinx, 1681 System setup, obstetric sonography and, 1035– 1036, 1035f–1037f Systemic lupus erythematosus, maternal, fetal AVB from, 1297 Systolic velocity, cerebral, factors changing, 1612t Systolic-to-diastolic ratio (S/D ratio), 27, 27f T “T” sign, in monochorionicity, 1119, 1119t, 1121f Tachyarrhythmias, fetal, hydrops from, 1424 Tachycardia fetal, 1296–1297, 1296f neonatal/infant, intracranial RI and, 1576 supraventricular with Ebstein anomaly, 1286–1287 fetal, 1296–1297, 1296f fetal, hydrops from, 1424, 1425f ventricular, 1296 Tactile sensation, in obstetric sonography, 1038 Tailgut cysts, 297, 298f

Takayasu arteritis aortic stenosis in, 444 of common carotid artery, 944–946, 947f Talipes equinovarus, fetal, 1406f, 1407 campomelic dysplasia and, 1395 Talipomanus, fetal, 1407 TAMM. See Time-averaged mean of maximum velocity Tamoxifen, 544–545, 545f Tandem plaques, in carotid stenosis, 923–924 TAPS. See Twin anemia polycythemia sequence Tardus-parvus waveform(s) arterial stenosis and, 969, 971f in hepatic artery thrombosis ater liver transplantation, 631, 633f in internal carotid artery stenosis, 934f, 938 pediatric renal artery stenosis and, 1809 in peripheral artery stenosis, 965–966 in popliteal artery occlusion, 968f in renal artery duplex Doppler sonography, 450, 450f in renal artery stenosis, 368, 368f in subclavian steal phenomenon, 953b, 954 Target pattern, in gut wall, 257, 260f Targeted organ lesion biopsy, 1961, 1961f–1962f TAS. See Transabdominal sonography TASC. See Trans-Atlantic Inter-Society Consensus TCC. See Transitional cell carcinoma TCD. See Transcranial Doppler sonography TDLUs. See Terminal ductolobular units Teale femoral hernia, 482, 485f Teen mothers, fetal gastroschisis and, 1322–1323 Tegmento-vermian angle, 1189–1190 Telangiectasia, hereditary hemorrhagic, 104 Telencephalon, formation of, 1077 “Telephone receiver” femur, 1380f Temporal average intensity, 36 Temporal bone approach, for duplex Doppler ultrasound of neonatal/infant brain, 1574, 1575f Temporal horns, of lateral ventricles, neonatal/ infant, in coronal imaging, 1514–1515 Temporal maximum intensity projection imaging, 64, 65f Temporal peak intensity, 36, 36f Temporal tap, in external carotid artery identiication, 918, 918f Tendinitis, calciic injections for, 909, 911f of supraspinatus tendon, 891–892, 892f Tendinosis, 859–861, 861f de Quervain, injection for, 904, 905f rotator cuf, 886, 886f in sports hernia, 486 of supraspinatus tendon, 886f Tendon(s) anatomy of, normal, 859, 860f anisotropy of, 859, 860f, 899 calciication of, 859–861 conjoined direct inguinal hernia and, 479–481, 483f–484f weakness/tear of, sports hernia and, 485–486, 489f inlammation of, 861–862, 862f injections of deep, 904–907 injuries to, 859–861, 861f tears to, 861, 861b, 862f ultrasound techniques for, 859–862 Tenosynovitis, 861–862, 862f long head of biceps, 892–893, 893f stenosing, injections for, 902 Tenotomy, percutaneous, 909–910, 913f Teratocarcinomas, pediatric, testicular, 1899 Teratogenic efects, from hyperthermia, 38 Teratogens, thermal efects of ultrasound and, 1037

Teratologic hip dislocation, pediatric, 1932 Teratoma(s). See also Sacrococcygeal teratomas cystic, ovarian, 582–584, 582b, 583f dacryocystocele diferentiated from, 1143 fetal cardiac, 1294 cervical, 1159, 1161f intracranial, 1208–1209, 1209f intrapericardial, hydrops from, 1424 neck, hydrops from, 1425, 1426f sacrococcygeal, 1238–1239, 1238b, 1239f, 1430–1431 immature, 584 neonatal/infant brain, 1562 cardiac, 1293 pediatric benign, ovarian, 1880, 1880f cervical, 1654, 1654f hemorrhagic ovarian cyst diferentiated from, 1877 pseudoprecocious puberty and, 1887 sacrococcygeal, 1691, 1691t, 1694f testicular, 1899 thymic, 1723–1724 testicular, 823–824, 825f thyroid gland, 1648 Teres minor tendon anatomy of, 878–879 ultrasound evaluation of, 884 Terminal ductolobular units (TDLUs), of breast, 760–761 carcinoma in, 789–790, 792f sonographic appearance of, 762, 766f Terminal ileitis, 288 Terminal myelocystocele, 1234 Terminal transverse limb defects, amniotic band sequence and, 1400 Terminal ventricle, persistent, pediatric, 1685 Tessier clets, classiication of, 1152–1153, 1153f Testicular appendage, pediatric, torsion of, 1897, 1897f Testicular artery(ies), 820f–821f, 821 Testicular duplication, pediatric, 1891 Testicular feminization, fetal, 1368 Testicular microlithiasis, pediatric, 1904, 1904f Testicular torsion, 844–846, 844f–845f pediatric acute, 1893–1894, 1894f acute scrotal pain from, 1892 chronic, 1895 color Doppler sonography in, 1895–1899, 1896b detorsion of, 1895–1896 extravaginal, 1892–1893, 1893f incomplete, 1896 intravaginal, 1893–1894, 1893f late, 1895 “missed”, 1895, 1895f within scrotal sac, 1893–1894 sonographic signs of, 1894b spontaneous detorsion of, 1896 types of, 1893–1894, 1893f Testis(es). See also Scrotum abscess of, 831–832, 831f adrenal rests and, 832–833, 833f, 1824 anatomy of, 819, 819f–820f appendix, 820–821, 820f pediatric, 1897 arterial supply of, 820f–821f, 821 cryptorchid, seminomas in, 823 cryptorchidism and, 851, 851f pediatric, 826 cystic dysplasia of, 830

Index Testis(es) (Continued) cysts of, 829, 829b cystic dysplasia and, 830 epidermoid, 830f, 831 intratesticular, 829, 830f tubular ectasia of rete testis and, 829–830, 830f ectopia of, transverse, 1890 feminization of, 826 dysplastic gonads and, 1899 primary amenorrhea in, 1887 fetal descent of, 1367 undescended, 1367 ibrosis of, ater orchitis, 846, 849f fracture of, 850, 850f gubernaculum, 851 hematoma of, 848–850, 850f heterogeneous “striped”, 846, 849f infarction of ater herniorrhaphy, 494–496, 495f segmental, 832, 832f in inguinal canal, 851, 851f malpositioned, 851 mediastinum, 819, 820f pediatric, 1888 metastases to, 822b, 826–829, 826b hamartomas as, 829, 829f leukemia as, 827, 828f lymphoma as, 826–827, 828f myeloma as, 827–829 microlithiasis of, 833, 833b, 834f pediatric accessory, 1891 anatomy of, 1888–1890, 1889f appendix, 1897 bilobed, 1891 congenital abnormalities of, 1890–1892, 1890f cystic dysplasia of, 1891–1892, 1891f cysts of, solitary simple, 1901–1902 detorsion of, 1895 hematomas of, 1897–1898 Henoch-Schönlein purpura and, 1899 hyperemia of, 1896 infarction of, 1895 newborn, 1888, 1889f ovotestis and, 1891, 1891f postpubertal, 1888–1890, 1889f rete, tubular ectasia of, 1891–1892, 1892f rupture of, 1897–1898, 1898f smaller than normal, 1891 torsion of, 1870, 1892–1899, 1893f–1894f, 1894b, 1896b undescended, right, 1890, 1890f rete, 819 tubular ectasia of, 829–830, 830f, 1891–1892, 1892f rupture of, 848, 850f seminomas in, 823, 823f–824f septula, 819, 820f splenogonadal fusion and, 833 supernumerary, 838–839, 841f torsion knot and, 844, 845f trauma to, 847–851, 850f tumors of, 822–834 choriocarcinoma as, 824, 825f, 1899 classiication of, 822b embryonal carcinoma as, 823, 825f, 1899 endodermal sinus, 823–824, 825f, 1899 germ cell, 822–825, 822b, 825f–826f gonadal stromal, 826, 827f Leydig cell, 826, 827f malignant, 822–826 markers of, 822

Testis(es) (Continued) metastatic, 822b mixed germ cell, 822–823, 822b, 825f non-germ cell, 825–826 nonseminomatous germ cell, 822b, 823–824, 825f pediatric, 1899–1902 regressed germ cell, 824–825, 825f–826f Sertoli cell, 826, 827f sex cord-stromal, 825–826, 827f stromal, 822, 822b teratocarcinomas as, 1899 teratomas as, 823–824, 825f, 1899 yolk sac, 823–824, 825f undescended, 851, 851f dysplastic gonads and, 1899 in prune belly syndrome, 1361–1362 right, pediatric, 1890, 1890f Testosterone, Leydig cells and secretion of, 819 Tethered cord, 1674 in diastematomyelia, 1236f fetal cloacal exstrophy and, 1328 pediatric, 1678–1679, 1681f spina biida occulta and, 1226 Tetralogy of Fallot (TOF), 1288, 1288f Tetraphocomelia, Roberts syndrome and, 1401 TGA. See Transposition of great arteries TGC. See Time gain compensation halamostriate vessels, mineralization of, 1203, 1204f halamus fetal, normal sonographic appearance of, 1168 neonatal/infant, sagittal imaging of, 1515, 1517f vasculopathy of, neonatal/infant brain and, 1556–1557 α-halassemia, nonimmune hydrops from, 1423, 1431 hanatophoric dysplasia bowing of long bones in, 1381–1382 campomelic dysplasia diferentiated from, 1388–1389 cloverleaf-shaped skull and, 1136, 1137f, 1389f craniosynostosis in, 1136–1138, 1137f diagnosis of, 1376–1377 homozygous achondroplasia diferentiated from, 1389, 1389f lethal skeletal dysplasia and, 1387–1390 megalencephaly associated with, 1194–1195 platyspondyly in, 1388–1389, 1390f sonographic appearance of, 1380f type 1, 1388–1389 type 2, 1388–1389, 1389f hanatophoric skeletal dysplasia, cortical malformations and, 1193–1194 heca externa, 1049 heca lutein cysts, 570, 572 pediatric, 1875 hecomas, ovarian, 585 helarche, pseudoprecocious puberty and, 1888 hermal efects, in ultrasound, 31. See also Bioefects, thermal obstetric, 1036–1038 hermal index (TI), 38–40, 38b for bone, in late pregnancy, 1039 obstetric sonography duration as function of, 1035–1036, 1036f, 1042t for sot tissue, in early pregnancy, 1039 tissue model of with bone at focus, 39 with bone at surface, 39–40 homogeneous, 39 high grat, hemodialysis and, preoperative mapping for, 1000, 1001f

I-57

horacentesis, pediatric, ultrasound-guided, 1725–1726 horacic ectopia cordis, 1295, 1296f horacic kidney, 318 horacic outlet syndrome, in upper extremity peripheral arteries, 976–977, 980f horacoabdominal ectopia cordis, 1295 horacoabdominal schisis, 1401 horax, fetal anomalies of, hydrops from, 1425–1427, 1427f circumference and length of gestational age correlated with, 1247t pulmonary hypoplasia and, 1382, 1384f circumference of, decreased in hypophosphatasia, 1392 severe micromelia with, 1387t echogenic lesions of, diferential diagnosis of, 1248t horotrast, 123 hree-dimensional (3-D) ultrasound, 15, 16f for breast lesions, 773 for fetal heart assessment, 1277 for fetal spine, 1216, 1221–1223 for neonatal/infant brain imaging, 1518 in placental volume assessment, 1466, 1468f for prostate cancer, 406–407 for skeletal dysplasia evaluation, 1384, 1385f for uterus, 529 hreshold level, for seeing gestational sac, 1056 hrill, from carotid stenosis, color Doppler, 933 hrombocytopenia, alloimmune, intracranial hemorrhage and, 1206 hrombocytopenia–absent radius syndrome, 1401, 1402f hrombophlebitis, ovarian vein, 589–590, 589f hrombosis. See also Deep venous thrombosis cerebral sinovenous, 1547–1548 dural sinus fetal, 1205–1206, 1206f neonatal/infant, 1585 hepatic artery, ater liver transplantation, 627, 628f, 631, 633f hepatic vein, pediatric, suprahepatic portal hypertension and, 1763, 1763f IJV, 955–956, 956f–957f central line placement causing, 1658, 1661f of iliac veins, 459–460, 459f–461f detection diiculties with, 988, 988f of IVC, 459–460 ater liver transplantation, 636–637, 642f, 1766, 1769f–1770f ovarian vein, 369, 589–590, 589f ater pancreas transplantation, 677–678, 678f–679f portal vein, 98, 99f–100f chronic pancreatitis and, 232–233, 235f from HCC, 120, 121f ater liver transplantation, 635–636, 639f–640f, 1766 malignant, 98, 99f pediatric, 1757, 1757b renal artery, ater renal transplantation, 653–655, 657f Doppler assessment of, pediatric, 1807–1809, 1808f renal vein, 369, 370f Doppler assessment of, pediatric, 1809 hyperechogenic kidneys and, 1351 pediatric, acute, Doppler assessment of, 1804–1805, 1804b, 1804f ater renal transplantation, 658, 662f round ligament, simulating groin hernia, 500, 501f Volume I pp 1–1014 • Volume II pp 1015–1968

I-58

Index

hrombosis (Continued) of splenic vein acute pancreatitis complicated by, 230, 231f chronic pancreatitis and, 232–233, 234f–235f SVC, pediatric, 1721, 1721b, 1722f vascular, pediatric chest and, 1716–1721, 1721f–1723f humb aplastic or hypoplastic, in Fanconi pancytopenia, 1400, 1402f hitchhiker in diastrophic dwarism, 1382, 1406 diastrophic dysplasia and, 1398, 1398f triphalangeal, in Aase syndrome, 1401 hump artifacts, 60 hymic cyst, 1652, 1653f, 1723–1724 hymic index, 1723, 1725f formula for calculation of, 1724t normal, for children under 2, 1726t hymopharyngeal ducts, formation of, 1652 hymus fetal, normal appearance of, 1244f pediatric benign abnormalities of, 1723–1724 cervical ectopic, 1723 ectopic, 1652, 1653f mediastinal masses and abnormal location of, 1723 normal, blood vessels of chest and, 1716– 1721, 1721f superior herniation of, 1723 hyroglossal duct cysts, pediatric, 1640, 1643, 1644f–1645f hyroid artery, superior, 918 hyroid gland. See also hyroiditis adenomas of, 697, 700f anatomy of, 692–694, 692f aplasia of, 694, 694f carcinoma of, 695, 698–708 anaplastic, 707–708, 708b, 709f follicular, 701, 701b, 706f–707f, 1648 incidence of, 722, 722f–723f medullary, 701–707, 707f–708f, 1648 papillary, 698–701, 701f–705f, 713, 1648, 1649f papillary microcarcinoma, 701, 706f CEUS for assessment of, 692, 714–715 congenital abnormalities of, 694, 694f cysts, calciications of, 695 difuse disease of, 723–728, 723b adenomatous goiter as, 727 Graves disease and, 727, 727f, 1646, 1646f ectopic, 694 elastography for assessment of, 692, 714–715, 715f–716f ethanol injection for nodular disease of for autonomously functioning nodules, 719–720 for benign cystic lesions, 719, 719f for solitary solid benign “cold” nodules, 720 fetal, normal sonographic appearance of, 1136f hypoplasia of, 694, 694f incidentally detected nodule and, 720–723, 722f–723f, 723b instrumentation for, 691–692, 692f lingual, pediatric, 1639 lobes of, 692 lymphoma of, 708–709, 709f metastases to, 709, 710f nodular disease of, 694–723 adenomas in, 697, 700f carcinoma in, 698–708 ine-needle aspiration biopsy in, 709–710, 710t, 722 hyperplasia and goiter in, 695–697, 695f–699f

hyroid gland (Continued) lymphoma in, 708–709, 709f, 1648 metastases in, 709, 710f parathyroid adenomas confused with, 745–746 pathologic features of, 695–709 sonographic correlates of, 695–709 sonographic evaluation of, 695b pediatric cancer of, 1648, 1648b, 1649f congenital lesions of, 1642–1643 cysts of, 1646, 1647f dimensions of, normal, 1642t dysgenesis of, 1642–1643 ectopic, 1642–1643, 1644f follicular adenoma of, 1646–1648, 1647f hemiagenesis of, 1642–1643, 1643f hemorrhage in, 1646, 1647f inlammatory disease of, 1643–1646, 1645f–1646f isthmus of, 1640–1642 lobes of, normal thickness of, 1643t masses of, 1646–1648, 1647f–1649f, 1648b normal anatomy of, 1640–1642, 1642f, 1642t–1643t pseudonodule of, 1646 pyramidal lobe of, 1640–1642 retrosternal, 1723 volume of, normal, 1643t sonographic applications in, 710–720 for benign and malignant nodule diferentiation, 696f–699f, 712–714, 712t CEUS for, 692, 714–715 elastography for, 692, 714–715, 715f–716f incidentally detected nodule and, 720–723, 722f–723f, 723b needle biopsy guidance for, 715–720, 718f–719f, 721f for thyroid mass detection, 710–712, 711f–712f TIRADS for, 714 sonographic technique for, 691–692, 692f vascularity of, 693, 694f volume of, measuring, 692–693, 693f hyroid Imaging Reporting and Data System (TIRADS), 714 hyroid inferno, in Graves disease, 727, 727f hyroiditis, 723b acute suppurative, 723–724 chronic autoimmune lymphocytic, 724, 725f–727f de Quervain, 1645 focal, pediatric, 1645 Hashimoto, 724, 725f–727f fetal goiter and, 1159–1163 pediatric, 1645, 1646f invasive ibrous, 727–728, 728f painless (silent), 725–727 subacute granulomatous, 724, 724f hyromegaly, fetal, 1159–1163 TI. See hermal index TIA. See Transient ischemic attack TIB. See hermal index for bone Tibia, dislocation of, pediatric, 1934f Tibial artery anterior, 966 normal appearance of, 966–967 posterior, 966 sonographic technique for, 967 Tibial hemimelia, pediatric, 1933 Tibial tendons, posterior, injection of, 902, 903f Tibial veins anterior, 981, 981f posterior, 981, 981f Tibioperoneal trunk, 966, 981

Time gain compensation (TGC) artifacts and settings of, 19–21 control of, 8–9, 8f output control and, 50 Time-averaged mean of maximum (TAMM) velocity, 1593, 1605–1606 Time-averaged peak velocity, 1593 “Tip of the iceberg” sign, 582–583 TIPS. See Transjugular intrahepatic portosystemic shunts TIRADS. See hyroid Imaging Reporting and Data System TIS. See hermal index for sot tissue Tissue harmonic imaging, 13, 13f–14f, 38, 61–62 Tissue heating spatial focusing and, 35 temporal considerations in, 36, 36f tissue type and, 36, 36f Tissue plasminogen activator (TPA), 1622 Tissue vibration artifact, 973–974, 974f T-lymphotropic virus, 1203–1204 TMPRSS2:ERG test, 396 Tobacco, fetal gastroschisis and, 1322–1323 Toe polydactyly, fetal, 1406f Toes, sandal, 1406f, 1407 TOF. See Tetralogy of Fallot Tongue, fetal, abnormally enlarged, 1153, 1153b, 1158f TORCH infections, 1203–1204 neonatal/infant brain and, 1511, 1558 Torsion, testicular. See Testicular torsion Torsion knot, 844, 845f Toxemia, pediatric pregnancy and, 1884 Toxoplasmosis fetal brain and, 1204 fetal hydrops from, 1432 prenatal, neonatal/infant brain and, 1558–1560 TPA. See Tissue plasminogen activator Trabecula septomarginalis, moderator band of, 1274–1275 Trachea, fetal, CHAOS and, 1253 Tracheal webs, fetal, CHAOS and, 1253 Tracheoesophageal istula, fetal CHAOS and, 1254–1255 esophageal atresia and, 1305 Transabdominal scanning, for placenta previa, 1469 Transabdominal sonography (TAS), for pelvis, 564 Trans-Atlantic Inter-Society Consensus (TASC), 970 Transcranial Doppler (TCD) sonography adult functional, 1622 indications for, 1598–1623, 1598b vasospasm and, 1608–1610, 1610t for carotid artery examination, 948–950, 950f pediatric ACA collateral low evaluation and, 1610, 1611f angle correction for, 1607 asphyxia and, 1614, 1616f AVM detection with, 1614, 1615f brain death and, 1618–1620, 1618b, 1619f–1620f in cardiopulmonary bypass, 1621–1622 in CEA, 1621 cerebral edema and, 1614, 1617f contrast enhancement for, 1597 ECMO monitoring with, 1622 equipment types for, 1591–1592 factors changing indices in, 1612t foramen magnum approach for, 1592, 1595f functional, 1622 headaches and, 1610–1611, 1612f hydrocephalus and, 1611–1614, 1613f hyperventilation therapy and, 1614

Index Transcranial Doppler (TCD) sonography (Continued) indications for, 1598–1623, 1598b in intraoperative neuroradiologic procedures, 1620–1622, 1621f–1622f limitations for, 1597, 1597t orbital approach for, 1592, 1596f pitfalls in, 1597, 1597t power settings for, 1597 right-to-let shunt evaluation with, 1614–1618 for SCD, 1591, 1598–1608, 1599b, 1599f–1608f sleep apnea and, 1611 submandibular approach for, 1592–1593 technique for, 1592–1596 TPA and, 1622 transtemporal approach for, 1592, 1593f–1594f vascular malformations and, 1614, 1615f vasospasm and, 1608–1610, 1609f, 1610t velocity evaluation in, 1593, 1595–1596 Transducer(s), 7–8 arrays, 11–12, 12f hand-held, for breast sonography, 788, 789f–790f heating, in obstetric sonography, 1038 heeling and toeing of, 768 in interventional sonography, pediatric, 1943 locating needle ater insertion and, 1946– 1947, 1947f for neonatal/infant brain imaging, 1512 output control and, 50 percutaneous needle biopsies and sterilization of, 600 second harmonic and, 105 selection of, 12 for obstetric sonography, 1035 Transfundal pressure, dynamic cervical change and, 1501–1503 Transfusion, fetomaternal, maternal serum alpha-fetoprotein elevation in, 1228. See also Twin-twin transfusion syndrome Transhepatic cholangiography, 614–615 Transient double-bubble sign, 1309 Transient elastography, 1764 Transient ischemic attack (TIA), 916 carotid artery embolism causing, 919 Transitional cell carcinoma (TCC) bladder, 347–348, 350f genitourinary tract tumors and, 346–348 nonpapillary, 346 ovarian, 581–582, 582f papillary, 346 renal, 346–347, 346f–349f synchronous, 346 ureteral, 347 Transitional cell papilloma, lower urinary tract, pediatric, 1910–1912 Transjugular intrahepatic portosystemic shunts (TIPS), 131–132, 132b, 132f–133f, 463, 1764 Translabial ultrasound of cervix, 1497 of female urethra, 315, 316f Transmediastinal artery, 820f, 821 Transmitter, 7 Transorbital approach, for duplex Doppler ultrasound of neonatal/infant brain, 1574, 1575f Transperineal biopsy, TRUS-guided, 411 Transperineal scanning, in Crohn disease, 276 Transperineal ultrasound cervix in, 1497, 1497f in ureteral calculi detection, 337

Transplantation, organ, 623–624. See also Liver transplantation; Pancreas transplantation; Posttransplant lymphoproliferative disorder; Renal transplantation Transposition of great arteries (TGA), 1289–1290, 1289f–1290f Transrectal ultrasound (TRUS) biopsy guided by, 407–411, 408f analgesia and, 407 antibiotic prophylaxis and, 407, 408f anticoagulation and, 407–408 bowel preparation and, 407 indications and sampling for, 409, 409b, 410f in men with absent anus, 411 mpMRI-TRUS fusion, 410–411 other applications of, 411–412 preparation for, 407–408 ater radical prostatectomy, 411, 411f side efects and complications in, 409 technique for, 408–409, 408f transperineal, 411 brachytherapy guided by, 401, 402f for drainage of pelvic abscesses, 612 for hematospermia, 394 infertility and, 392–394, 393f of male urethra, 315, 316f probes for, 386–387, 386f of prostate, 381–382 prostate cancer, mpMRI fusion with, 406–407, 410–411 prostate cancer and, 302, 302f, 403–406, 403f–405f, 406b in rectal carcinoma staging, 301 rectal cleansing prior to, 387 Transtemporal window for TCD sonography, 1592, 1593f–1594f for transcranial Doppler sonography, 948 Transurethral resection of ejaculatory ducts, 393 Transurethral resection of prostate (TURP), 385f–386f, 388 Transvaginal sonography, in peritoneal disease evaluation, 506, 506f–507f Transvaginal ultrasound for acute appendicitis diagnosis, 283, 285f for adnexa assessment, 566 cervical abnormal indings on, 1503b for cervix, 1497–1498, 1497f–1498f diagnostic value of, 258 for drainage of pelvic abscesses, 612, 613f endometrial thickness assessment with, 545–546 in gestational sac identiication, 1054–1055 for pediatric pelvis, 1870–1871 for placenta previa, 1469 in pregnancy, safety of, 1049 thermal efects of, 38 in ureteral calculi detection, 337, 338f for uterus, 529, 529b in yolk sac identiication, 1057 Transventricular valvotomy, 1292 Transverse abdominis tendon, torn, in spigelian hernia, 483–484, 487f Transverse mesocolon, 219, 220f Transverse myelitis, pediatric, neurogenic bladder in, 1907 Transverse testicular ectopia, 1890 Transverse waves, 2–3 TRAP. See Twin reversed arterial perfusion Trauma biliary, hemobilia from, 174, 175f bladder, 366 cervical, carotid artery damage from, 946, 948f dural sinus thrombosis from, 1205–1206 focused abdominal sonography for, 508 to genitourinary tract, 365–366

I-59

Trauma (Continued) to liver, 129–132, 131f to lower urinary tract, pediatric, 1912 to musculoskeletal system pediatric, 1938–1939, 1939f pediatric epididymitis following, 1897 scrotum and, 1897–1898, 1898f renal, 365–366, 366f scrotal, 847–851, 850f splenic, 158, 159f–160f testicular, 847–851, 850f ureteral, 366 Treacher Collins syndrome clets of secondary palate in, 1153 midface hypoplasia in, 1148 Triangular cord sign, in biliary atresia, 1734–1735, 1737, 1738f Trichobezoars, 300, 1840, 1841f Tricuspid atresia fetal, hydrops from, 1423–1424 hypoplastic right ventricle with, 1287 Tricuspid insuiciency, fetal, spectral Doppler assessment of, 1281f Tricuspid regurgitation in aneuploidy screening, 1095 in Ebstein anomaly, 1286 neonatal/infant, cardiac pulsations in veins and, 1578, 1578f “Trident hand” coniguration, achondroplasia and, 1407, 1408f Triggered imaging, 65 Trigone, 314 neonatal/infant, in coronal imaging, 1515 pediatric, identiication of, 1871, 1872f Triorchidism, 1891 Triphalangeal thumb, in Aase syndrome, 1401 Triphasic waveform, 966–967 Triplets, amnionicity and chorionicity and, 1122f Triploid karyotype, partial molar pregnancy and, 1078 Triploidy, 1078 common sonographic indings in, 1104–1106, 1104b, 1105f Dandy-Walker malformation in, 1105f fetal hydrops from, 1429–1430 IUGR in, 1105f omphalocele in, 1105f ovarian cysts in, 1105f skeletal indings in, 1408–1409 syndactyly of ingers in, 1105f, 1406 Triradiate cartilage of hip, 1923 in sonogram of hip from transverse/neutral view, 1927 Trisomy 9, horseshoe kidney in, 1345–1346 Trisomy 13 (Patau syndrome) common sonographic indings in, 1104, 1104b, 1105f facial clets in, 1151 fetal hydrops from, 1429–1430 fetal omphalocele and, 1325 fetal pentalogy of Cantrell and, 1329 HPE in, 1104, 1105f hyperechogenic kidneys in, 1351 NT in, 1093 polydactyly in, 1104, 1105f proboscis in, 1104, 1105f skeletal indings with, 1408, 1408b umbilical cord cysts in, 1483 Trisomy 17, biliary atresia and, 1737 Trisomy 18 (Edwards syndrome) biliary atresia and, 1737 CDH and, 1263 Volume I pp 1–1014 • Volume II pp 1015–1968

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Index

Trisomy 18 (Edwards syndrome) (Continued) choroid plexus cyst in, 1103f, 1104 clenched hands in, 1103, 1103f common sonographic indings in, 1103–1104, 1103b, 1103f congenital heart defects in, 1103 ectopia cordis and, fetal, 1329 facial clets in, 1151 fetal hydrops from, 1429–1430 fetal pentalogy of Cantrell and, 1329 horseshoe kidney in, 1345–1346 hydrocephalus in, 1103 IUGR and, 1104 mega-cisterna magna and, 1168–1169 NT in, 1093 omphalocele in, 1103, 1103f fetal, 1325 polyhydramnios in, 1104 skeletal indings with, 1408, 1408b umbilical cord cysts in, 1103f, 1483 Trisomy 21 (Down syndrome) absent nasal bone in, 1150 adjunct features of, 1101 A-V canal, 1098f AVSD and, 1101, 1284 β-hCG concentration in, 1089–1090 choroid plexus cysts and, 1101 congenital heart defects in, 1097, 1098f duodenal atresia in, 1097, 1098f ear length in, 1101 echogenic bowel in, 1100f, 1101 echogenic intracardiac focus in, 1100f, 1101 femur length in, 1100–1101 fetal hepatomegaly and, 1316 fetal hydrops from, 1429–1430 frontothalamic distance in, 1101 genetic sonography in, 1102–1103 humerus length in, 1101 hypoplasia of middle phalanx in, 1101 iliac angle measurements in, 1101 macroglossia in, 1153 markers in, 1097 cluster of, likelihood ratios of, 1098t combined, 1100t, 1101–1103 common second-trimester, 1099b isolated, likelihood ratios of, 1097t midface hypoplasia in, 1148 nasal bone in, 1099–1100, 1099f NT in, 1089, 1090f nuchal fold in, 1097–1099, 1099f, 1154–1159 prevalence of, 1088–1089 risk for, short femur indicating, 1381 risk ratio for, revised, 1102b screening for, second-trimester, 1097–1103, 1098f skeletal indings with, 1408, 1408b structural anomalies in, 1101 urinary tract dilation in, 1100f, 1101 VM in, 1098f VSDs in, 1098f, 1101 wormian bones in, 1139 Trocar technique, for drainage catheter placement, 611, 611f Trophoblastic blood low, 1083 Trophoblastic tumor, placental-site, 1082 True hermaphroditism, pediatric, 1891, 1899 Truncal artery, 1288 Truncal valve, 1288 Truncus arteriosus, 1288, 1289f Trunk, length of, shortened, in achondrogenesis, 1391 TRUS. See Transrectal ultrasound TSC. See Tuberous sclerosis T-shaped uterus, 1881 TTT. See Twin-twin transfusion syndrome Tubal occlusion devices, 553f, 554

Tubal ring, ectopic, 1072, 1073f Tuberculosis of adrenal glands, 423 epididymitis associated with, 841, 843f spleen and, 150, 151f–152f urinary tract, 329–330, 330f Tuberculosis colitis, 287–288 Tuberculous peritonitis, 517–521, 522f Tuberous sclerosis (TSC) angiomyolipoma and, 351 cardiac rhabdomyomas and, 1293, 1424 fetal brain and, 1198, 1200f hemimegalencephaly associated with, 1195 pediatric, renal cysts in, 1816, 1817f pheochromocytomas with, 1826, 1910–1912 prenatal intracranial tumors in, 1208 renal cysts in, 364–365, 365f Tubo-ovarian abscess, in pelvic inlammatory disease, 588–589, 588f, 1886–1887, 1886f Tubo-ovarian complex, in pelvic inlammatory disease, 588–589, 588f, 1886–1887, 1886f Tubular ectasia, 359 of rete testis, 829–830, 830f pediatric, 1891–1892, 1892f Tubular necrosis, acute, 370 acute kidney injury and, 1795–1796, 1797f renal transplantation complication with, 649–651, 653f, 1809 Tubuli recti, 819 Tubulointerstitial ibrosis, 359 Tumefactive chronic pancreatitis, 236 Tumefactive sludge, 195, 196f, 1741 Tunica albuginea ovarian, 565 testicular, 819, 819f–820f cysts of, 829, 830f pediatric, 1888 Tunica vaginalis, 819, 819f cysts of, 829, 830f pediatric, 1902–1903 pathologic lesions of, 834–836, 835f pediatric, 1902 Tunica var, 819 Tunica vasculosa, 821 Turner syndrome (monosomy X) anasarca in fetus with, 1417, 1420f cystic hygromas in, 1106–1107, 1106f fetal hydrops from, 1429–1430, 1430f horseshoe kidney in, 1345–1346 lymphatic malformation in, 1159 midface hypoplasia in, 1148 primary amenorrhea in, 1887 small aorta in, 1106f, 1107 sonographic indings in, 1106–1107, 1106f TURP. See Transurethral resection of prostate Turribrachycephaly, 1138f Twin anemia polycythemia sequence (TAPS), 1126–1127 “Twin peak” sign, 1119, 1119t, 1120f Twin pregnancies, skeletal abnormalities in, 1384 Twin reversed arterial perfusion (TRAP), 1127–1129, 1127f–1128f, 1429 Twinkling artifacts bezoars and, 1840 mimicking AVMs ater renal transplantation, 662–664, 668f renal calculi indicated by, 336, 337f urolithiasis and, 1799–1801, 1799f Twin(s) acardiac, hydrops and, 1429 aneuploidy screening for, 1091 congenital malformation of, 1123 conjoined, 1115–1116 complications with, 1129–1130, 1130f

Twin(s) (Continued) dichorionic diamniotic, 1019f, 1115–1116, 1116f growth discrepancy in, 1123f placental indings in, 1119 sonographic indings of, chorionicity and, 1119, 1120f dizygotic, 1115–1116, 1116f growth discrepancy in, 1123, 1123f hydrops in, 1429, 1429f IUFD and, 1123–1125, 1124f monochorionic diamniotic, 1019f, 1058f, 1115–1116, 1116f CHD risk with, 1270–1273 complications of, 1125–1129 growth discrepancy in, 1123f IUFD and, 1124f sonographic indings of, chorionicity and, 1119, 1121f TAPS complications with, 1126–1127 TRAP and, 1127–1129, 1127f–1128f TTTS complications and, 1125–1126, 1125t, 1126f monochorionic monoamniotic, 1057, 1115– 1116, 1116f complications of, 1125–1129, 1129f conjoined twins as, 1130f IUFD and, 1124f sonographic indings of, chorionicity and, 1119, 1121f TAPS complications with, 1126–1127 TRAP and, 1127–1129, 1127f–1128f TTTS complications and, 1125–1126, 1125t, 1126f at 12 weeks, 1129f at 28 weeks, 1129f monozygotic, 1115, 1116f vanishing, 1117 Twin-twin transfusion syndrome (TTTS), 1203 advanced, 1125–1126, 1126f complications of, 1125–1126, 1125t, 1126f early identiication of, 1125, 1126f hydrops from, 1429, 1429f pulmonic stenosis and, 1292 staging system for, 1125t 2-D echocardiography, 10 Two-dimensional array transducers, 12, 12f Typhlitis, acute, 287–288, 289f Tyrosinemia GSD and, 1740f management of, 1738 staghorn calculus and, 1799, 1800f U Uhl anomaly, 1286 UKCTOCS. See United Kingdom Collaborative Trial of Ovarian Cancer Screening Ulcer craters, in plaque ulceration, 923, 924f Ulcerative colitis, 266–267 Ulcer(s) duodenal, perforated, gallbladder wall thickening signs in, 201f gastric, pediatric, 1839–1840, 1840f penetrating, in abdominal aorta, 441, 444f peptic, 299, 300f Ulnar nerve, dislocation of, at elbow, 865–866, 866f Ulnar ray defects, 1399 Ulnar veins, normal anatomy of, 990–991 Ultrasound speckle, 4, 5f Umbilical artery(ies), 1059 aneurysms of, 1483 fetal assessment of, Doppler ultrasound for, 1458, 1459f fetal cloacal exstrophy and single, 1328 single, 1484, 1484f spontaneous rupture of, 1483 Umbilical coiling index, twisting of, 1482, 1482f

Index Umbilical cord, 1481–1487 abnormalities of, in monochorionic twins, 1119 appearance of, 1481–1484 cysts of, 1483, 1483f sonographic appearance of, 1061, 1061f in trisomy 18, 1103f diameter of, 1482 edematous, 1484f entangled, chorionicity and, 1119, 1121f excessive length of, 1481 fetal, amniotic band syndrome and, 1330 funic presentation of, 1485–1487, 1489f hemangiomas of, 1483 insertion of marginal, 1484–1485, 1487f into placenta, 1484, 1485f velamentous, 1119, 1122f, 1484–1485, 1486f knots of, true, 1482–1483 normal sonographic appearance of, 1059–1061 nuchal, 1483–1484 prolapse of, fetal hydrops and, 1436 pseudocysts of, 1483, 1484f routine sonographic views of, 1021, 1029f short, 1481 size of, 1481–1484 tumors of, 1483 twisting of, 1482 absent, 1482, 1482f vasa previa and, 1485–1487, 1488f–1489f Umbilical hernias, 491–492, 492f–493f Umbilical veins, 1059 pediatric, recanalized, in portal hypertension, 1758f Uncinate process, pancreatic head and, 212, 213f Undescended testis, 851, 851f right, pediatric, 1890, 1890f Unfused amnion, 1057 Unicornuate uterus, 536f–537f, 538, 1881 United Kingdom Collaborative Trial of Ovarian Cancer Screening (UKCTOCS), 578 Univentricular heart, 1287–1288, 1287f UPJ obstruction. See Ureteropelvic junction obstruction Upright positioning, for dynamic ultrasound of hernias, 474 Urachal sinus, pediatric, 1907–1908, 1909f Urachus, 1337f, 1338 adenocarcinomas of, 355 in bladder development, 311, 312f cysts of, 322, 323f ovarian cysts diferentiated from, 1369 pediatric, 1907–1908, 1909f pediatric hydronephrosis and, 1791, 1792f–1793f pediatric ovarian cysts diferentiated from, 1875 diverticula of, 322, 323f pediatric, 1907–1908, 1909f patent, 322 pediatric, 1791 pediatric cysts of, 1907–1908, 1909f diverticula of, 1907–1908, 1909f patent, 1907–1908, 1909f remnant of, normal, 1871 sinus of, 1791 sinus of, 322, 323f pediatric, 1791 Ureteral bud congenital anomalies related to, 318–321 congenital megacalices and, 321 congenital megaureter and, 321, 322f duplex collecting system and, 319, 320f

Ureteral bud (Continued) renal agenesis and, 318–319 supernumerary kidneys and, 319 UPJ obstruction and, 321, 321f ureteroceles and, 310, 319, 321f in kidney development, 311, 312f Ureteral jets, color Doppler ultrasound for, 1781f Ureteral relux, bladder augmentation and, 1912–1913 Ureteral reimplantation, pediatric, 1912, 1913f Ureteric bud, 1336–1338 Ureteric jets, pediatric, 1781f, 1906–1907 Ureterocele(s) congenital anomalies related to, 310, 319, 321f fetal, in duplication anomalies, 1359–1360, 1359f, 1360b pediatric in duplication anomalies, 1783–1784, 1784f ectopic, 1904–1905, 1905f Ureteropelvic junction (UPJ) obstruction, 318 congenital anomalies related to, 321, 321f fetal hydronephrosis from, 1358, 1358f perirenal urinomas from, 1358, 1358f pediatric, hydronephrosis and, 1786, 1787f VUR with, 1360 Ureterovesical junction obstruction, pediatric, 1906–1907, 1907f Ureter(s) adenocarcinoma of, 348 anastomosis of, in renal transplantation, 643, 648f anatomy of, 313f, 314 atretic, with MCDK, 1346 calculi in, 325, 325f, 337–338, 338f–339f bladder augmentation and, 1912–1913 complicating renal transplantation, 659–660, 663f–664f congenital megaureter and, 321, 322f development of, 311, 312f distal, dilated, 592 lymphomas of, 353 metastases to, 354 obstruction of, renal transplantation complications from, 659–660, 663f–664f pediatric, 1906–1907, 1907f–1908f duplication of, 1783–1784, 1784f, 1904–1905 ectopic, 1904–1905 ectopic insertion of, hydronephrosis and, 1788 obstruction of, hydronephrosis and, 1786–1788, 1787f reimplantation of, 1912, 1913f retrocaval, 322 sonographic technique for, 314 squamous cell carcinoma of, 348 transitional cell carcinoma of, 347 trauma to, 366 Urethra development of, 311 congenital anomalies of, 323, 323f diverticula of, 323, 323f fetal atresia, lower urinary tract obstruction from, 1361, 1361f megalourethra and atresia of, 1362 obstruction of, renal pelvic dilation and, 1355–1356 pediatric diverticulum of, anterior, bladder outlet obstruction from, 1906 duplication of, bladder outlet obstruction from, 1906 normal, 1872f

I-61

Urethra (Continued) polyp of, posterior, bladder outlet obstruction from, 1906, 1906f sonographic technique for, 315, 316f Urethral valve(s) anterior, pediatric, bladder outlet obstruction from, 1906 fetal lower urinary tract obstruction from, 1361, 1361f megalourethra and, 1362 pediatric hydronephrosis and, 1788, 1789f posterior, 1905–1906, 1906f Urinary diversion, evaluation ater, 375, 375f Urinary stasis, pediatric, 1799, 1800f Urinary tract congenital anomalies of, 1336 dilation of, in trisomy 21, 1100f, 1101 echinococcal disease of, 331, 332f LUTS and, 387–388 masses of, 592 obstruction of, 387–388 schistosomiasis of, 331 tuberculosis of, 329–330, 330f Urinary tract, fetal. See also Hydronephrosis abnormalities of, 1340–1366 bilateral renal agenesis as, 1342–1344, 1343f–1344f, 1344b characterizing, 1341 evaluation of, 1342b horseshoe kidney as, 1345–1346, 1345f MRI for diagnosing, 1342, 1342f prenatal diagnosis of, 1340, 1340b prevalence of, 1340 renal cystic disease as, 1346–1352 (See also Kidneys, fetal, cystic disease of) renal ectopia as, 1344–1345, 1344f–1345f unilateral renal agenesis as, 1344 embryology of, 1336–1338, 1337f lower, obstruction of, 1360–1363 cloacal malformation and, 1363, 1363f cystoscopy for, 1363–1365 hydrops from, 1428, 1429f from megacystis, 1360, 1360b, 1360f from megalourethra, 1362, 1362f MMIHS and, 1362–1363 from posterior urethral valves, 1361, 1361f from prune belly syndrome, 1361–1362 from urethral atresia, 1361, 1361f in utero intervention for, 1363–1365, 1364f, 1365t vesicoamniotic shunts for, 1363–1365, 1364f, 1365t normal, 1336–1340 sonographic appearance of, 1338–1339, 1338f upper, dilation of, 1354–1360, 1354f–1355f, 1356t, 1357f duplication anomalies and, 1359–1360, 1359f, 1360b management of, 1356–1358 UPJ obstruction and, 1358, 1358f vesicoureteral junction obstruction and, 1358–1359 VUR and, 1360 Urinary tract, pediatric. See also Bladder, pediatric; Kidneys, pediatric calciication of, 1798–1801 cortical nephrocalcinosis and, 1798, 1798b, 1798f dystrophic, 1799 medullary nephrocalcinosis of, 1798–1799, 1799f Volume I pp 1–1014 • Volume II pp 1015–1968

I-62

Index

Urinary tract, pediatric (Continued) renal vein thrombosis and, 1799, 1800f urinary stasis and, 1799, 1800f urolithiasis and, 1799–1801, 1799f congenital anomalies of, 1783–1785 renal duplication as, 1783–1784, 1784f dilation of, classiication of, 1785–1786, 1786f infection of, 1791–1794 cystitis and, 1794, 1796f–1797f, 1908, 1910f–1911f jaundice in, 1738 neonatal candidiasis and, 1794, 1795f pyelonephritis, acute, and, 1792–1793, 1793f–1794f pyelonephritis, chronic, and, 1794, 1795f lower, 1904–1913 congenital anomalies of, 1904–1906, 1905f–1907f infection of, 1904–1905, 1908, 1910f–1911f neoplasms of, 1908–1912, 1912f trauma to, 1912 obstruction of, renal transplantation and, 1811 sonography of, 1776–1783 patient preparation for, 1776, 1776t technique for, 1776–1781 Urinary tract dilation (UTD), 1785–1786, 1786f Urine leak, renal transplantation and, 1810–1811 Urinoma(s) bladder augmentation and, 1912–1913 pelvic, 591 perirenal, from UPJ obstruction, 1358, 1358f ater renal transplantation, 665, 672f pediatric, 1809 Urogenital sinus, in bladder development, 311, 312f Urolithiasis, pediatric calciication and, 1799–1801, 1799f Uropathy pediatric, obstructive, CKD and, 1796–1798 postnatal, pyelectasis as marker for, 1355 U.S. Preventive Services Task Force (USPSTF), 397, 434–435 U-shaped coniguration, 1927, 1928f UTD. See Urinary tract dilation Uterine artery(ies), 528–529, 565–566, 565f embolization of, for uterine ibroids, 540 pediatric, 1875 Uterine septum, circumvallate placenta confused with, 1479–1480, 1481f Uterine synechia, circumvallate placenta confused with, 1479–1480, 1481f Uterine veins, 531–532, 533f Uterocervical anomalies, cervical assessment in, 1505 Utero-ovarian ligament, 565 Uterus. See also Cervix; Endometrium; Myometrium accessory and cavitated mass of, 541 anatomy of, 528–530, 529f sections in, 530 arcuate, 534, 536–538, 536f–537f bicornuate, 534, 536f–537f, 538, 1881, 1881f cervical abnormalities and, 541–544, 543f DES exposure of, 534, 536f, 1881 didelphys, 534, 536f–537f, 1881 endometrial abnormalities and, 544–552 enlargement of, 538b hypoplasia of, 538 isolated, primary amenorrhea in, 1887 leiomyomas of, 538–540, 539f, 540b leiomyosarcomas of, 540, 541f müllerian duct anomalies and, 529, 533–538, 537f categories of, 534, 536f

Uterus (Continued) myometrial abnormalities of, 538–541 neonatal, 1872–1873, 1873f obstruction of, 546–547, 546f–547f pediatric, 1872–1873 abnormalities of, 1881–1887 agenesis of, primary amenorrhea in, 1887 congenital anomalies of, 1881–1883 endocrine abnormalities and, 1887–1888 infection and, 1885–1887 neoplasms of, 1883–1884 PID and, 1885–1887, 1886b, 1886f postpubertal, 1872–1873, 1873t precocious puberty and, 1887–1888 pregnancy and, 1884–1885 prepubertal, 1872–1873, 1873f, 1873t postpartum indings in, 554–557 AVMs and, 556, 556f bleeding and, 554 ater cesarean section, 556–557, 557f–558f endometritis and, 555–556 normal, 554, 554f placental site trophoblastic tumor and, 530–531 RPOC and, 554–555, 555f pregnant dehiscence or rupture of, assessing risk for, 1020 second-trimester scan of, 1020, 1021f sarcomas of, 551 septate, 534–536, 536f–537f size of, 531 sonographic techniques for, 528–530, 529b IUDs and, 552–554, 553f normal indings in, 530–533 positioning in, 530–531, 530f tubal occlusion devices and, 553f, 554 sonohysterography for, 529 three-dimensional ultrasound for, 529 transvaginal ultrasound for, 529, 529b T-shaped, 1881 unicornuate, 536f–537f, 538, 1881 Utricle cysts, prostatic, 391f, 392 V VACTERL association, 1689 duodenal atresia and, 1308 fetal renal anomalies for, 1341 ribs in, 1382–1384 sacral agenesis in, 1237 VACTERL sequence, 1306, 1311 Vagina, 528–529 bleeding in, hydatidiform molar pregnancy and, 1078 pediatric, 1873 abnormalities of, 1881–1887 atretic, vaginal obstruction from, 1881 congenital anomalies of, 1881–1883 endocrine abnormalities and, 1887–1888 foreign bodies in, 1887 infection and, 1885–1887 neoplasms of, 1883–1884, 1883f precocious puberty and, 1887–1888 pregnancy and, 1884–1885 stenotic, vaginal obstruction from, 1881 Peutz-Jeghers syndrome and watery discharge of, 544 Vaginal fornix, 528–529 Vaginal pessary, cervical incompetence and, 1507 Vaginal progesterone, 17α-OHPC compared to, 1507 Vaginal septum, 538 transverse, vaginal obstruction from, 1881 Vaginitis, pediatric, 1887

Vallecula cysts, pediatric, 1640, 1641f neonatal/infant, in mastoid fontanelle imaging, 1517–1518, 1519f Valproic acid, NTDs from, 1218 Valsalva maneuver, 471, 992 for dynamic ultrasound of hernias femoral, 472f, 483 inguinal, 473, 474f Valve lealet morphology, 1285f Valvular aortic stenosis, 1292 Varicella fetal brain and, 1203–1204 fetal hydrops from, 1432 Varices gallbladder wall, in chronic pancreatitis, 233, 235f gastric mural, in chronic pancreatitis, 233, 235f gastrointestinal, endosonographic identiication of, 301 round ligament, simulating groin hernias, 500, 501f Varicocele(s) idiopathic, 837–838 pediatric, 1902–1903, 1903f scrotal, 837–838, 838f–839f Vas aberrans of Haller, 1897f inferior, 820–821 Vas deferens, 819–820 absence of, 394 calciication of, 392 cysts of, 842f Vasa aberrantia, 820–821 Vasa previa, 1480, 1485–1487, 1488f–1489f Vascular abnormalities, in liver. See Liver, vascular abnormalities in Vascular anomalies, of neck, pediatric, 1654–1655, 1655b malformations, 1655–1658, 1655b, 1657f, 1659f tumors, 1655, 1655b, 1656f Vascular malformations fetal, 1204–1208, 1206f dural sinus thrombosis as, 1205–1206, 1206f hydranencephaly as, 1208, 1208f intracranial hemorrhage as, 1206, 1207f pediatric in masticator space, 1640, 1641f in neck, 1655–1658, 1655b, 1657f, 1659f Vasculitis acute, gut edema and, 295, 297f autoimmune, Henoch-Schönlein purpura and, 1853 mesenteric ischemia from, 453 renal artery stenosis and, 447 Vasectomy, epididymis changes following, 841, 843f Vasodilation, 27 Vasospasm, 950 pediatric, TCD sonography for, 1608–1610, 1609f, 1610t VATER syndrome fetal renal anomalies in, 1341 spina biida and, 1226 Vein mapping before hemodialysis, 996–1000 upper extremity, 996–998, 998f–1000f of lower extremity peripheral veins, 989–990 Vein of Galen aneurysms of, 1204, 1206f arachnoid cysts diferentiated from, 1192–1193 in neonatal/infant brain, duplex Doppler sonography of, 1583–1584, 1585f–1586f cavum veli interpositi cysts diferentiated from aneurysm of, 1170

Index Vein of Galen (Continued) malformations of, neonatal/infant brain and, 1566, 1567f Vein of Markowski, 1180 fetal brain and, 1204 Velamentous umbilical cord insertion, 1484–1485, 1486f multifetal pregnancy and, 1119, 1122f Velocardiofacial syndrome, clets of secondary palate in, 1153 Velocity arterial stenosis and, 969, 970f diastolic, end, in assessing degree of carotid stenosis, 930 in Doppler spectral analysis of carotid artery, 925 stroke and SCD indications with, 1605–1607 systolic cerebral, factors changing, 1612t peak, in determining carotid stenosis, 929–930 TCD sonography evaluation of, 1593, 1595–1596 time-averaged mean of maximum, 1593, 1605–1606 time-averaged peak, 1593 Velocity range, in obstetric Doppler sonography, 1036 Velocity ratios, in carotid artery stenosis evaluation, 937 Venography in IJV, 955–956 wedge hepatic, 1764 Veno-occlusive disease, hepatic, 103 Venous drainage, in pancreas transplantation, 672 Venous insuiciency deep, causes of, 989, 990f supericial, 981–982 Venous malformations, pediatric of neck, 1657 of salivary gland, 1636 Venous occlusive disease, hepatic, small-vessel, 1762–1763 Venous venous (VV) anastomoses, 1125, 1125f Ventilation, mechanical, in neonatal/infant brain, 1578, 1579f Ventral hernias, 488–494 Ventral induction errors, fetal brain and, 1186–1203 arachnoid cysts as, 1192–1193, 1193f in cerebellum, 1189–1192 Dandy-Walker malformation as, 1190, 1190f HPE as, 1186–1189, 1187b, 1188f, 1189b mega-cisterna magna as, 1192, 1193f in posterior fossa, 1189–1192 rhombencephalosynapsis as, 1192 vermis hypoplasia or dysplasia as, 1190–1192, 1192f Ventricle(s) cardiac double-outlet right, fetal, 1288–1289, 1289f echogenic foci, signiicance of, 1294, 1294f hypoplastic let, fetal, 1292 hypoplastic right, fetal, 1287, 1287f neonatal/infant, let, dysfunction of, intracranial RI and, 1576 cerebral, fetal, sonographic view of, 1024f fourth cisterna magna clot of, 1546f trapped, in intraventricular hemorrhage, 1545–1547

Ventricle(s) (Continued) lateral, neonatal/infant coarctation of, 1566 in coronal imaging, 1513–1515, 1514f–1515f in sagittal imaging, 1515–1517, 1517f measurement technique for, 1174–1176, 1175f medial wall of, separation of choroid from, in VM evaluation, 1176, 1176f persistent terminal, pediatric, 1685 third in corpus callosum agenesis, 1528, 1531f fetal, normal sonographic appearance of, 1168 Ventricular aneurysms, congenital, 1294 Ventricular diverticula, 1294 Ventricular septal defects (VSDs), 1270, 1281– 1284, 1283f–1284f with spina biida, 1233 in trisomy 21, 1098f, 1101 Ventricular tachycardia, fetal, 1296 Ventriculitis chemical, 1206 in intraventricular hemorrhage, 1545–1547 neonatal/infant brain and, 1560, 1563f Ventriculoarterial discordance, in TGA, 1289 Ventriculomegaly (VM) CDH and, 1263 conditions associated with, 1178b fetal brain and, 1174–1178 hydrocephalus diferentiated from, 1611–1612 isolated, 1176 IUFD and, 1124f marked, 1176, 1177f measurement technique for, 1174–1176, 1175f mild, 1176, 1177f neonatal/infant hydranencephaly compared to, 1538f pathogenesis of, 1177–1178 in rhombencephalosynapsis, 1192 in spina biida, 1184f, 1230–1232 in trisomy 21, 1098f ultrasound evaluation of, 1177f, 1178 Ventriculus terminalis formation of, 1673, 1673f normal anatomy of, 1674, 1677f Verma-Naumof syndrome, 1396 Vermian agenesis, 1190 Vermian dysplasia, Dandy-Walker malformation diferentiated from, 1190 Vermis abnormalities of, 1192 cerebellar, 1167, 1515, 1516f, 1524 dysplasia of, 1190–1192, 1192f embryology of, 1167 hypoplasia of, 1190–1192, 1192f inferior, arachnoid cysts diferentiated from, 1192–1193 hypoplasia/dysgenesis/agenesis of, 1190–1191 keyhole-shaped defect in, 1191–1192 neonatal/infant in coronal imaging, 1514–1515, 1514f development of, 1524 trapezoidal vermian defect in, 1191–1192 Vertebral artery, 950–955 anatomy of, 951, 951f occlusion of, 954–955 stenosis of, 954–955, 955f subclavian steal phenomenon and, 952–954, 953b, 953f–954f subclavian steal with transient low reversal in, 979f technique and normal examination of, 951–952, 951f–952f Vertebral vein, 951f, 952

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Vertebrobasilar insuiciency, symptoms of, 950–951 Vertical talus, congenital, 1932–1933, 1932f Verumontanum, 382f–383f, 384 Vesicoamniotic shunts, for lower urinary tract obstruction, 1363–1365, 1364f, 1365t Vesicocentesis, 1363–1364 Vesicocolic istulas, 1310–1312 Vesicocutaneous istulas, 334 Vesicoenteric istulas, 334 Vesicourachal diverticulum, pediatric, 1775, 1791 Vesicoureteral istulas, 334 Vesicoureteral junction obstruction, fetal, megaureters from, 1358–1359 Vesicoureteral relux (VUR), 1906–1907 fetal, 1360 nephropathy associated with, 327 pediatric, 1905 hydronephrosis and, 1788, 1790f renal transplantation and, 1811 unilateral renal agenesis and, 1344 Vesicouterine istulas, 334 Vesicouterine pouch, 528 Vesicovaginal istulas, 334 Vessel stenosis, 25 VHL disease. See von Hippel-Lindau disease Villi, in placental development, 1465–1466, 1466f Villitis, thick placenta and, 1467f Virus(es) fetal, IUGR and, 1455 hepatitis, 83–85 pediatric infections from cervical lymphadenopathy in, 1660 salivary gland, 1632, 1632f Visceral heterotaxy, splenic abnormalities in, 159–160 Vitelline arteries and veins, 1057, 1059 Vitelline duct, 1057, 1059 VM. See Ventriculomegaly VMCs. See Von Meyenburg complexes Voltage, 7 Volume imaging, in obstetric sonography, 1030 Volumetric imaging, of liver, 75 Volvulus of gallbladder, 201 midgut intestinal malrotation with, 1841–1842, 1843f–1844f “whirlpool” sign of, 1841–1842, 1843f small bowel obstruction and, 1308 Vomer, deviation of, in clet palate, 1151 von Gierke disease, 1740f von Hippel-Lindau (VHL) disease epididymal cystadenomas and, 1904 pancreatic cysts and, 243, 244f fetal, 1320 papillary cystadenoma with, 840–841 pediatric, renal cysts in, 1816 pheochromocytomas with, 1826, 1910–1912 renal cell carcinoma and, 340 renal cysts in, 364, 364f von Hippel-Lindau syndrome, prenatal intracranial tumors in, 1208 Von Meyenburg complexes (VMCs), 83, 83f–84f VSDs. See Ventricular septal defects VUR. See Vesicoureteral relux VV anastomoses. See Venous venous anastomoses W WAGR syndrome, pediatric, 1818 “Waist sign”, 587–588 Waldeyer fossa, 566, 567f Volume I pp 1–1014 • Volume II pp 1015–1968

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Index

Walker-Warburg syndrome cobblestone lissencephaly in, 1195 Dandy-Walker malformation diferentiated from, 1190 diagnosis of, 1195 vermian hypoplasia with, 1191 Wall ilters in Doppler ultrasound, 29, 30f in renal artery duplex Doppler sonography, 449 Wall-echo-shadow complex, 194, 195f Wandering spleen, 159, 161f pediatric, 1770–1772 Warfarin, 598 Warthin tumor, 1638 Watchful waiting, for prostate cancer, 401 Water enema technique, contrast agents in, 1870–1871, 1871f Waterhouse-Friderichsen syndrome, 422 Waveform(s). See also Tardus-parvus waveform(s) of carotid arteries, 925–926, 925f intrarenal, in renal artery duplex Doppler sonography, 450, 450f Wavelength, in sound waves, 2, 2f Weaver syndrome, megalencephaly associated with, 1194–1195 Wedge hepatic venography, 1764 Weigert-Meyer rule, 1359, 1783 Weight, fetal assessment of, 1450–1453 in relation to gestational age, 1451–1453, 1452t, 1453f estimation for, 1450–1453 formulas in, 1451, 1451t gestational age compared to, 1453, 1453f recommended approach in, 1451, 1452t Weight, pediatric, kidney length compared to, 1777f at birth, 1776–1778, 1780f

Weighted mean frequency, in color Doppler ultrasound, 28 Wells score, 979 Weyers acrodental dysostosis, 1395 WFUMB. See World Federation for Ultrasound in Medicine and Biology Wharton duct, pediatric, 1630–1631, 1631f Wharton jelly, 1059, 1482 Whipple resection, 233 “Whirlpool” sign, of midgut volvulus, 1841–1842, 1843f White matter injury of prematurity (WMIP), 1512, 1550–1553. See also Periventricular leukomalacia Wilms tumor, 1352–1353, 1804 neuroblastomas mistaken for, 1818 pediatric kidneys and, 1818, 1818f–1820f liver metastases from, 1746 metastasis of, to teste, 1901 Windsock coniguration, duodenal diaphragm in, 1842, 1844f WMIP. See White matter injury of prematurity Wolian (mesonephric) duct, 820–821 Wolf-Hirschhorn syndrome (4p−), 1139, 1140f midface hypoplasia in, 1148 World Federation for Ultrasound in Medicine and Biology (WFUMB), 1041 Wormian bones, 1139, 1139b, 1139f Wrist, injection of, 901 supericial peritendinous and periarticular, 904, 905f X Xanthogranulomatous cholecystitis, 202 Xanthogranulomatous pyelonephritis (XGP), 328, 329f, 348 X-linked hydrocephalus, 1177 X-linked NTDs, 1226

Y Yersinia, 1852–1853, 1852f “Yin-yang” pattern, in renal biopsy pseudoaneurysms, 1809, 1811f Yolk sac tumors, 585, 823–824, 825f Yolk sac(s) angiogenesis wall of, 1057 assessment of, 1016, 1016b calciication of, 1067, 1068f diameter of, measurement, 1017f echogenic material in, 1067–1068 embryo in, 1058f hematopoiesis in, 1057 identiication of, in gestational age determination, 1445, 1445f, 1446t MSD and, 1057 normal sonographic appearance of, 1057, 1058f number of, amnionicity and, 1117 in nutrient transfer, 1057 primary, formation of, 1051, 1052f secondary, formation of, 1051, 1053f size and shape of, in early pregnancy failure, 1067–1068, 1068f transvaginal ultrasound for identiication of, 1057 Yolk stalk, 1059 Z Zellweger syndrome, 1196, 1399 subependymal cysts from, 1566 Zero baseline, shiting, to overcome aliasing, 939 Zika virus, 1194, 1203–1204 congenital, neonatal/infant brain and, 1560 Zona fasciculata, 417 Zona glomerulosa, 417 Zona reticularis, 417 Zuckerkandl fascia, 314 Zygosity, in multifetal pregnancy, 1115–1116, 1116f Zygote, formation of, 1051, 1051f

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DIAGNOSTIC ULTRASOUND

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DIAGNOSTIC ULTRASOUND 5TH EDITION CAROL M. RUMACK, MD, FACR Vice Chair of Education and Professional Development Professor of Radiology and Pediatrics Associate Dean for GME University of Colorado School of Medicine Denver, Colorado

DEBORAH LEVINE, MD, FACR Co-Chief of Ultrasound Director of OB/Gyn Ultrasound Vice Chair of Academic Afairs Department of Radiology Beth Israel Deaconess Medical Center Professor of Radiology Harvard Medical School Boston, Massachusetts

1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103-2899

DIAGNOSTIC ULTRASOUND, FIFTH EDITION

ISBN: 978-0-323-40171-5

Copyright © 2018 by Elsevier, Inc. All rights reserved. Chapter 32: Mary C. Frates retains copyright for the original igures appearing in the chapter. Chapter 42: Carol B. Benson and Peter M. Doubilet retain copyright for their original igures appearing in the chapter. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. his book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).

Notices Knowledge and best practice in this ield are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identiied, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. Previous editions copyrighted 2011, 2005, 1998, and 1993. Library of Congress Cataloging-in-Publication Data Names: Rumack, Carol M., editor. | Levine, Deborah, 1962- editor. Title: Diagnostic ultrasound / [edited by] Carol M. Rumack, Deborah Levine. Other titles: Diagnostic ultrasound (Rumack) Description: 5th edition. | Philadelphia, PA : Elsevier, [2018] | Includes bibliographical references and index. Identiiers: LCCN 2017019887 | ISBN 9780323401715 (hardcover : alk. paper) Subjects: | MESH: Ultrasonography Classiication: LCC RC78.7.U4 | NLM WN 208 | DDC 616.07/543–dc23 LC record available at https://lccn.loc.gov/2017019887 Executive Content Strategist: Robin Carter Senior Content Development: Manager: Taylor Ball Publishing Services Manager: Catherine Jackson Senior Project Manager: Daniel Fitzgerald Design Manager: Amy Buxton Illustrations Manager: Nichole Beard Printed in China. Last digit is the print number: 9

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ABOUT THE EDITORS

Carol M. Rumack, MD, FACR, is Professor of Radiology and Pediatrics at the University of Colorado School of Medicine in Denver, Colorado. Her clinical practice is based at the University of Colorado Hospital. Her primary research has been in neonatal sonography of high-risk infants, particularly the brain, on which she has published and lectured widely. She is a Fellow, previous Chair of the Ultrasound Commission, past president of the American College of Radiology, and American Association for Women Radiologists, and a Fellow of both the American Institute of Ultrasound in Medicine and the Society of Radiologists in Ultrasound. She and her husband, Barry, have two children, Becky and Marc, and ive grandchildren.

Deborah Levine, MD, FACR, is Professor of Radiology at Beth Israel Deaconess Medical Center, Boston, and Harvard Medical School. At Beth Israel Deaconess Medical Center she is Vice Chair of Academic Afairs of the Department of Radiology, Co-Chief of Ultrasound, and Director of Ob/Gyn Ultrasound. Her main areas of clinical and research interest are obstetric and gynecologic imaging. She is a Fellow and past Vice President of the American College of Radiology and a Fellow (and 2016-2017 President) of the Society of Radiologists in Ultrasound. She and her husband, Alex, have two children, Becky and Julie.

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Contributors

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CONTRIBUTORS Jacques S. Abramowicz, MD, FACOG, FAIUM Professor and Director Ultrasound Services Department of Obstetrics and Gynecology University of Chicago Chicago, Illinois United States

Diane S. Babcock, MD Professor Emerita of Radiology and Pediatrics University of Cincinnati College of Medicine Cincinnati Children’s Hospital Medical Center Cincinnati, Ohio United States

Ronald S. Adler, MD, PhD Professor of Radiology New York University School of Medicine Department of Radiology NYU Langone Medical Center New York, New York United States

Beryl Benacerraf, MD Clinical Professor of Obstetrics and Gynecology and Radiology Brigham and Women’s Hospital Clinical Professor of Obstetrics and Gynecology Massachusetts General Hospital Harvard Medical School Boston, Massachusetts United States

Allison Aguado, MD Assistant Professor Department of Radiology Cincinnati Children’s Hospital Medical Center Cincinnati, Ohio United States Rochelle Filker Andreotti, MD Professor of Clinical Radiology Associate Professor of Clinical Obstetrics and Gynecology Department of Radiology and Radiological Sciences Vanderbilt University Nashville, Tennessee United States Elizabeth Asch, MD Instructor in Radiology Harvard Medical School Brigham and Women’s Hospital Boston, Massachusetts United States homas D. Atwell, MD Professor of Radiology Department of Radiology Mayo Clinic Rochester, Minnesota United States Amanda K. Auckland, BS, RT(R), RDMS, RVT, RDCS Diagnostic Medical Sonographer Division of Ultrasound/Prenatal Diagnosis and Genetics University of Colorado Hospital Aurora, Colorado United States

Carol B. Benson, MD Professor of Radiology Harvard Medical School Director of Ultrasound and Co-Director of High Risk Obstetrical Ultrasound Department of Radiology Brigham and Women’s Hospital Boston, Massachusetts United States Raymond E. Bertino, MD, FACR, FSRU Medical Director of Vascular and General Ultrasound OSF Saint Francis Medical Center Clinical Professor of Radiology and Surgery University of Illinois College of Medicine Peoria, Illinois United States Edward I. Bluth, MD, FACR, FSRU Chairman Emeritus Ochsner Clinic Foundation Professor Ochsner Clinical School University of Queensland, School of Medicine New Orleans, Louisiana United States Bryann Bromley, MD Professor of Obstetrics, Gynecology and Reproductive Biology, part time Harvard Medical School Department of Obstetrics and Gynecology Massachusetts General Hospital Brigham and Women’s Hospital Boston, Massachusetts United States

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Contributors

Olga R. Brook, MD Assistant Professor Harvard Medical School Associate Director of CT Department of Radiology Beth Israel Deaconess Medical Center Boston, Massachusetts United States Douglas Brown, MD Professor of Radiology Department of Radiology Mayo Clinic College of Medicine and Science Rochester, Minnesota United States Dorothy Bulas, MD Professor of Pediatrics and Radiology George Washington University Medical Center Pediatric Radiologist Children’s National Health Systems Washington DC United States Peter N. Burns, PhD Professor and Chairman Department of Medical Biophysics University of Toronto Senior Scientist, Imaging Research Sunnybrook Research Institute Toronto, Ontario Canada Vito Cantisani, MD, PhD Department of Radiologic, Oncologic and Pathologic Sciences Policlinic Umberto I Sapienza University Rome Italy Ilse Castro-Aragon, MD Assistant Professor of Radiology Boston University School of Medicine Section Head, Pediatric Radiology Boston Medical Center Boston, Massachusetts United States J. William Charboneau, MD Emeritus Professor of Radiology Department of Radiology Mayo Clinic Rochester, Minnesota United States

Humaira Chaudhry, MD Section Chief, Abdominal Imaging Assistant Professor Department of Radiology Rutgers-New Jersey Medical School Newark, NJ United States Tanya Punita Chawla, MBBS, FRCR, MRCP, FRCPC Assistant Professor and Staf Radiologist Joint Department of Medical Imaging University of Toronto Toronto, Ontario Canada Christina Marie Chingkoe, MD Department of Radiology Beth Israel Deaconess Medical Center Boston, Massachusetts United States David Chitayat, MD Professor Department of Pediatrics, Obstetrics and Gynecology, Molecular Genetics and Laboratory Medicine and Pathobiology Medical Director he MSc program in Genetic Counselling, Department of Molecular Genetics University of Toronto Head he Prenatal Diagnosis and Medical Genetics Program Mount Sinai Hospital Staf Pediatrics, Division of Clinical and Metabolic Genetics Hospital for Sickkids Toronto, Ontario Canada Peter L. Cooperberg, OBC, MDCM, FRCP(C), FACR Professor Emeritus Department of Radiology University of British Columbia Vancouver, British Columbia Canada Lori A. Deitte, MD, FACR Vice Chair of Education and Professor Department of Radiology and Radiological Sciences Vanderbilt University Nashville, Tennessee United States

Contributors Peter M. Doubilet, MD, PhD Professor of Radiology Harvard Medical School Senior Vice Chair Department of Radiology Brigham and Women’s Hospital Boston, Massachusetts United States Julia A. Drose, RDMS, RDCS, RVT Associate Professor Department of Radiology University of Colorado Hospital Aurora, Colorado United States Alexia Eglof, MD Diagnostic Imaging and Radiology Children’s National Health Systems Washington DC United States Judy A. Estrof, MD Instructor Boston University School of Medicine Department of Radiology Boston Children’s Hospital Boston, Massachusetts United States Katherine W. Fong, MBBS, FRCPC Associate Professor Medical Imaging and Obstetrics and Gynecology University of Toronto Co-director, Centre of Excellence in Obstetric Ultrasound Mount Sinai Hospital Toronto, Ontario Canada J. Brian Fowlkes, PhD Professor Department of Radiology University of Michigan Ann Arbor, Michigan United States Mary C. Frates, MD Associate Professor of Radiology Department of Radiology Harvard Medical School Brigham and Women’s Hospital Boston, Massachusetts United States

Hournaz Ghandehari, MD, FRCPC Department of Medical Imaging Abdominal Division University of Toronto Sunnybrook Health Sciences Centre Toronto, Ontario Canada Phyllis Glanc, MDCM Associate Professor University of Toronto Department Medical Imaging, Obstetric & Gynecology Sunnybrook Health Sciences Centre Toronto, Ontario Canada S. Bruce Greenberg, MD Professor of Radiology and Pediatrics Department of Radiology University of Arkansas for Medical Sciences Little Rock, Arkansas United States Leslie E. Grissom, MD Clinical Professor of Radiology and Pediatrics Department of Radiology Sidney Kimmel Medical College at homas Jeferson University Philadelphia, Pennsylvania Attending Radiologist Department of Medical Imaging Nemours Alfred I. duPont Hospital for Children Wilmington, Delaware United States Anthony E. Hanbidge, MB, BCh, FRCPC Associate Professor Department of Medical Imaging University of Toronto Site Director, Abdominal Imaging Toronto Western Hospital Joint Department of Medical Imaging University Health Network, Mount Sinai Hospital and Women’s College Hospital Toronto, Ontario Canada H. heodore Harcke, MD, FACR, FAIUM Sidney Kimmel Medical College at homas Jeferson University Chairman, Emeritus Department of Medical Imaging Nemours/A I duPont Hospital for Children Wilmington, Delaware United States

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Christy K. Holland, PhD Scientiic Director of the Heart, Lung, and Vascular Institute Professor Department of Internal Medicine Division of Cardiovascular Health and Disease University of Cincinnati Cincinnati, Ohio United States hierry A.G.M. Huisman, MD Professor of Radiology, Pediatrics, Neurology, and Neurosurgery Director Pediatric Radiology and Pediatric Neuroradiology Russell H. Morgan Department of Radiology and Radiological Science he Johns Hopkins University School of Medicine Baltimore, Maryland United States Bonnie J. Huppert, MD Assistant Professor of Radiology Consultant in Radiology Department of Radiology Mayo Clinic Rochester, Minnesota United States

Anne Kennedy, MB, BCh Vice Chair Clinical Operations Department of Radiology University of Utah Salt Lake City, Utah United States Julia Eva Kfouri, BSc, MD, FRCSC-MFM Clinical Associate Division of Maternal Fetal Medicine Department of Obstetrics and Gynecology Mount Sinai Hospital Toronto, Ontario Canada Korosh Khalili, MD, FRCPC Associate Professor Department of Medical Imaging University of Toronto University Health Network Princess Margaret Hospital Toronto, Ontario Canada

Alexander Jesurum, PhD Weston, Massachusetts United States

Beth M. Kline-Fath, MD Professor of Radiology Department of Radiology Cincinnati Children’s Hospital Medical Center Cincinnati, Ohio United States

Susan D. John, MD Professor and Chair Department of Diagnostic and Interventional Imaging University of Texas Medical School Houston Houston, Texas United States

Elizabeth Lazarus, MD Associate Professor Department of Diagnostic Imaging Warren Alpert Medical School of Brown University Providence, Rhode Island United States

Neil Johnson, MBBS, FRANZCR, MMed Professor Department of Radiology and Pediatrics Cincinnati Children’s Hospital Medical Center Cincinnati, Ohio United States

Deborah Levine, MD, FACR Co-Chief of Ultrasound Director of OB/Gyn Ultrasound Vice Chair of Academic Afairs Department of Radiology Beth Israel Deaconess Medical Center Professor of Radiology Harvard Medical School Boston, Massachusetts United States

Stephen I. Johnson, MD Staf Radiologist Department of Radiology Ochsner Clinic Foundation New Orleans, Louisiana United States

Mark E. Lockhart, MD, MPH Professor of Radiology and Chief, Body Imaging Department of Radiology University of Alabama at Birmingham Birmingham, Alabama United States

Contributors Ana P. Lourenco, MD Associate Professor of Diagnostic Imaging Diagnostic Imaging Alpert Medical School of Brown University Providence, Rhode Island United States Martha Mappus Munden, MD Associate Professor of Radiology Department of Pediatric Radiology Texas Children’s Hospital Houston, Texas United States John R. Mathieson, MD Clinical Associate Professor University of British Columbia Vancouver, British Columbia Medical Director and Department Head Vancouver Island Health Authority Victoria, British Columbia Canada Giovanni Mauri, MD Division of Interventional Radiology European Institute of Oncology Milan Italy Colm McMahon, MB, BAO, BCh, MRCPI, FFR(RCSI) Assistant Professor Department of Radiology Harvard Medical School Beth Israel Deaconess Medical Center Brookline, Massachusetts United States Rashmi J. Mehta, MD, MBA Clinical Radiology Fellow Department of Radiology Beth Israel Deaconess Medical Center Boston, Massachusetts United States Nir Melamed, MD, MSc Associate Professor Department of Obstetrics and Gynecology University of Toronto Sunnybrook Health Sciences Center Toronto, Ontario Canada Christopher R.B. Merritt, MD New Orleans, Louisiana United States

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Derek Muradali, MD, FRCPC Associate Professor and Staf Radiologist Department of Medical Imaging St Michaels Hospital University of Toronto Toronto, Ontario Canada Elton Mustafaraj, DO Resident, Department of Radiology University of Illinois College of Medicine Peoria, Illinois United States Lisa Napolitano, RDMS Department of Radiology Beth Israel Deaconess Medical Center Boston, Massachusetts United States Sara M. O’Hara, MD Professor of Radiology & Pediatrics Department of Radiology Cincinnati Children’s Hospital Cincinnati, Ohio United States Harriet J. Paltiel, MDCM Associate Professor of Radiology Harvard Medical School Department of Radiology Boston Children’s Hospital Boston, Massachusetts United States Jordana Phillips, MD Department of Radiology Beth Israel Deaconess Medical Center Boston, Massachusetts United States Andrea Poretti, MD Assistant Professor of Radiology Section of Pediatric Neuroradiology Division of Pediatric Radiology Russell H. Morgan Department of Radiology and Radiological Science he Johns Hopkins University School of Medicine Baltimore, Maryland United States heodora A. Potretzke, MD Assistant Professor Department of Radiology Mayo Clinic Rochester, Minnesota United States

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Contributors

Rupa Radhakrishnan, MBBS Assistant Professor Department of Radiology Cincinnati Children’s Hospital Medical Center Cincinnati, Ohio United States Carl Reading, MD Professor of Radiology Department of Radiology Mayo Clinic Rochester, Minnesota United States Michelle L. Robbin, MD, MS Professor of Radiology and Biomedical Engineering Department of Radiology University of Alabama at Birmingham Birmingham, Alabama United States Henrietta Kotlus Rosenberg, MD Radiologist-in-Chief Kravis Children’s Hospital at Mount Sinai Director of Pediatric Radiology Department of Radiology Mount Sinai Hospital Professor of Radiology and Pediatrics Icahn School of Medicine at Mount Sinai New York, New York United States Carol M. Rumack, MD, FACR Vice Chair of Education and Professional Development Professor of Radiology and Pediatrics Associate Dean for GME University of Colorado School of Medicine Denver, Colorado United States Eric Sauerbrei, BSc, MSc, MD, FRCPC Professor of Radiology Diagnostic Imaging Queens University Kingston, Ontario Canada Chetan Chandulal Shah, MD, MBA Faculty, Department of Radiology Mayo Clinic Pediatric Radiologist Department of Pediatric Radiology Nemours Wolfson Children’s Hospital Jacksonville, Florida United States

homas D. Shipp, MD Associate Professor of Obstetrics, Gynecology & Reproductive Biology Harvard Medical School Department of Obstetrics & Gynecology Brigham & Women’s Hospital Boston, Massachusetts United States William L. Simpson, Jr., MD Associate Professor Department of Radiology Icahn School of Medicine at Mount Sinai New York, New York United States Luigi Solbiati, MD Professor of Radiology Department of Radiology Humanitas University and Research Hospital Rozzano (Milan) Italy Daniel Sommers, MD Associate Professor Department of Radiology University of Utah Salt Lake City, Utah United States Elizabeth R. Stamm, MD Associate Professor Department of Radiology University of Colorado Hospital Aurora, Colorado United States A. homas Stavros, MD, FACR Medical Director Ultrasound Invision Sally Jobe Breast Center Englewood, Colorado United States Maryellen R.M. Sun, MD Department of Radiology Lowell General Hospital Lowell, Massachusetts United States

Contributors Wendy hurston, MD Assistant Professor Department of Medical Imaging University of Toronto Chief, Diagnostic Imaging Department of Diagnostic Imaging St. Joseph’s Health Centre Courtesy Staf Department of Medical Imaging University Health Network Toronto, Ontario Canada Ants Toi, MD, FRCPC, FAIUM Professor of Radiology and of Obstetrics and Gynecology University of Toronto Radiologist Medical Imaging Mt. Sinai Hospital Toronto, Ontario Canada Laurie Troxclair, BS, RDMS, RVT Ochsner Clinic Foundation New Orleans, Louisiana United States Mitchell Tublin, MD Professor and Vice Chair Department of Radiology University of Pittsburgh School of Medicine Pittsburgh, Pennsylvania United States Heidi R. Umphrey, MD, MS Associate Professor of Radiology Department of Radiology University of Alabama at Birmingham Birmingham, Alabama United States Sheila Unger, MD University of Lausanne Lausanne Switzerland Patrick M. Vos, MD Clinical Assistant Professor Department of Radiology University of British Columbia Vancouver, British Columbia Canada

herese M. Weber, MD, MS Professor of Radiology Department of Radiology University of Alabama at Birmingham Birmingham, Alabama United States Kirsten L. Weind Matthews, PhD, MBBS, FRCPC Lecturer, Medical Imaging University of Toronto Department of Medical Imaging Mount Sinai Hospital Toronto, Ontario Canada Stephanie R. Wilson, MD Clinical Professor Department of Radiology Department of Medicine, Division of Gastroenterology University of Calgary Calgary, Alberta Canada homas Winter, MD Professor and Chief of Abdominal Imaging Department of Radiology University of Utah Salt Lake City, Utah United States Cynthia E. Withers, MD Radiologist (retired) Sansum Clinic and Santa Barbara Cottage Hospital Santa Barbara, California United States Corrie Yablon, MD Assistant Professor Department of Radiology University of Michigan Ann Arbor, Michigan United States Hojun Yu, MD Radiologist Department of Diagnostic Imaging Queen Elizabeth II Hospital Grande Prairie, Alberta Canada

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In memory of my parents, Drs. Ruth and Raymond Masters, who encouraged me to enjoy the intellectual challenge of medicine and the love of making a diference in patients’ lives. Carol M. Rumack To Alex, Becky, and Julie—your love and support made this work possible. Debbie Levine

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Preface

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PREFACE he ith edition of Diagnostic Ultrasound is a major revision. Previous editions have been very well accepted as reference textbooks and have been the most commonly used reference in ultrasound education and practices worldwide. he text and references have all been updated and are now all available online. We are pleased to provide over 2500 new/revised images (with over 5800 images total) and over 380 new videos (with 480 total videos). he display of real-time ultrasound has helped to capture those abnormalities that require a sweep through the pathology to truly appreciate the lesion as well. Daily we ind that cine or video clips show important areas between still images that help to make certain a diagnosis or relationships between lesions. Now we rarely need to go back to reevaluate a lesion with another scan, making patient imaging more eicient. Another new ofering in this textbook is a completely online “virtual” chapter on artifacts. PowerPoint videos explain many of the artifacts that are linked to images and videos in the text. he ith edition was a major change for our editorial team, as we said a fond farewell to Stephanie Wilson and Bill Charboneau. heir expertise is still felt in this edition, as they have contributed chapters on gastrointestinal ultrasound (liver, biliary tree, and gastrointestinal tract, which are all some of Stephanie’s passions) and thyroid and interventional ultrasound (just some of Bill’s areas of expertise). Nearly 100 outstanding new and continuing authors have contributed to this edition, and all are recognized experts in the ield of ultrasound. As in prior editions, we have emphasized the use of collages to show many examples of similar anatomy and pathology. hese images relect the spectrum of sonographic changes that may occur in a given disease, instead of the most common manifestation only. he book’s format has been redesigned with key points in addition to the outline at the beginning of each chapter. here

are again colored boxes to highlight the important or critical features of sonographic diagnoses. Key terms and concepts are emphasized in boldface type. To direct the readers to other research and literature of interest, comprehensive reference lists are provided. Diagnostic Ultrasound is again divided into two volumes. Volume I consists of Parts I to III. Part I contains chapters on physics and biologic efects of ultrasound and includes descriptions of elastography and contrast agents. Part II covers abdominal sonography and includes two completely revised chapters on pelvic sonography, along with chapters on interventional procedures (including those in the thorax) and organ transplantation. Part III presents small parts imaging, including thyroid, breast, scrotum, carotid, a completely revised chapter on imaging of the extracranial vessels, and two completely revised musculoskeletal imaging chapters, as well as an updated chapter on musculoskeletal intervention. Volume II begins with Part IV, with obstetric ultrasound, which has important updates in irst-trimester scanning and screening for aneuploidy including cell-free DNA. Part V comprehensively covers pediatric sonography, including pediatric interventional sonography. Completely revised chapters on the pediatric spinal canal and pediatric kidney are replete with new images and scanning techniques. Diagnostic Ultrasound is for practicing physicians, residents, medical students, sonographers, and others interested in understanding the vast applications of diagnostic sonography in patient care. Our goal is for Diagnostic Ultrasound to continue to be the most comprehensive reference book available in the sonographic literature, with a highly readable style and superb images. Carol M. Rumack, MD, FACR Deborah Levine, MD, FACR

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Acknowledgments

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ACKNOWLEDGMENTS We wish to express our deepest appreciation and sincerest gratitude: To all of our outstanding authors, who have contributed extensive, newly updated, and authoritative text and images and videos. We cannot thank them enough for their eforts on this project. To Alexander Jesurum, PhD, whose outstanding eforts kept the references updated for all of our authors and who helped in author contact and communication. To Lisa Napolitano, RDMS, who spent hours inding and cropping videos to supplement our online edition. To Robin Carter, Executive Content Strategist at Elsevier, who has worked closely with us on this project from the very beginning of the ith edition. To Taylor Ball and Dan Fitzgerald at Elsevier, who kept us on track for the process of updating and copyediting the entire manuscript. It has been an intense year for everyone, and we are very proud of this superb edition of Diagnostic Ultrasound.

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Contents

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CONTENTS VOLUME I

15 The Uterus, 528

PART I Physics

16 The Adnexa, 564

Douglas Brown and Deborah Levine

Rochelle Filker Andreotti and Lori A. Deitte

1 Physics of Ultrasound, 1 Christopher R.B. Merritt

2 Biologic Effects and Safety, 34 J. Brian Fowlkes and Christy K. Holland

3 Contrast Agents for Ultrasound, 53 Peter N. Burns

PART II Abdominal and Pelvic Sonography 4 The Liver, 74 Stephanie R. Wilson and Cynthia E. Withers

5 The Spleen, 139 Patrick M. Vos, John R. Mathieson, and Peter L. Cooperberg

6 The Biliary Tree and Gallbladder, 165 Korosh Khalili and Stephanie R. Wilson

7 The Pancreas, 210 Thomas Winter and Maryellen R.M. Sun

8 The Gastrointestinal Tract, 256 Stephanie R. Wilson

9 The Kidney and Urinary Tract, 310 Mitchell Tublin, Deborah Levine, Wendy Thurston, and Stephanie R. Wilson

10 The Prostate and Transrectal Ultrasound, 381 Ants Toi

11 The Adrenal Glands, 416 Christina Marie Chingkoe, Olga R. Brook, and Deborah Levine

12 The Retroperitoneum, 432 Raymond E. Bertino and Elton Mustafaraj

13 Dynamic Ultrasound of Hernias of the Groin and Anterior Abdominal Wall, 470 Deborah Levine, Lisa Napolitano, and A. Thomas Stavros

17 Ultrasound-Guided Biopsy of Chest, Abdomen, and Pelvis, 597 Theodora A. Potretzke, Thomas D. Atwell, J. William Charboneau, and Carl Reading

18 Organ Transplantation, 623 Derek Muradali and Tanya Punita Chawla

PART III Small Parts, Carotid Artery, and Peripheral Vessel Sonography 19 The Thyroid Gland, 691 Luigi Solbiati, J. William Charboneau, Vito Cantisani, Carl Reading, and Giovanni Mauri

20 The Parathyroid Glands, 732 Bonnie J. Huppert and Carl Reading

21 The Breast, 759 Jordana Phillips, Rashmi J. Mehta, and A. Thomas Stavros

22 The Scrotum, 818 Daniel Sommers and Thomas Winter

23 Overview of Musculoskeletal Ultrasound Techniques and Applications, 856 Colm McMahon and Corrie Yablon

24 The Shoulder, 877 Colm McMahon and Corrie Yablon

25 Musculoskeletal Interventions, 898 Ronald S. Adler

26 The Extracranial Cerebral Vessels, 915 Edward I. Bluth, Stephen I. Johnson, and Laurie Troxclair

27 Peripheral Vessels, 964 Mark E. Lockhart, Heidi R. Umphrey, Therese M. Weber, and Michelle L. Robbin

14 The Peritoneum, 504 Anthony E. Hanbidge, Korosh Khalili, and Stephanie R. Wilson

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Contents

VOLUME II PART IV Obstetric and Fetal Sonography 28 Overview of Obstetric Imaging, 1015 Deborah Levine

29 Bioeffects and Safety of Ultrasound in Obstetrics, 1034 Jacques S. Abramowicz

30 The First Trimester, 1048 Elizabeth Lazarus and Deborah Levine

31 Chromosomal Abnormalities, 1088 Bryann Bromley and Beryl Benacerraf

32 Multifetal Pregnancy, 1115 Mary C. Frates

33 The Fetal Face and Neck, 1133 Ana P. Lourenco and Judy A. Estroff

34 The Fetal Brain, 1166 Ants Toi and Deborah Levine

35 The Fetal Spine, 1216 Elizabeth Asch and Eric Sauerbrei

36 The Fetal Chest, 1243 Dorothy Bulas

37 The Fetal Heart, 1270 Elizabeth R. Stamm and Julia A. Drose

38 The Fetal Gastrointestinal Tract and Abdominal Wall, 1304 Nir Melamed, Anne Kennedy, and Phyllis Glanc

39 The Fetal Urogenital Tract, 1336 Katherine W. Fong, Julia Eva Kfouri, and Kirsten L. Weind Matthews

40 The Fetal Musculoskeletal System, 1376 Phyllis Glanc, David Chitayat, and Sheila Unger

41 Fetal Hydrops, 1412 Deborah Levine

42 Fetal Measurements: Normal and Abnormal Fetal Growth and Assessment of Fetal Well-Being, 1443 Carol B. Benson and Peter M. Doubilet

43 Sonographic Evaluation of the Placenta, 1465 Thomas D. Shipp

44 Cervical Ultrasound and Preterm Birth, 1495 Hournaz Ghandehari and Phyllis Glanc

PART V Pediatric Sonography 45 Neonatal and Infant Brain Imaging, 1511 Carol M. Rumack and Amanda K. Auckland

46 Duplex Sonography of the Neonatal and Infant Brain, 1573 Thierry A.G.M. Huisman and Andrea Poretti

47 Doppler Sonography of the Brain in Children, 1591 Dorothy Bulas and Alexia Egloff

48 The Pediatric Head and Neck, 1628 Rupa Radhakrishnan and Beth M. Kline-Fath

49 The Pediatric Spinal Canal, 1672 Ilse Castro-Aragon, Deborah Levine, and Carol M. Rumack

50 The Pediatric Chest, 1701 Chetan Chandulal Shah and S. Bruce Greenberg

51 The Pediatric Liver and Spleen, 1730 Sara M. O’Hara

52 The Pediatric Urinary Tract and Adrenal Glands, 1775 Harriet J. Paltiel and Diane S. Babcock

53 The Pediatric Gastrointestinal Tract, 1833 Susan D. John and Martha Mappus Munden

54 Pediatric Pelvic Sonography, 1870 William L. Simpson, Jr., Humaira Chaudhry, and Henrietta Kotlus Rosenberg

55 The Pediatric Hip and Other Musculoskeletal Ultrasound Applications, 1920 Leslie E. Grissom and H. Theodore Harcke

56 Pediatric Interventional Sonography, 1942 Neil Johnson and Allison Aguado

Appendix: Ultrasound Artifacts: A Virtual Chapter Korosh Khalili, Hojun Yu, Alexander Jesurum, and Deborah Levine

Index, I-1

Video Contents

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VIDEO CONTENTS 4 The Liver Stephanie R. Wilson and Cynthia E. Withers Video 4.1 Normal liver, sagittal sweep Video 4.2 Normal liver, subcostal sweep Video 4.3 Focal fat in the liver Video 4.4 Geographic fatty iniltration of the liver Video 4.5 CEUS of FNH with classic enhancement features Video 4.6 CEUS of the lash-illing hemangioma shown in Fig. 4.47 Video 4.7 CEUS of focal nodular hyperplasia Video 4.8 CEUS of focal nodular hyperplasia Video 4.9 CEUS of hepatic adenoma in a young woman Video 4.10 CEUS of small hepatocellular carcinoma Video 4.11 CEUS of hepatocellular carcinoma Video 4.12 Classic colorectal metastasis Video 4.13 CEUS of liver metastasis Video 4.14 CEUS of liver metastasis

5 The Spleen Patrick M. Vos, John R. Mathieson, and Peter L. Cooperberg Video 5.1 Normal spleen in sagittal plane Video 5.2 Normal spleen in transverse plane Video 5.3 Contrast study of lymphoma manifesting as a hypoechoic solitary splenic lesion

6 The Biliary Tree and Gallbladder Korosh Khalili and Stephanie R. Wilson Video 6.1 Distal common bile duct and ampulla of Vater Video 6.2 Intrahepatic bile duct stones Video 6.3 Distal common bile duct stone Video 6.4 Choledochoduodenal istula Video 6.5 Primary sclerosing cholangitis Video 6.6 Primary sclerosing cholangitis Video 6.7 Cholangiocarcinoma complicating primary sclerosing cholangitis Video 6.8 Cholangiocarcinoma complicating primary sclerosing cholangitis Video 6.9 Cholelithiasis Video 6.10 Acute cholecystitis Video 6.11 Perforated cholecystitis with liver abscess

7 The Pancreas Thomas Winter and Maryellen R.M. Sun Video 7.1 Normal pancreas Video 7.2 Acute pancreatitis Video 7.3 Acute pancreatitis Video 7.4 Chronic pancreatitis Video 7.5 Chronic pancreatitis Video 7.6 Pancreatic pseudocyst Video 7.7 Pancreatic carcinoma Video 7.8 Pancreatic carcinoma Video 7.9 Intraductal papillary mucinous neoplasm Video 7.10 Mucinous cystic neoplasm

8 The Gastrointestinal Tract Stephanie R. Wilson Video 8.1 An incidentally detected neuroendocrine tumor (carcinoid) of the small bowel Video 8.2 Classic features of Crohn disease on a sweep through the terminal ileum Video 8.3 Loss of stratiication of the bowel wall layers in severe subacute inlammation of the sigmoid colon in a patient with Crohn disease Video 8.4 Stricture in Crohn disease Video 8.5 Color Doppler shows hyperemia in thickened bowel wall in Crohn disease Video 8.6 Contrast-enhanced longitudinal image of Crohn disease Video 8.7 Contrast-enhanced cross-sectional image of Crohn disease Video 8.8 Severe ixation and acute angulation of the ileum with stricture and enteroenteric istula Video 8.9 Incomplete small bowel obstruction in patient with Crohn disease Video 8.10 Dysfunctional and excess peristalsis Video 8.11 Localized perforation with a phlegmonous inlammatory mass Video 8.12 Enteroenteric istula Video 8.13 Normal appendix Video 8.14 Perforated appendix Video 8.15 Acute diverticulitis in second trimester of pregnancy Video 8.16 Paralytic ileus Video 8.17 Incomplete bowel obstruction due to an inlammatory stricture from Crohn disease seen only on endovaginal scan

9 The Kidney and Urinary Tract Mitchell Tublin, Deborah Levine, Wendy Thurston, and Stephanie R. Wilson Video 9.1 Video 9.2 Video 9.3 Video 9.4

Doppler jet Renal cell carcinoma Transitional cell carcinoma of the bladder Bladder diverticula

11 The Adrenal Glands Christina Marie Chingkoe, Olga R. Brook, and Deborah Levine Video 11.1 Video 11.2 Video 11.3 Video 11.4

Normal adrenal gland Adrenal adenoma Adrenal adenoma Adrenal gland with calciication

12 The Retroperitoneum Raymond E. Bertino and Elton Mustafaraj Video 12.1 Video 12.2 scan Video 12.3 Video 12.4 Video 12.5 image Video 12.6 Video 12.7 artery

Type 2 endoleak from inferior mesenteric artery–aorta Type 2 endoleak on enhanced computed tomography Type 3 endoleak, transverse image Type 3 endoleak, longitudinal image Aortic pseudoaneurysm (contained rupture), longitudinal Restenosis of stented accessory left renal artery Angiogram of restenosis of stented accessory left renal

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Video 12.8 Angiogram of stented accessory left renal artery restenosis after restenting Video 12.9 Normal right renal artery Video 12.10 Left renal artery stenosis with color bruit and aliasing throughout cardiac cycle Video 12.11 Nutcracker syndrome Video 12.12 Nutcracker syndrome after stent placement Video 12.13 Prominent arcuate veins Video 12.14 Mildly prominent arcuate veins Video 12.15 Angiogram of left ovarian vein during coil placement

13 Dynamic Ultrasound of Hernias of the Groin and Anterior Abdominal Wall Deborah Levine, Lisa Napolitano, and A. Thomas Stavros Video 13.1 Fat-containing indirect inguinal hernia Video 13.2 Direct inguinal hernia with intraperitoneal and preperitoneal fat Video 13.3 Note bowel peristalsis in this inguinal hernia Video 13.4 Large fat-containing direct inguinal hernia Video 13.5 Change in hernia contents during Valsalva maneuver Video 13.6 Completely reducible large wide-necked fat-containing ventral hernia Video 13.7 Partially reducible indirect inguinal hernia containing fat and bowel Video 13.8 Nonreducible fat-containing epigastric linea alba hernia Video 13.9 Large bowel-containing indirect inguinal hernia extending into scrotum Video 13.10 Fat-containing femoral hernia Video 13.11 Moderate-sized fat-containing nonreducible left spigelian hernia Video 13.12 Large fat- and bowel-containing incompletely reducible spigelian hernia Video 13.13 Diastasis recti abdominis Video 13.14 Fat-containing ventral hernia Video 13.15 Small fat-containing nonreducible epigastric linea alba hernia Video 13.16 Two adjacent moderate-sized fat-containing incompletely reducible epigastric linea alba hernias Video 13.17 Mesh with strong shadow makes evaluation for recurrent hernia dificult Video 13.18 Two adjacent moderate-sized fat-containing incisional hernias in patient after transverse rectus abdominis myocutaneous (TRAM) lap breast reconstruction Video 13.19 Fat-containing incisional hernia Video 13.20 Moderate-sized fat-containing reducible incisional hernia Video 13.21 Moderate-sized fat-containing reducible recurrent inguinal hernia at the edge of mesh Video 13.22 Pantaloon hernias Video 13.23 Strangulated right femoral hernia Video 13.24 Round ligament and inguinal canal (canal of Nuck) in a female with hydrocele

Video 14.7 Peritoneal mesothelioma Video 14.8 Endometrioma in the pouch of Douglas Video 14.9 Endometriotic plaque Video 14.10 Endometriotic plaque

15 The Uterus Douglas Brown and Deborah Levine Video 15.1 Unicornuate uterus Video 15.2 Bicornuate uterus Video 15.3 Fibroid with cystic necrotic change Video 15.4 Adenomyosis Video 15.5 Prolapsing polyp Video 15.6 Endometrial polyp Video 15.7 Endometrial polyp Video 15.8 Endometrial carcinoma Video 15.9 Endometrial carcinoma with hematometra Video 15.10 Synechia Video 15.11 Low position of intrauterine device (IUD) Video 15.12 Vascularized retained products of conception Video 15.13 Bladder lap hematoma and sutures after cesarean section

16 The Adnexa Rochelle Filker Andreotti and Lori A. Deitte Video 16.1 Bowel peristalsis Video 16.2 Hemorrhagic cyst Video 16.3 Endometrioma Video 16.4 Atypical endometrioma Video 16.5 Deep iniltrating endometriosis Video 16.6 Ovarian torsion Video 16.7 Clear cell carcinoma in endometrioma Video 16.8 Yolk sac tumor Video 16.9 Hydrosalpinx in 70-year-old woman with adnexal cyst Video 16.10 Hydrosalpinx in 35-year-old with complex left adnexal cyst Video 16.11 Pelvic inlammatory disease caused by Neisseria Gonorrhoeae

17 Ultrasound-Guided Biopsy of Chest, Abdomen, and Pelvis Theodora A. Potretzke, Thomas D. Atwell, J. William Charboneau, and Carl Reading Video 17.1 Ultrasound-guided omental core biopsy Video 17.2 Ultrasound-guided liver core biopsy Video 17.3 Ultrasound-guided liver mass biopsy using “freehand” technique Video 17.4 Ultrasound-guided liver mass biopsy using “freehand” technique Video 17.5 Power Doppler imaging improving drain conspicuity Video 17.6 Transvaginal adnexal cyst local anesthesia Video 17.7 Transvaginal adnexal cyst aspiration

18 Organ Transplantation 14 The Peritoneum Anthony E. Hanbidge, Korosh Khalili, and Stephanie R. Wilson Video 14.1 Video 14.2 Video 14.3 Video 14.4 Video 14.5 Video 14.6

Tumor iniltration of the omentum Tumor implant in the pouch of Douglas Tumor implant in the pouch of Douglas Peritoneal carcinomatosis—parietal peritoneum Peritoneal carcinomatosis—visceral peritoneum Peritoneal carcinomatosis—visceral peritoneum

Derek Muradali and Tanya Punita Chawla Video 18.1 Normal renal transplant, sagittal Video 18.2 Normal renal transplant, transverse Video 18.3 Arteriovenous malformation renal transplant Video 18.4 Partially thrombosed pseudoaneurysm in hilum of renal transplant Video 18.5 Normal pancreas transplant, sagittal Video 18.6 Normal pancreas transplant, transverse

Video Contents 19 The Thyroid Gland Luigi Solbiati, J. William Charboneau, Vito Cantisani, Carl Reading, and Giovanni Mauri Video 19.1 Video 19.2 Video 19.3 Video 19.4 Video 19.5 Video 19.6 Video 19.7

Colloid cysts Honeycomb pattern of benign nodule Adenoma Papillary carcinoma: ine calciications Papillary carcinoma: coarse and ine calciications Fine-needle aspiration (FNA) Hashimoto thyroiditis

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23 Overview of Musculoskeletal Ultrasound Techniques and Applications Colm McMahon and Corrie Yablon Video 23.1 Video 23.2 Video 23.3 Video 23.4 Video 23.5

Normal biceps muscle and distal tendon Normal Achilles tendon Normal inger lexor tendons—dynamic imaging Dynamic ulnar nerve subluxation Short-axis imaging of a Baker cyst

24 The Shoulder Colm McMahon and Corrie Yablon

20 The Parathyroid Glands Bonnie J. Huppert and Carl Reading Video 20.1 Cystic and solid parathyroid adenoma Video 20.2 Small parathyroid adenoma Video 20.3 Multiple gland parathyroid hyperplasia Video 20.4 Multiple gland parathyroid hyperplasia Video 20.5 Superior parathyroid adenoma Video 20.6 Superior parathyroid adenoma Video 20.7 Inferior parathyroid adenoma Video 20.8 Inferior parathyroid adenoma Video 20.9 Ectopic superior parathyroid adenoma Video 20.10 Intrathyroid parathyroid adenoma Video 20.11 Intrathyroid parathyroid adenoma Video 20.12 Ectopic parathyroid adenoma Video 20.13 Parathyromatosis in the postoperative neck Video 20.14 Parathyroid adenoma Video 20.15 Small inferior parathyroid adenoma and multinodular goiter Video 20.16 Small inferior parathyroid adenoma and multinodular thyroid Video 20.17 Ectopic intrathyroid parathyroid adenoma biopsy Video 20.18 Ectopic parathyroid adenoma biopsy Video 20.19 Ethanol ablation of recurrent graft-dependent hyperparathyroidism

21 The Breast Jordana Phillips, Rashmi J. Mehta, and A. Thomas Stavros Video 21.1 Importance of light pressure for color Doppler examination Video 21.2 Importance of light pressure for color Doppler examination Video 21.3 Normal cyst Video 21.4 Intraductal papilloma Video 21.5 Percutaneous biopsy using spring-loaded biopsy device

22 The Scrotum Daniel Sommers and Thomas Winter Video 22.1 Atrophic testis with seminoma Video 22.2 Epidermoid cyst Video 22.3 Varicocele in patient performing a Valsalva maneuver, with gray-scale and color Doppler sonography Video 22.4 Postvasectomy appearance of epididymis and vas deferens Video 22.5 “Dancing sperm” postvasectomy image of scrotum Video 22.6 Acute orchitis Video 22.7 Inferior traumatic tunica albuginea rupture, hematoma in testis, and extrusion of seminiferous tubules

Video 24.1 Dynamic assessment for subcoracoid impingement Video 24.2 Illustration of imaging the supraspinatus in long axis and the transition to infraspinatus posteriorly Video 24.3 Dynamic assessment for subacromial impingement Video 24.4 Dynamic imaging showing increased prominence of glenohumeral effusion on external rotation Video 24.5 Short-axis imaging of the supraspinatus tendon

25 Musculoskeletal Interventions Ronald S. Adler Video 25.1 Intraarticular injection of a hip under ultrasound guidance Video 25.2 Biceps tendon sheath injection using a rotator interval approach Video 25.3 Aspiration of a spinoglenoid notch cyst Video 25.4 Injection of calciic tendinosis Video 25.5 Autologous blood injection of 50-year-old woman with lateral epicondylitis Video 25.6 Depiction of Tenex procedure Video 25.7 Posthydrodissection of sural nerve in a 59-year-old female patient

26 The Extracranial Cerebral Vessels Edward I. Bluth, Stephen I. Johnson, and Laurie Troxclair Video 26.1 Minimal homogeneous plaque at carotid bulb (gray-scale) Video 26.2 Considerable homogenous plaque at ICA (gray-scale) Video 26.3 Type 3 homogeneous plaque with less than 50% sonolucency (gray-scale) Video 26.4 Type 3 homogeneous plaque with low-grade stenosis of the ICA (gray-scale) Video 26.5 Calciied plaque in the CCA (gray-scale) Video 26.6 Heterogeneous plaque in the left ICA (type 1) (gray-scale) Video 26.7 Heterogeneous plaque (type 1) with greater than 50% sonolucency within the plaque of the left ICA (gray-scale) Video 26.8 Heterogeneous plaque (type 2) in the ICA (gray-scale) Video 26.9 High-grade stenosis in the proximal right ICA (color Doppler) Video 26.10 Heterogeneous plaque in the ICA (color Doppler) Video 26.11 Heterogeneous plaque in the left ICA (power Doppler) Video 26.12 High-grade stenosis in the ICA (power Doppler) Video 26.13 High-grade stenosis of the ICA (power Doppler) Video 26.14 Low-grade stenosis in the ICA (color Doppler) Video 26.15 Normal spectral waveform of the proximal ICA Video 26.16 Normal spectral waveform of the mid ICA Video 26.17 Normal spectral waveform of the distal ICA Video 26.18 Normal spectral waveform of the right distal CCA Video 26.19 High-grade stenosis in the ICA (power Doppler)

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Video 26.20 High-grade stenosis in the ICA (color Doppler) Video 26.21 High-grade stenosis with spectral broadening (color and spectral Doppler) Video 26.22 Color and spectral Doppler of low-grade stenosis in the ICA

27 Peripheral Vessels Mark E. Lockhart, Heidi R. Umphrey, Therese M. Weber, and Michelle L. Robbin Video 27.1 Acute thrombus in the supericial femoral artery Video 27.2 Occlusion of the supericial femoral artery with a large collateral exiting proximal to the occlusion Video 27.3 Severe calciication of the supericial femoral artery limits ability to see within the artery lumen with gray-scale imaging Video 27.4 Common femoral artery pseudoaneurysm Video 27.5 Common femoral artery to common femoral vein arteriovenous istula (AVF) Video 27.6 Arterial bypass graft stenosis on grayscale and color Doppler Video 27.7 Large radial artery pseudoaneurysm with rent in arterial wall Video 27.8 Large radial artery pseudoaneurysm Video 27.9 Subclavian steal Video 27.10 Normal femoral vein compression during study to assess for deep venous thrombosis Video 27.11 Acute common femoral vein (CFV) thrombus Video 27.12 Nonocclusive slightly mobile thrombus within the great saphenous vein (GSV) with extension into the common femoral vein (CFV) Video 27.13 Acute deep venous thrombosis in right lower extremity Video 27.14 Chronic vein occlusion with collaterals Video 27.15 Chronic common femoral vein (CFV) occlusion with normal antegrade low in the femoral vein, and low reversal in the profunda femoral vein Video 27.16 Slow low in patent, compressible vein without deep venous thrombosis, longitudinal cine clip Video 27.17 Slow low in patent, compressible vein without deep venous thrombosis, transverse cine clip Video 27.18 Thrombus in one of paired femoral veins Video 27.19 Normal femoral vein valve Video 27.20 Normal internal jugular vein (IJV) on gray scale compression cine clip Video 27.21 Acute internal jugular thrombus Video 27.22 Nonocclusive thrombus in one brachial vein in the paired brachial veins Video 27.23 Acute thrombus around peripherally inserted central catheter (PICC) line in the basilic vein Video 27.24 Acute thrombus around peripherally inserted central catheter (PICC) line in the basilic vein Video 27.25 Thick-walled cephalic vein with chronic thrombus Video 27.26 Large hematoma adjacent to arteriovenous istula (AVF) Video 27.27 Small AVF basilic vein pseudoaneurysm Video 27.28 Graft wall irregularity and degeneration from repeated punctures Video 27.29 Graft venous anastomosis stenosis with peak systolic velocity measuring 6.1 m/sec in highest velocity portion of jet

28 Overview of Obstetric Imaging Deborah Levine Video 28.1 Normal 6-week embryo with cardiac activity Video 28.2 Normal irst-trimester embryo with rhombencephalon appearing as a luid collection in the region of the head Video 28.3 Sagittal view of uterus with 17-week gestational age fetus in cephalic presentation and anterior placenta Video 28.4 Normal intracranial anatomy at 19 weeks’ gestation Video 28.5 Four-chamber view of beating fetal heart Video 28.6 Scan through the heart Video 28.7 Normal kidneys and lumbosacral spine Video 28.8 Transverse fetal spine Video 28.9 Bladder and umbilical arteries

30 The First Trimester Elizabeth Lazarus and Deborah Levine Video 30.1 Early embryonic cardiac activity Video 30.2 Early pregnancy failure at 7 weeks Video 30.3 Expanded amnion in nonviable pregnancy Video 30.4 Ten-week demise with calciied yolk sac Video 30.5 Small subchorionic hemorrhage Video 30.6 Right ectopic pregnancy with adnexal mass separating from the ovary with manual pressure Video 30.7 Ruptured ectopic pregnancy Video 30.8 Cesarean section implantation in retrolexed uterus Video 30.9 Normal rhombencephalon Video 30.10 Persistent trophoblastic neoplasia Video 30.11 Choriocarcinoma

31 Chromosomal Abnormalities Bryann Bromley and Beryl Benacerraf Video 31.1 Nuchal translucency Video 31.2 Cystic hygroma Video 31.3 Nasal bone in irst trimester Video 31.4 Echogenic bowel Video 31.5 Amniocentesis needle being withdrawn from amniotic luid cavity

32 Multifetal Pregnancy Mary C. Frates Video 32.1 Quintuplets, 9 weeks’ gestational age Video 32.2 Conjoined embryos, 7 weeks’ gestational age Video 32.3 Monochorionic monoamniotic twins, 26 weeks’ gestational age Video 32.4 Three separate placentas in a trichorionic triplet pregnancy at 13 weeks’ gestational age Video 32.5 Velamentous cord insertion in a twin, 34 weeks’ gestational age Video 32.6 Growth and luid discrepancies in dichorionic twins, 24 weeks’ gestational age Video 32.7 Twin-twin transfusion syndrome, 22 weeks’ gestational age Video 32.8 Twin reversed arterial perfusion sequence, 16 weeks’ gestational age Video 32.9 Monochorionic monoamniotic twins, 12 weeks’ gestational age Video 32.10 Monochorionic monoamniotic twins, 28 weeks’ gestational age Video 32.11 Monochorionic monoamniotic conjoined twins, 35 weeks’ gestational age

Video Contents 33 The Fetal Face and Neck Ana P. Lourenco and Judy A. Estroff Video 33.1 Left 2 complete cleft lip, cleft alveolus, and cleft palate in sagittal plane in 20-week gestational age fetus Video 33.2 Left unilateral complete cleft lip, cleft alveolus, and cleft palate in axial plane in 20-week gestational age fetus Video 33.3 Left unilateral complete cleft lip, cleft alveolus, and cleft palate in coronal plane in 20-week gestational age fetus Video 33.4 Micrognathia at gestational age 20 weeks

34 The Fetal Brain Ants Toi and Deborah Levine Video 34.1 Normal brain, axial Video 34.2 Normal brain, coronal Video 34.3 Normal brain, sagittal Video 34.4 Choroid plexus cysts Video 34.5 Bilateral ventriculomegaly Video 34.6 Chiari malformation in fetus with spinal neural tube defect Video 34.7 Holoprosencephaly Video 34.8 Second trimester agenesis of corpus callosum Video 34.9 Agenesis of corpus callosum in coronal plane Video 34.10 Agenesis of corpus callosum in sagittal plane Video 34.11 Agenesis of corpus callosum in axial plane with midline cyst Video 34.12 Absence of septal lealets

35 The Fetal Spine Elizabeth Asch and Eric Sauerbrei Video 35.1 Video 35.2 Video 35.3 Video 35.4 Video 35.5 Video 35.6

Normal transaxial spine Normal longitudinal spine Myelomeningocele Closed neural tube defect: transaxial Closed neural tube defect: longitudinal Sacrococcygeal teratoma

36 The Fetal Chest

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Video 37.7 Aortic arch Video 37.8 Aortic arch Video 37.9 Atrioventricular septal defect Video 37.10 Hypoplastic left heart syndrome Video 37.11 Hypoplastic right heart Video 37.12 Ebstein anomaly Video 37.13 Tetralogy of Fallot

38 The Fetal Gastrointestinal Tract and Abdominal Wall Nir Melamed, Anne Kennedy, and Phyllis Glanc Video 38.1 Esophageal atresia Video 38.2 Gastric debris Video 38.3 Gastric debris Video 38.4 Duodenal atresia Video 38.5 Jejunal atresia Video 38.6 Duplication cyst Video 38.7 Meconium peritonitis Video 38.8 Echogenic bowel Video 38.9 Normal gallbladder Video 38.10 Annular pancreas Video 38.11 Splenic cyst Video 38.12 Gastroschisis Video 38.13 Omphalocele Video 38.14 Bladder exstrophy Video 38.15 Cloacal exstrophy

39 The Fetal Urogenital Tract Katherine W. Fong, Julia Eva Kfouri, and Kirsten L. Weind Matthews Video 39.1 “Lying down” adrenal sign due to unilateral renal agenesis Video 39.2 Bilateral renal agenesis Video 39.3 Pelvic kidney Video 39.4 Cross-fused renal ectopia Video 39.5 Horseshoe kidney Video 39.6 Autosomal recessive polycystic kidney disease Video 39.7 Perinephric urinoma Video 39.8 Primary megaureter Video 39.9 Megalourethra Video 39.10 Cloacal dysgenesis Video 39.11 Ovarian cyst

Dorothy Bulas Video 36.1 Congenital pulmonary adenomatoid malformation Video 36.2 Small pleural effusion at 16 weeks’ gestational age Video 36.3 Left-sided congenital diaphragmatic hernia at 32 weeks’ gestational age (transverse view) Video 36.4 Left-sided congenital diaphragmatic hernia at 32 weeks’ gestational age (sagittal view) Video 36.5 Large left-sided congenital diaphragmatic hernia with large amount of liver in chest Video 36.6 Right-sided congenital diaphragmatic hernia

37 The Fetal Heart Elizabeth R. Stamm and Julia A. Drose Video 37.1 Normal apical four-chamber view Video 37.2 Normal sub-costal four-chamber view Video 37.3 Normal appearance of the aorta and pulmonary artery Video 37.4 Color Doppler of the aorta and pulmonary artery Video 37.5 Short-axis view of the color Doppler of the ventricles and great arteries Video 37.6 Three-vessel and trachea view

40 The Fetal Musculoskeletal System Phyllis Glanc, David Chitayat, and Sheila Unger Video 40.1 Thanatophoric dysplasia Video 40.2 Clubfeet at 21 weeks

41 Fetal Hydrops Deborah Levine Video 41.1 Fetal abdomen at 30 weeks gestational age in fetus with a small amount of ascites and polyhydramnios Video 41.2 Bilateral pleural effusions, left greater than right Video 41.3 Large unilateral pleural effusion inverts the hemidiaphragm and is associated with ascites Video 41.4 Small pericardial effusion in fetus with poorly contractile and echogenic heart Video 41.5 Anasarca in fetus with congenital pulmonary airway malformation Video 41.6 Middle cerebral artery Doppler Video 41.7 Poorly contractile heart abnormal appearing heart, bilateral pleural effusions, and marked anasarca

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42 Fetal Measurements: Normal and Abnormal Fetal Growth and Assessment of Fetal Well-Being Carol B. Benson and Peter M. Doubilet Video 42.1 Early embryonic heartbeat Video 42.2 Fetal movement Video 42.3 Fetal breathing movements

43 Sonographic Evaluation of the Placenta Thomas D. Shipp Video 43.1 Placental lake Video 43.2 Thick placenta Video 43.3 Placenta accreta Video 43.4 Placenta increta Video 43.5 Placenta percreta Video 43.6 Abruption Video 43.7 Abruption Video 43.8 Preplacental hematoma Video 43.9 Preplacental hematoma Video 43.10 Placental infarction Video 43.11 Placental infarction Video 43.12 Circumvallate placenta Video 43.13 Circumvallate placenta Video 43.14 Bilobed placenta Video 43.15 Velamentous cord insertion and two-vessel cord Video 43.16 Umbilical cord insertion into placenta Video 43.17 Vasa previa

44 Cervical Ultrasound and Preterm Birth Hournaz Ghandehari and Phyllis Glanc Video 44.1 Open cervix with large funnel and bulging membranes Video 44.2 Closed cervix with mobile debris at the internal os Video 44.3 Open cervix with mobile debris in the dilated cervical canal and adjacent to the external os

Video 45.16 Video 45.17 Video 45.18 Video 45.19

Cystic periventricular leukomalacia Cytomegalovirus with punctate calciications Multiple focal calciications Ventricular septation

47 Doppler Sonography of the Brain in Children Dorothy Bulas and Alexia Egloff Video 47.1 Normal color Doppler of circle of Willis in 6-year-old Video 47.2 Spectral wave form of the right middle cerebral artery Video 47.3 Normal spectral Doppler of right bifurcation Video 47.4 Four-year-old pending brain death after fall from second story Video 47.5 Eight-year-old pending brain death after motor vehicle accident postcraniectomy for hematoma

48 The Pediatric Head and Neck Rupa Radhakrishnan and Beth M. Kline-Fath Video 48.1 Video 48.2 Video 48.3 Video 48.4

Wharton duct stone Multinodular goiter Infantile hemangioma Lymphatic malformation

49 The Pediatric Spinal Canal Ilse Castro-Aragon, Deborah Levine, and Carol M. Rumack Video 49.1 Normal cauda equina Video 49.2 Normal ilum terminale Video 49.3 Skin dimple and hypoechoic tract in subcutaneous tissues extending to normal coccyx Video 49.4 Lipomyelocele in sagittal view Video 49.5 Sagittal lipomyelocele Video 49.6 Lipomyelocele in transverse view Video 49.7 Lipomyelomeningocele Video 49.8 Segmental spinal dysgenesis in sagittal view Video 49.9 Segmental spinal dysgenesis patient with fatty ilum

50 The Pediatric Chest 45 Neonatal and Infant Brain Imaging Carol M. Rumack and Amanda K. Auckland Video 45.1 Normal coronal sweep Video 45.2 Normal sagittal sweep Video 45.3 Normal mastoid sweep Video 45.4 Chiari II malformation Video 45.5 Ventriculomegaly in association with Chiari II malformation (seen in Video 45.4) Video 45.6 Chiari II malformation, pointed frontal and large occipital horn; partial absence of corpus callosum (same neonate as in Videos 45.4 and 45.5) Video 45.7 Tethered cord in patient with Chiari II malformation, sagittal scan Video 45.8 Absence of cavum septi pellucidi, coronal scan Video 45.9 Right subacute subependymal, intraventricular, and right frontal intraparenchymal hemorrhages, coronal scan Video 45.10 Right subependymal, caudothalamic groove, and hemorrhage and intraventricular hemorrhage, sagittal scan Video 45.11 Cisterna magna clot Video 45.12 Acute intraventricular echogenic blood Video 45.13 Bilateral intraventricular hemorrhage and intraparenchymal hemorrhage Video 45.14 Acute highly echogenic hemorrhage Video 45.15 Intraventricular hemorrhage

Chetan Chandulal Shah and S. Bruce Greenberg Video 50.1 Video 50.2 Video 50.3 child Video 50.4 surgery

Moving septations within pleural luid Hemidiaphragmatic motion in an infant Hemidiaphragmatic movement in healthy 31-month-old Hemidiaphragmatic paralysis in an infant after cardiac

51 The Pediatric Liver and Spleen Sara M. O’Hara Video 51.1 Normal porta hepatis showing portal vein, hepatic artery, and common bile duct Video 51.2 Neonatal hepatitis Video 51.3 Steatosis from obesity Video 51.4 Multiple cutaneous hemangiomas in a 1-month-old infant Video 51.5 Multiple cutaneous hemangiomas in a 1-month-old infant Video 51.6 Hepatic abscess Video 51.7 Normal low in the main portal vein Video 51.8 Normal branching vessels in the liver Video 51.9 Normal third- and fourth-order branches in the liver Video 51.10 Cavernous transformation of the portal vein Video 51.11 Pneumobilia, an expected inding following portoenterostomy

Video Contents 52 The Pediatric Urinary Tract and Adrenal Glands Harriet J. Paltiel and Diane S. Babcock Video 52.1 Crossed renal ectopia Video 52.2 Contrast-enhanced urosonography depicts a normal bladder Video 52.3 Contrast-enhanced urosonography demonstrates vesicoureteral relux Video 52.4 Contrast-enhanced urosonography shows a normal male urethra Video 52.5 Inlammatory pseudotumor Video 52.6 Laceration of the mid-lateral aspect of the left kidney and perirenal hematoma Video 52.7 Multicystic dysplastic kidney Video 52.8 Burkitt lymphoma involving kidney Video 52.9 Neuroblastoma

54 Pediatric Pelvic Sonography William L. Simpson, Jr., Humaira Chaudhry, and Henrietta Kotlus Rosenberg Video 54.1 Video 54.2 Video 54.3 Video 54.4 Video 54.5

Water vaginogram Normal postpubertal ovary Polycystic ovarian morphology Normal postpubertal testis Testicular microlithiasis

55 The Pediatric Hip and Other Musculoskeletal Ultrasound Applications Leslie E. Grissom and H. Theodore Harcke Video 55.1 Video 55.2 Video 55.3 Video 55.4 Video 55.5 Video 55.6 Video 55.7 Video 55.8

Normal coronal/lexion view, midacetabulum Normal coronal/lexion view, posterior lip Subluxation, coronal/lexion view, midacetabulum Dislocatable hip, coronal/lexion view, midacetabulum Dislocatable hip, coronal/lexion view, posterior lip Normal transverse/lexion view Subluxation, transverse/lexion view Dislocation, transverse/lexion view

56 Pediatric Interventional Sonography Neil Johnson and Allison Aguado Video 56.1 Peripherally inserted central catheter (PICC) line placement

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Video 56.2 Video loops showing debris attached to and obstructing the drainage catheter during diagnostic and therapeutic aspiration of heavily bloodstained abdominal luid with loating debris Video 56.3 Video loops showing debris attached to and obstructing the drainage catheter during diagnostic and therapeutic aspiration of heavily bloodstained abdominal luid with loating debris Video 56.4 Appendiceal abscess with catheter touching fecalith Video 56.5 Gaucher disease patient rib biopsy Video 56.6 Gaucher rib osteomyelitis drain catheter being advanced Video 56.7 Gaucher rib prebiopsy showing pus and displaceable rib Video 56.8 Juvenile rheumatoid arthritis tendon sheath steroid injection

Appendix: Ultrasound Artifacts: A Virtual Chapter Korosh Khalili, Hojun Yu, Alexander Jesurum, and Deborah Levine Video A.1 Propagation velocity artifact Video A.2 Attenuation-related artifacts Video A.3 Shadowing Video A.4 Showing in region of cauda equina Video A.5 Increased through transmission Video A.6 Path of sound assumption Video A.7 Mirror image artifact Video A.8 Comet-tail artifact Video A.9 Comet-tail artifact in adenomyomatosis Video A.10 Refraction from the anterior abdominal wall Video A.11 Anisotropy Video A.12 Anisotropy at supraspinatus tendon insertion Video A.13 Reverberation artifact from free intraperitoneal gas Video A.14 Ring-down artifact Video A.15 Ring-down artifact from air in bile ducts Video A.16 Dirty shadowing Video A.17 Side lobe artifact Video A.18 Partial volume averaging explanation Video A.19 Tissue vibration artifact Video A.20 Tissue vibration artifact from left renal artery stenosis with color bruit and aliasing Video A.21 Aliasing seen in common femoral artery to common femoral vein arteriovenous istula Video A.22 Twinkle explanation Video A.23 Twinkle

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DIAGNOSTIC ULTRASOUND

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PART FOUR: Obstetric and Fetal Sonography CHAPTER

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Overview of Obstetric Imaging Deborah Levine

SUMMARY OF KEY POINTS • Ultrasound allows for accurate prediction of gestational age. • The appropriate training and skills are necessary for safely performing and accurately interpreting obstetric ultrasound • There are many options for screening pregnant women, most of which include ultrasound.

• Routine obstetric ultrasound has speciic recommended views that allow for depiction of many, but not all, fetal anomalies. • Three-dimensional ultrasound, fetal Doppler examinations, and fetal magnetic resonance imaging may be used when additional information is needed beyond that available with routine gray-scale ultrasound.

CHAPTER OUTLINE TRAINING, PERSONNEL, AND EQUIPMENT ULTRASOUND GUIDELINES First Trimester Second and Third Trimesters ROUTINE ULTRASOUND SCREENING

T

Estimation of Gestational Age Identiication of Twin/Multiple Pregnancies Screening and Perinatal Outcomes Fetal Malformations: Diagnostic Accuracy

here were more than 3.9 million live births in the United States in 2013.1 Ultrasound is the most frequently used imaging modality for assessment of pregnancy. With care being taken to keep exposure to ultrasound limited to medically needed information, and with imaging performed at the appropriate power settings, ultrasound is safe for use in pregnancy. Indications for ultrasound during the irst trimester include pregnancy dating, assessment of women with bleeding or pain, and assessment of nuchal translucency in screening for aneuploidy. In the second trimester, ultrasound is used for pregnancy dating, assessment of interval growth, assessment of patients with abnormal pain or bleeding, assessment of size-to-dates discrepancy, routine survey of fetal anatomy, and assessment of maternal complications due to conditions such as age, drug use, or history of previous abnormalities. In cases of multiple gestations, ultrasound is used to assess growth and complications of twinning. In women with history of cervical incompetence, ultrasound is used to screen for cervical changes that put a patient at risk for preterm delivery. In the third trimester, ultrasound is predominantly used to assess fetal growth and well-being. Ultrasound is increasingly used for fetal procedures such as testing for aneuploidy, drainage of abnormal fetal luid collections, and guidance for fetal surgery. Ultrasound is well recognized as the screening modality of choice, but

Three-Dimensional Ultrasound Prudent Use of Ultrasound MAGNETIC RESONANCE IMAGING CONCLUSION

additional information may be needed beyond that available with ultrasound. In many of these cases, especially those with fetal central nervous system abnormalities, fetal magnetic resonance imaging (MRI) can help clarify the diagnosis. Part IV of this textbook focuses on obstetric ultrasound and reviews speciic fetal organ system anatomy and pathology, with chapters also on safety of ultrasound in pregnancy, assessment of twins, and growth. Fetal magnetic resonance (MR) and threedimensional (3D) ultrasound images are added throughout to illustrate the beneit of these techniques in select cases.

TRAINING, PERSONNEL, AND EQUIPMENT Obstetric ultrasound diagnosis is critically dependent on examiner training and experience.2,3 Physicians and sonographers performing obstetric ultrasound examinations should have completed appropriate training and should be appropriately credentialed and/or boarded. Accreditation of ultrasound laboratories improves compliance with published minimum standards and guidelines.4 Ultrasound practitioners should be knowledgeable regarding the basic physical principles of ultrasound, equipment, record-keeping requirements, indications, and safety of using ultrasound in pregnancy. Studies should be conducted with real-time scanners

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Indications for First-Trimester Ultrasound Conirmation of the presence of an intrauterine pregnancy Suspected ectopic pregnancy Vaginal bleeding Pelvic pain Estimation of gestational age Diagnosis or evaluation of multiple gestations Conirmation of cardiac activity Adjunct to chorionic villus sampling, embryo transfer, and localization, and removal of an intrauterine device Assessment for certain fetal anomalies, such as anencephaly, in high-risk patients Measurement of nuchal translucency when part of a screening program for fetal aneuploidy Suspected ectopic pregnancy Suspected hydatidiform mole Maternal pelvic masses and/or uterine abnormalities Modiied from Collaborative Subcommittee. ACR–ACOG–AIUM–SRU practice parameter for the performance of obstetrical ultrasound. American College of Radiology; 2014.5

using a transabdominal and/or transvaginal approach, depending on the gestational age and the region of interest. he choice of transducer frequency is a trade-of between beam penetration and resolution. In general, a 3- to 5-MHz transducer frequency provides suicient resolution with adequate depth penetration in all but the extremely obese patient. During early pregnancy, a 4- to 7-MHz abdominal transducer or a 5- to 10-MHz vaginal transducer can provide superior resolution while still allowing adequate penetration. Higher-frequency transducers are most useful in achieving high-resolution scans of anatomy close to the probe, and lower-frequency transducers are useful when increased penetration of the sound beam is necessary and when a wider ield of view is needed. Use of Doppler ultrasound and 3D imaging depends on the speciic indication. As in all imaging studies, complete documentation of the images and a formal written interpretation are essential for quality assurance, accreditation, and medicolegal issues.

Indications for Second- and Third-Trimester Ultrasound Estimation of gestational (menstrual) age Evaluation of fetal growth Evaluation of fetal anatomy and fetal well-being Vaginal bleeding Abdominal or pelvic pain Cervical insuficiency Determination of fetal presentation Suspected multiple gestation Adjunct to amniocentesis or other procedure Evaluation of discrepancy between uterine size (as measured by fundal height) and clinical dates Pelvic mass Suspected hydatidiform mole Adjunct to cervical cerclage placement Suspected ectopic pregnancy Suspected fetal death Suspected uterine abnormality Suspected amniotic luid abnormalities Suspected placental abruption Adjunct to external cephalic version Premature rupture of membranes and/or premature labor Previous abnormal screening exams Follow-up evaluation of placental location for suspected placenta previa or accreta Previous congenital anomaly Screening for or follow-up of fetal anomalies Modiied from Collaborative Subcommittee. ACR–ACOG–AIUM–SRU practice parameter for the performance of obstetrical ultrasound. American College of Radiology; 2014.5

dating can be performed with measurement of the biparietal diameter and head circumference rather than crown-rump length. Videos 28.1 and 28.2 show normal irst-trimester indings of an early embryo with cardiac activity (Video 28.1) and normal indings of rhombencephalon (Video 28.2). In the irst trimester it is important to not only establish the location of the pregnancy (intrauterine versus extrauteruine) but when intrauterine, to carefully determine if it is a potentially viable pregnancy or if it is a nonviable pregnancy.6-9 Due to the

ULTRASOUND GUIDELINES First Trimester he current guidelines of the American College of Radiology (ACR) and American Institute of Ultrasound in Medicine (AIUM) for the performance of irst-trimester obstetric ultrasound examination include documentation of the location of the pregnancy (intrauterine vs. extrauterine), documentation of the appearance of the maternal uterus and ovaries (Fig. 28.1), and assessment of gestational age, either by measurement of mean sac diameter (before visualization of embryonic pole; Fig. 28.2) or by embryonic/fetal pole crown-rump length5 (Fig. 28.3). Another important structure to assess is the yolk sac. An image of the heart rate is taken using M-mode ultrasound. It is important to use M-mode rather than spectral Doppler ultrasound on the embryo to limit power deposition. Late in the irst trimester,

General Survey Guidelines for First-Trimester Ultrasound Gestational sac Location of pregnancy: intrauterine vs. extrauterine Gestational age (as appropriate) Mean sac diameter Embryonic pole length or crown rump length Yolk sac Cardiac activity on M-mode ultrasound Embryo/fetal number (amnionicity/chorionicity) Maternal anatomy: uterus and adnexa Modiied from Collaborative Subcommittee. ACR–ACOG–AIUM–SRU practice parameter for the performance of obstetrical ultrasound. American College of Radiology; 2014.5

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FIG. 28.1 Normal First-Trimester Ultrasound Images: Pregnancy Location and Adnexa. (A) Transabdominal sagittal sonogram shows an intrauterine gestational sac. (B) Transverse image to the left of uterus shows normal appearance for the ovary (arrow). (C) Transvaginal color Doppler image shows normal hypervascular rim around corpus luteum.

FIG. 28.2 Normal First-Trimester Measurement of Sac Diameter. Transvaginal sagittal image shows sagittal measurement of sac diameter (calipers). Measurements in three orthogonal planes are averaged to calculate the mean sac diameter. Note yolk sac within the gestational sac.

variety of medical professionals performing and interpreting ultrasound in a variety of clinical settings, thresholds for the diagnosis of a failed pregnancy have been increased in order to not misdiagnose a potentially viable pregnancy. hese issues are discussed in detail in Chapter 30. In cases of multiple gestation, irst-trimester scans should document the fetal number as well as the amnionicity and chorionicity (Fig. 28.4). Chapter 32 discusses the assessment of multifetal pregnancies. In addition, the American College of Obstetricians and Gynecologists (ACOG) recommends that prenatal testing for aneuploidy be ofered to all pregnant women.10 Clinicians must understand current screening options (and the tradeofs between them), including traditional serum analysis (with or without nuchal translucency ultrasonography) or cell-free DNA so that they can discuss these options appropriately with the patient. Cell-free DNA testing uses DNA from the placenta to assess the risk of the fetus having a chromosomal abnormality; it does not assess risk for fetal anomalies such as neural tube defects or ventral wall defects. Management decisions, including termination of the pregnancy, should not be based on the results of the cell-free

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D

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FIG. 28.3 First-Trimester Ultrasound Images: Embryo and Fetus. (A) Normal embryo at 6.5 weeks’ gestation. Note embryonic pole (calipers) adjacent to yolk sac. (B) Normal embryo at 8 weeks’ gestation. Note embryo (calipers) and adjacent yolk sac (arrow). (C) M-mode ultrasound from same embryo as in B. Note normal heart rate of 160 beats/min. (D) Normal embryo at 9 weeks’ gestational age. Note embryo within amnion (arrow) and umbilical cord (arrowhead). (E) Just lateral to image in D, note yolk sac (arrowhead) is located outside the amnion (arrow). (F) Sagittal ultrasound at 10.5 weeks’ gestation. (G) Sagittal ultrasound at 11.5 weeks’ gestation. (H) Coronal view of face at 13 weeks’ gestation. (I) Sagittal ultrasound of nuchal translucency (calipers) at 13 weeks’ gestation. See also Videos 28.1 and 28.2.

DNA screening alone.10 Patients should be counseled that a negative cell-free DNA test result does not ensure an unafected pregnancy. According to a 2015 ACOG committee opinion, “Given the performance of conventional screening methods, the limitations of cell-free DNA screening performance, and the limited data on cost-efectiveness in the low-risk obstetric population, conventional screening methods remain the most appropriate choice for irst-line screening for most women in the general obstetric population.”10 hus despite increased use of cell-free DNA testing, ultrasound screening is still being performed by measuring nuchal translucency between 11 and 14 weeks of gestation (see Fig. 28.3I). his measurement, in conjunction with maternal age

and serology, can be used to determine an individualized risk of fetal aneuploidy (see Chapter 31). Increased use of maternal serum screening, as well as irst- and second-trimester ultrasound have reduced the number of interventional procedures to detect aneuploidy while increasing the number of prenatal diagnoses of aneuploidy.11 Given the increased scanning late in the irst trimester, it is also increasingly common for a limited anatomic survey to be conducted in the late irst trimester. Anomalies that should be detected this early include anencephaly (Fig. 28.5) and omphalocele (Fig. 28.6). Although substantial information can be obtained at this time, the irsttrimester anatomic survey is unlikely to replace the secondtrimester anatomic survey, since many structures are diicult

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FIG. 28.4 Multiple Gestations. The entire gestational sac should be examined to identify multiple gestations. (A) Transabdominal image of diamniotic dichorionic twins. Note the thick, dividing membrane that separates twin A (A), the presenting twin, from twin B (B). (B) Transvaginal image of diamniotic monochorionic twins at 8 weeks’ gestational age (calipers denote crown rump length [CRL]) with two thin membranes (arrows, amnion) still close to embryonic poles.

A

B

FIG. 28.5 Anencephaly. (A) Sagittal ultrasound at 10 weeks’ gestation. (B) Sagittal ultrasound in a different fetus at 12 weeks’ gestation. Note the orbits (arrow) with absent ossiied cranium above this level with angiomatous stroma. The calipers mark the estimate of the crown rump length, made dificult due to angiomatous stroma above the orbits.

to visualize completely early in the second trimester, particularly the heart, cardiac outlow tracts, posterior fossa, and distal spine.

Second and Third Trimesters he current ACR/AIUM guidelines for the performance of the second- and third-trimester obstetric ultrasound examinations

describe the standard sonographic examination.5 It is important to understand that the guidelines were written to maximize detection of many fetal abnormalities but are not expected to allow for detection of all structural abnormalities. he terminology level I and level II examinations refer to “standard” or “routine” (level I) and “high risk,” “specialized,” or “detailed” (level II) obstetric ultrasound. he concept of these

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FIG. 28.6 Omphalocele at 11 Weeks’ Gestational Age. Sagittal view of fetus (calipers) shows a large, abdominal wall defect (arrow).

two levels of scanning is that the standard, basic, routine, or level I examination is performed routinely on pregnant patients (Figs. 28.7 to 28.15, Videos 28.3) to 28.9. he methods to obtain all the required images are described in detail in subsequent chapters. his chapter provides a collage of igures as a guide for the anatomic survey and common additional views obtained during a fetal survey. In general, the “standard fetal anatomic survey” refers to the second-trimester scan, typically performed between 16

and 22 weeks of gestation. When anatomic surveys are performed at 20 to 22 weeks’ gestational age, there is less need for repeat scans to document normal anatomy compared to studies performed earlier in pregnancy.12 However, there are practical considerations when determining the optimal timing of studies. In well-dated pregnancies in women who are unlikely to want amniocentesis, a survey at 20 to 22 weeks’ gestation is optimal. However, if a pregnancy is not well-dated, an earlier scan may be needed both to establish accurate dates for the pregnancy and to assess the anatomy. Some centers ofer the scan at 16 weeks’ gestation to coincide with performance of genetic amniocentesis and/or midtrimester quadruple serum screening. he level I examination consists of investigation of the maternal uterus and ovaries, the cervix, and placenta (Fig. 28.7, Video 28.3), as well as a systematic review of fetal anatomy. Adnexal cysts are common in pregnant women. In early pregnancy a cyst is most likely the corpus luteum. If a cyst appears atypical or enlarges beyond the middle second trimester, it should be further assessed. Leiomyoma position and size should be documented. If the myometrium appears thin in the lower uterine segment (e.g., 1000) populations. Oten, however, these studies describe no anomalies in the study group or in the control population; in a survey of more than 121,000 patients among 68 examiners, combining 292 institute-years of experience, 3000 to 5000 anomalies would be expected as background rate, but none were reported.121 In fact, rigorous epidemiologic studies of the adverse bioefects of ultrasound are scarce. Several biologic end points have been analyzed in the human fetus or neonate to determine whether prenatal exposure to diagnostic ultrasound had observable efects: intrauterine growth restriction and low birth weight,122 delayed speech,123 vision and hearing,124 dyslexia,125 neurologic and mental development or behavioral issues,126,127 malignancies,128 and nonright-handedness.129,130 Most indings have never been duplicated, and the majority of studies have been negative for any association, with the possible exception of low birth weight. here are no epidemiologic studies related to the output display standard (thermal and mechanical indices) and clinical

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outcomes. Only a few clinical studies describe routine scan,131 irst-trimester scan,132 particularly, nuchal translucency screening,133 as well as Doppler132 and three-dimensional (3D)/fourdimensional (4D) ultrasound.134 Furthermore, although some studies address the issue of repeat scans,135,136 it was not as an analysis of potential cumulative efects for which no information is available.

Birth Weight In one oten-quoted study of more than 2000 infants, a small (116 g at term) but statistically signiicant lower mean birth weight was found in the half exposed to ultrasound compared with the nonexposed group.137 However, information was collected several years ater exposure, with no indications known and no exposure information available. Moreover, in a later study, the authors concluded that the relationship of ultrasound exposure to reduced birth weight may be caused by shared common risk factors, which lead to both exposure and a reduction in birth weight,138 an association but not a causal relationship. A twice-greater risk of low birth weight was reported in another retrospective study ater four or more exposures to diagnostic ultrasound.14 hese results were not reproduced in another retrospective study with a large population, originally of 10,000 pregnancies exposed to ultrasound matched with 500 controls and with 6-year follow-up.139 No increased congenital malformations, chromosomal abnormalities, infant neoplasms, speech or hearing impairment, or developmental problems were observed in this latter study. In a randomized controlled trial of more than 2800 pregnant women, about half received ive ultrasound imaging and Doppler low studies at 18, 24, 28, 34, and 38 weeks of gestation, and half received a single ultrasound imaging at 18 weeks.122 An increased risk of intrauterine growth restriction was detected in those exposed to frequent Doppler ultrasound examinations, possibly through efects on bone growth. However, when children were examined at 1 year of age, there were no diferences between the study and control groups. In addition, ater examining their original subjects ater 8 years, the investigators found no evidence of adverse neurologic outcome.136 Similarly, other randomized studies found no harmful efect of one or two prenatal scans on growth.140,141 Curiously, in some studies, birth weight was slightly higher in the scanned group, but not signiicantly, except in one group of newborns exposed to ultrasound in utero who weighed on average 42 g (75 g in reported smokers) more than the control group.141 hus ultrasound exposure in utero does not appear to be associated with reduced birth weight, although Doppler ultrasound exposure may have some risks.114 Delayed Speech To determine if an association exists between prenatal ultrasound exposure and delayed speech in children, Campbell et al.123 studied 72 children with delayed speech and found a higher rate of ultrasound exposure in utero compared with the 144 control subjects. However, this retrospective study used records more than 5 years old, with neither a dose-response efect nor any relationship to time of exposure. A much larger study of more than 1100 children exposed in utero and 1000 controls found

no signiicant diferences in delayed speech, limited vocabulary, or stuttering.142

Dyslexia Dyslexia has been extensively studied. Stark et al.125 compared more than 4000 children (ages 7-12 years) exposed to ultrasound in utero to matched controls, analyzing outcome measures at birth (Apgar scores, gestational age, head circumference, birth weight, length, congenital abnormalities, neonatal/congenital infection) or in early infancy (hearing, visual acuity/color vision, cognitive function, behavior). No signiicant diferences were found, except for a signiicantly greater proportion of dyslexia in children exposed to ultrasound. Given the design of the study and the presence of several possible confounding factors, the authors indicated that dyslexia could be incidental. Subsequently, long-term follow-up studies of more than 600 children with various tests for dyslexia (e.g., spelling, reading) were performed.143-147 End points included evaluation for dyslexia along with examination of nonright-handedness, said to be associated with dyslexia. No statistically signiicant diferences were found between ultrasound-exposed children and controls for reading, spelling, arithmetic, or overall performance, as reported by teachers. Speciic dyslexia tests showed similar incidence rates among scanned children and controls in reading, spelling, and intelligence scores and no discrepancy between intelligence and reading or spelling. herefore the original inding of dyslexia was not conirmed in subsequent randomized controlled trials. It is considered unlikely that routine ultrasound screening can cause dyslexia. Nonright-Handedness A possible link between prenatal exposure to ultrasound and subsequent nonright-handedness at age 8 to 9 years in children exposed to ultrasound in utero was irst reported in 1993 from Norway.146 According to the authors, however, the diference was “only barely signiicant at the 5% level” and was restricted to boys.148 A second group of researchers (including Salvesen, main author of the irst study), studying a new population of more than 3000 children from Sweden, reported similar indings of a statistically signiicant association between ultrasound exposure in utero and nonright-handedness in males.129 An intriguing recent study showed that fetuses self-touched their faces more oten with the let hand than the right, as observed by ultrasound, in correlation to stress levels of the mother.149 Furthermore, laterality is, mostly, genetically determined150 but could, naturally, be modiied by external factors. Evidence is insuicient to infer a direct efect on brain structure or function, or even that nonright-handedness is an adverse efect. Neurologic Development and Behavioral Issues Neurons of the cerebral neocortex in mammals, including humans, are generated during fetal life in the brain proliferative zones and then migrate to their inal destination by following an inside-to-outside sequence. his neuronal migration occurs in the human fetal brain mainly from 6 to 11 weeks of gestation151 but continues until 32 weeks. It has long been theorized that

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external factors such as ultrasound could afect this process.152 In another study, only 2 of 123 variables were found to be disturbed at birth, but not at 1 year of age, in children exposed in utero; these variables are grasp relex and tonic neck relex.153 he signiicance was not elaborated, and some doubts exist regarding statistical validity. Stark et al.125 reported that vision and intelligence scores were identical among 425 exposed infants and 381 controls. A large report found no association between routine exposure to prenatal ultrasound and school performance (deicits in attention, motor control, perception, vision, and hearing).154 In more than 4900 children age 15 to 16 years, no diferences were found in school performance between exposed and nonexposed children, except for a lower score for exposed boys in physical education.155 Behavioral changes may be a more sensitive marker of subtle brain damage than obvious structural alterations.156 Such changes have been described in animals,84,105 although oten transient.97 An interesting study in mice was recently published.157 As detailed earlier, there may be male preponderance of nonright-handedness ater in utero ultrasound exposure. Furthermore, an increased prevalence of autism exists in males and there are reports of excess nonright-handedness in this population. Pregnant mice were exposed to 30 minutes of diagnostic ultrasound at embryonic day 14.5. Social behavior of their male pups was analyzed 3 weeks ater birth. Ultrasound-exposed pups were signiicantly (P < .01) less interested in social interaction than sham-exposed pups and demonstrated signiicantly (P < .05) more activity relative to the sham-exposed pups (only in the presence of an unfamiliar mouse). hese results suggest that social behavior in young mice was altered by in utero exposure to diagnostic ultrasound. he authors’ conclusions are that this may be relevant for autism but that major diferences between the exposure of diagnostic ultrasound of mice and humans preclude conclusions regarding human exposure and require further studies. Indeed, no such changes have been reported in humans. In particular, schizophrenia and other psychoses have not been found to be associated with prenatal ultrasound exposure.158 he question has been raised about the increased rate of autism observed over the past few years and its relation to the greatly increased use of ultrasound in obstetrics. Although a major upsurge in both have occurred, there is no cause and efect demonstrable between the two.159

Congenital Malformations In humans, prenatal ultrasound has not been shown to result in an increased incidence of congenital anomalies, as found in animals. Childhood Malignancies No association has been found between ultrasound exposure in utero and the later development of leukemia160,161 or solid tumors in children.128,162-166 Again, although some of these studies were published in 2007 or 2008, the populations studied were exposed to ultrasound in utero 20 to 30 years ago, that is, with instruments generating lower outputs and with minimal or no information available on exposure conditions.

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IS DOPPLER DIFFERENT? Spectral (pulsed) Doppler uses high pulse repetition frequencies, generating greater temporal average intensities and powers than B- or M-mode, and hence greater heating potential (see “hermal Efects”).75 Adequate diagnostic information may be obtained with low output levels (as documented by values of the TI), as demonstrated in Fig. 29.1. his has been reported in the literature, speciically for Doppler, the mode with the highest output, both in early and later pregnancy.167,168 In fact, under pressure from bioefects and safety committees of various professional organizations (American Institute of Ultrasound in Medicine [AIUM], European Federation of Societies of Ultrasound in Medicine and Biology [EFSUMB], International Society for Ultrasound in Obstetrics and Gynecology [ISUOG], and World Federation for Ultrasound in Medicine and Biology [WFUMB]), several manufacturers have changed their default settings, speciically for pulsed Doppler in fetal mode, from very high (as it was originally, presumably in an attempt to obtain better images) to very low, with the end user capable of raising the output, if desired. Because acoustic output is high in Doppler, special precaution is recommended, particularly in early gestation.169

SAFETY GUIDELINES It is diicult to issue precise safety recommendations because of the multitude of ultrasound instruments, each with a selection of transducers and used in a variety of applications. Patient characteristics further complicate the task.170 Safety guidelines are very important, however, given the very low level of knowledge about bioefects and safety of ultrasound among clinical end users. In a questionnaire distributed to ultrasound active end users (of which 82% were obstetricians), only 17.7% gave the correct answer of the deinition of the TI. Approximately 96% did not know the proper deinition for MI. Almost 80% of respondents did not know the correct answer to the multiple choice question of where to ind the acoustic indices; answer options were the machine documentation, a textbook, a complicated calculation or in real time on the ultrasound monitor (the correct answer).171 Similar results were recorded in surveys abroad, performed in Europe, Asia, or the Middle East,172-174 indicating that clinical end users worldwide show poor knowledge regarding safety issues of ultrasound during pregnancy.30 More recently, knowledge among residents in obstetrics and gynecology was also found to be grossly lacking.175 Similar results were obtained in a survey of sonographers, and years of experience made no diference.176 In another study, compliance with the ALARA (as low as reasonably achievable) principle by practitioners seeking credentialing for nuchal translucency (NT) measurement between 11 and 14 weeks’ gestation was evaluated. Only 5% of the providers used the correct TI type (TIB) at lower than 0.5 for all submitted images, 6% at lower than 0.7, and 12% at 1.0 or lower. A TI (TIB or TIS) higher than 1.0 was used by almost 20% of the providers. Proiciency in NT measurement and educational background (physician or sonographer) did not inluence compliance with ALARA. he authors concluded that clinicians seeking

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credentialing in NT do not demonstrate compliance with the recommended use of the TI in monitoring acoustic output.177 An easy way to reduce exposure is to reduce the TI and MI, using the appropriate controls, and/or reduce the dwell time. he 1999 statement of the British Medical Ultrasound Society, reconirmed in 2009, declares178: For equipment for which the safety indices are displayed over their full range of values, the TI should always be less than 0.5 and the MI should always be less than 0.3. When the safety indices are not displayed, Tmax should be less than 1°C and MImax should be less than 0.3. Frequent exposure of the same subject is to be avoided. he British Medical Ultrasound Society has strict recommendations for maximum allowed exposure time (Tmax), depending on the TI (Table 29.1). Miller and Ziskin57 demonstrated a logarithmic relationship between exposure duration and temperature elevation in producing harmful bioefects in animal fetuses. For temperatures below 43°C, the exposure time necessary for every 1°C increase in temperature was decreased by a factor of 4. Using a maximum “safe” exposure time of 4 minutes for a temperature elevation of 4°C, based on these calculations, the following maximal exposure times are allowable with no apparent obvious risks: 128 minutes at 1°C, 64 at 2°C, 16 at 3°C, and only 4 minutes at 4°C. Precautions are, naturally, of particular importance in early gestation179,180 and for Doppler exposure.181 General recommendations from major professional organizations follow. It is strongly recommended to consult various safety statements published on these organizations’ websites.182-192 1. A diagnostic ultrasound exposure that produces a maximum in situ temperature rise of no more than 1.5°C above normal physiologic levels (37°C) may be used clinically without reservation on thermal grounds.193 2. A diagnostic ultrasound exposure that elevates embryonic and fetal in situ temperature above 41°C (4°C above normal temperature) for 5 minutes or more should be considered potentially hazardous.193,194 In this regard, maternal temperature elevation (e.g., from viral disease) should be considered because body temperature of the fetus will also be increased above normal.48

TABLE 29.1 Duration of Obstetric Ultrasound as a Function of Thermal Index Thermal Index (TI) 0.7 1 1.5 2 2.5

Recommended Upper Limit 60 30 15 4 1

min min min min min

Modiied from British Medical Ultrasound Society (BMUS) Safety Group. Guidelines for the safe use of diagnostic ultrasound equipment. Ultrasound. 2010;18:52-59.178

3. he risk of adverse efects is increased with the duration of exposure (dwell time).195 4. Based on available information, there is no reason to withhold scanning in B-mode for medical indications. he risk of thermal damage secondary to heating appears to be negligible.193 5. M-mode ultrasound appears to be safe and not to cause thermal damage (Fig. 29.5).48 6. Spectral Doppler ultrasound may produce high intensities, and routine Doppler examination during the embryonic period is rarely indicated.196 7. hree-dimensional (3D) and four-dimensional (4D) ultrasound are based on two-dimensional (2D) B-mode imaging with multiple 2D planes obtained and assembled (reconstructed) into a volume. Hence the exposure is really to B-mode and is, most likely, safe. Time of exposure has to be watched to avoid long episodes of scanning to obtain the “ideal” 3D volume (Fig. 29.6). 8. Education of ultrasound operators is crucial; the responsibility for the safe use of ultrasound devices is shared between the users and the manufacturers, who should ensure the accuracy of the output display.196 9. he AIUM advocates the responsible use of diagnostic ultrasound and strongly discourages the nonmedical use of ultrasound for “entertainment” purposes. he use of ultrasound without a medical indication to view the fetus, obtain a picture of the fetus, or determine the fetal gender is inappropriate and contrary to responsible medical practice. Ultrasound should be used by qualiied health professionals to provide medical beneit to the patient.28 10. Examinations should be kept as short as possible and with as low MI and TI outputs as possible, but without sacriicing diagnostic accuracy. Follow the as low as reasonably achievable (ALARA) principle.197

CONCLUSION Diagnostic ultrasound has been used in medicine in general and obstetrics and gynecology in particular for more than half a century. No conirmed biologic efects have been described in patients as a result of exposure to diagnostic ultrasound. Such efects, however, have been described in animals, oten at exposure levels higher than, but also occasionally equivalent to, those used in clinical practice. Epidemiologic information available is from studies performed on instruments with acoustic output much lower than current machines. Oten, exposure data are insuicient and number of subjects too small. Furthermore, “no reported efects” does not mean “no efects,” and such biologic efects may be identiied in the future. Prudent use of ultrasound in fetal scanning, following the ALARA principle, is therefore recommended. Based on known mechanisms, there is no contraindication to the use of B-mode, M-mode, 3D/4D, and color Doppler ultrasound, when clinically indicated. However, special precaution is necessary when applying pulsed Doppler ultrasound, particularly in the irst trimester.

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FIG. 29.5 M-Mode Tracing, Obtained With Low TI (0.3) and MI (0.8).

FIG. 29.6 Multiplanar Images and Three-Dimensional Reconstructed Volume With Low TI (0.1) and MI (0.9).

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69. Makikallio K, Tekay A, Jouppila P. Uteroplacental hemodynamics during early human pregnancy: a longitudinal study. Gynecol Obstet Invest. 2004;58(1):49-54. 70. Wloch A, Rozmus-Warcholinska W, Czuba B, et al. Doppler study of the embryonic heart in normal pregnant women. J Matern Fetal Neonatal Med. 2007;20(7):533-539. 71. Russell NE, McAulife FM. First-trimester fetal cardiac function. J Ultrasound Med. 2008;27(3):379-383. 72. Duck FA. Is it safe to use diagnostic ultrasound during the irst trimester? Ultrasound Obstet Gynecol. 1999;13(6):385-388. 73. Smythe GE, MacRae DJ. Letter: doppler ultrasound and fetal hazard. Lancet. 1975;2(7925):134. 74. Calvert J, Duck F, Clit S, Azaime H. Surface heating by transvaginal transducers. Ultrasound Obstet Gynecol. 2007;29(4):427-432. 75. Ziskin MC. Intrauterine efects of ultrasound: human epidemiology. Teratology. 1999;59(4):252-260. 76. O’Brien WD, Siddiqi TA. Obstetric sonography: the output display standard and ultrasound bioefects. In: Fleischer AC, Manning FA, Jeanty P, Romero R, editors. Sonography in obstetrics and gynecology: principles and practice. 6th ed. New York: McGraw-Hill; 2001. p. 29-48. 77. Bly SH, Vlahovich S, Mabee PR, Hussey RG. Computed estimates of maximum temperature elevations in fetal tissues during transabdominal pulsed Doppler examinations. Ultrasound Med Biol. 1992;18(4):389397. 78. Carstensen EL, Gates AH. he efects of pulsed ultrasound on the fetus. J Ultrasound Med. 1984;3(4):145-147. 79. Dalecki D, Raeman CH, Child SZ, et al. Hemolysis in vivo from exposure to pulsed ultrasound. Ultrasound Med Biol. 1997;23(2):307-313. 80. Abramowicz JS. Ultrasonographic contrast media: has the time come in obstetrics and gynecology? J Ultrasound Med. 2005;24(4):517-531. 81. Miller MW, Brayman AA, Sherman TA, et al. Comparative sensitivity of human fetal and adult erythrocytes to hemolysis by pulsed 1 MHz ultrasound. Ultrasound Med Biol. 2001;27(3):419-425. 82. Fatemi M, Ogburn Jr PL, Greenleaf JF. Fetal stimulation by pulsed diagnostic ultrasound. J Ultrasound Med. 2001;20(8):883-889. 83. Duck FA. Acoustic streaming and radiation pressure in diagnostic applications: what are the implications? In: Barnett SB, Kossof G, editors. Safety of diagnostic ultrasound. New York: Parthenon; 1998. p. 8798. 84. Jensh RP, Brent RL. Intrauterine efects of ultrasound: animal studies. Teratology. 1999;59(4):240-251. 85. Harvey EN, Loomis AL. High-frequency sound waves of small intensity and their biological efects. Nature. 1928;121:622-624. 86. Sikov MR. Efect of ultrasound on development. Part 1: introduction and studies in inframammalian species. Report of the Bioefects Committee of the American Institute of Ultrasound in Medicine. J Ultrasound Med. 1986;5(10):577-583. 87. Sikov MR. Efect of ultrasound on development. Part 2: studies in mammalian species and overview. J Ultrasound Med. 1986;5(11):651-661. 88. Fry FJ, Kossof G, Eggleton RC, Dunn F. hreshold ultrasonic dosages for structural changes in the mammalian brain. J Acoust Soc Am. 1970;48(6):Suppl 2:1413. 89. Frizzell LA, Carstensen EL, Davis JD. Ultrasonic absorption in liver tissue. J Acoust Soc Am. 1979;65(5):1309-1312. 90. Frizzell LA, Lee CS, Aschenbach PD, et al. Involvement of ultrasonically induced cavitation in the production of hind limb paralysis of the mouse neonate. J Acoust Soc Am. 1983;74(3):1062-1065. 91. Borrelli MJ, Frizzell LA, Dunn F. Ultrasonically induced morphological changes in the mammalian neonatal spinal cord. Ultrasound Med Biol. 1986;12(4):285-295. 92. Frizzell LA, Linke CA, Carstensen EL, Fridd CW. hresholds for focal ultrasonic lesions in rabbit kidney, liver, and testicle. IEEE Trans Biomed Eng. 1977;24(4):393-396. 93. Carnes KI, Hess RA, Dunn F. he efect of ultrasound exposure in utero on the development of the fetal mouse testis: adult consequences. Ultrasound Med Biol. 1995;21(9):1247-1257. 94. Hynynen K. he threshold for thermally signiicant cavitation in dog’s thigh muscle in vivo. Ultrasound Med Biol. 1991;17(2):157-169.

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95. Dalecki D, Raeman CH, Child SZ, Carstensen EL. Intestinal hemorrhage from exposure to pulsed ultrasound. Ultrasound Med Biol. 1995;21(8): 1067-1072. 96. Dalecki D, Child SZ, Raeman CH, et al. Ultrasonically induced lung hemorrhage in young swine. Ultrasound Med Biol. 1997;23(5):777-781. 97. Tarantal AF, Hendrickx AG. Evaluation of the bioefects of prenatal ultrasound exposure in the cynomolgus macaque (Macaca fascicularis): II. Growth and behavior during the irst year. Teratology. 1989;39(2):149-162. 98. Hande MP, Devi PU. Efect of in utero exposure to diagnostic ultrasound on the postnatal survival and growth of mouse. Teratology. 1993; 48(5):405-411. 99. O’Brien WD. Dose-dependent efects of ultrasound on fetal weight in mice. J Ultrasound Med. 1983;2:1-8. 100. Vorhees CV, Acuf-Smith KD, Schilling MA, et al. Behavioral teratologic efects of prenatal exposure to continuous-wave ultrasound in unanesthetized rats. Teratology. 1994;50(3):238-249. 101. O’Brien Jr WD, Januzik SJ, Dunn F. Ultrasound biologic efects: a suggestion of strain speciicity. J Ultrasound Med. 1982;1(9):367-370. 102. Hande MP, Devi PU. Efect of prenatal exposure to diagnostic ultrasound on the development of mice. Radiat Res. 1992;130(1):125-128. 103. Rao S, Ovchinnikov N, McRae A. Gestational stage sensitivity to ultrasound efect on postnatal growth and development of mice. Birth Defects Res A Clin Mol Teratol. 2006;76(8):602-608. 104. Borrelli MJ, Bailey KI, Dunn F. Early ultrasonic efects upon mammalian CNS structures (chemical synapses). J Acoust Soc Am. 1981;69(5):1514-1516. 105. Norton S, Kimler BF, Cytacki EP, Rosenthal SJ. Prenatal and postnatal consequences in the brain and behavior of rats exposed to ultrasound in utero. J Ultrasound Med. 1991;10(2):69-75. 106. Devi PU, Suresh R, Hande MP. Efect of fetal exposure to ultrasound on the behavior of the adult mouse. Radiat Res. 1995;141(3):314-317. 107. Hande MP, Devi PU, Karanth KS. Efect of prenatal ultrasound exposure on adult behavior in mice. Neurotoxicol Teratol. 1993;15(6):433-438. 108. Schneider-Kolsky ME, Ayobi Z, Lombardo P, et al. Ultrasound exposure of the foetal chick brain: efects on learning and memory. Int J Dev Neurosci. 2009;27(7):677-683. 109. Milunsky A, Ulcickas M, Rothman KJ, et al. Maternal heat exposure and neural tube defects. JAMA. 1992;268(7):882-885. 110. Ang Jr ES, Gluncic V, Duque A, et al. Prenatal exposure to ultrasound waves impacts neuronal migration in mice. Proc Natl Acad Sci USA. 2006;103(34):12903-12910. 111. Abramowicz JS. Prenatal exposure to ultrasound waves: is there a risk? Ultrasound Obstet Gynecol. 2007;29(4):363-367. 112. Kieler H. Epidemiological studies on adverse efects of prenatal ultrasound— which are the challenges? Prog Biophys Mol Biol. 2007;93(1-3):301-308. 113. Newman PG. Studies of ultrasound safety in humans: clinical beneit vs. risk. In: Barnett SB, Kossof G, editors. Safety of diagnostic ultrasound. New York: Parthenon; 1998. 114. Salvesen KA. Epidemiological prenatal ultrasound studies. Prog Biophys Mol Biol. 2007;93(1-3):295-300. 115. Ziskin MC, Petitti DB. Epidemiology of human exposure to ultrasound: a critical review. Ultrasound Med Biol. 1988;14(2):91-96. 116. Edmonds PD, Abramowicz JS, Carson PL, et al. Guidelines for Journal of Ultrasound in Medicine authors and reviewers on measurement and reporting of acoustic output and exposure. J Ultrasound Med. 2005;24:1171-1179. 117. Carvalho JS. Fetal heart scanning in the irst trimester. Prenat Diagn. 2004;24(13):1060-1067. 118. Makikallio K, Jouppila P, Rasanen J. Human fetal cardiac function during the irst trimester of pregnancy. Heart. 2005;91(3):334-338. 119. Becker R, Wegner RD. Detailed screening for fetal anomalies and cardiac defects at the 11-13-week scan. Ultrasound Obstet Gynecol. 2006;27(6):613-618. 120. Vinals F, Ascenzo R, Naveas R, et al. Fetal echocardiography at 11 + 0 to 13 + 6 weeks using four-dimensional spatiotemporal image correlation telemedicine via an Internet link: a pilot study. Ultrasound Obstet Gynecol. 2008;31(6):633-638. 121. Ziskin MC. Survey of patients exposed to diagnostic ultrasound. In: Reid JM, Sikov MR, editors. Interactions of ultrasound and biological tissues.

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PART IV

Obstetric and Fetal Sonography

Proceedings of a workshop, Battelle Seattle Research Center, Seattle, 1971. Rockville, Md: Bureau of Radiological Health, U.S. Department of Health, Education and Welfare; 1973. pp. 203-206. Newnham JP, Evans SF, Michael CA, et al. Efects of frequent ultrasound during pregnancy: a randomised controlled trial. Lancet. 1993;342(8876): 887-891. Campbell JD, Elford RW, Brant RF. Case-control study of prenatal ultrasonography exposure in children with delayed speech. CMAJ. 1993;149(10): 1435-1440. Kieler H, Haglund B, Waldenstrom U, Axelsson O. Routine ultrasound screening in pregnancy and the children’s subsequent growth, vision and hearing. Br J Obstet Gynaecol. 1997;104(11):1267-1272. Stark CR, Orleans M, Haverkamp AD, Murphy J. Short- and long-term risks ater exposure to diagnostic ultrasound in utero. Obstet Gynecol. 1984;63(2):194-200. Bricker L, Neilson JP, Dowswell T. Routine ultrasound in late pregnancy (ater 24 weeks’ gestation). Cochrane Database Syst Rev. 2008;(4): CD001451. Kieler H, Haglund B, Cnattingius S, et al. Does prenatal sonography afect intellectual performance? Epidemiology. 2005;16(3):304-310. Cartwright RA, McKinney PA, Hopton PA, et al. Ultrasound examinations in pregnancy and childhood cancer. Lancet. 1984;2(8410):999-1000. Kieler H, Axelsson O, Haglund B, et al. Routine ultrasound screening in pregnancy and the children’s subsequent handedness. Early Hum Dev. 1998;50(2):233-245. Salvesen KA. Ultrasound and let-handedness: a sinister association? Ultrasound Obstet Gynecol. 2002;19(3):217-221. Sheiner E, Freeman J, Abramowicz JS. Acoustic output as measured by mechanical and thermal indices during routine obstetric ultrasound examinations. J Ultrasound Med. 2005;24(12):1665-1670. Sheiner E, Shoham-Vardi I, Pombar X, et al. An increased thermal index can be achieved when performing Doppler studies in obstetric sonography. J Ultrasound Med. 2007;26(1):71-76. Sheiner E, Abramowicz JS. Acoustic output as measured by thermal and mechanical indices during fetal nuchal translucency ultrasound examinations. Fetal Diagn her. 2009;25(1):8-10. Sheiner E, Hackmon R, Shoham-Vardi I, et al. A comparison between acoustic output indices in 2D and 3D/4D ultrasound in obstetrics. Ultrasound Obstet Gynecol. 2007;29(3):326-328. Bellieni CV, Buonocore G, Bagnoli F, et al. Is an excessive number of prenatal echographies a risk for fetal growth? Early Hum Dev. 2005;81(8): 689-693. Newnham JP, Doherty DA, Kendall GE, et al. Efects of repeated prenatal ultrasound examinations on childhood outcome up to 8 years of age: follow-up of a randomised controlled trial. Lancet. 2004;364(9450): 2038-2044. Moore Jr RM, Barrick MK, Hamilton TM. Efect of sonic radiation on growth and development. Am J Epidemiol. 1982;116:571. Moore Jr RM, Diamond EL, Cavalieri RL. he relationship of birth weight and intrauterine diagnostic ultrasound exposure. Obstet Gynecol. 1988;71(4): 513-517. Lyons EA, Dyke C, Toms M, Cheang M. In utero exposure to diagnostic ultrasound: a 6-year follow-up. Radiology. 1988;166(3):687-690. Saari-Kemppainen A, Karjalainen O, Ylostalo P, Heinonen OP. Ultrasound screening and perinatal mortality: controlled trial of systematic one-stage screening in pregnancy. he Helsinki Ultrasound Trial. Lancet. 1990; 336(8712):387-391. Waldenstrom U, Axelsson O, Nilsson S, et al. Efects of routine one-stage ultrasound screening in pregnancy: a randomised controlled trial. Lancet. 1988;2(8611):585-588. Salvesen KA, Vatten LJ, Bakketeig LS, Eik-Nes SH. Routine ultrasonography in utero and speech development. Ultrasound Obstet Gynecol. 1994;4(2): 101-103. Bakketeig LS, Eik-Nes SH, Jacobsen G, et al. Randomised controlled trial of ultrasonographic screening in pregnancy. Lancet. 1984;2(8396): 207-211. Eik-Nes SH, Okland O, Aure JC, Ulstein M. Ultrasound screening in pregnancy: a randomised controlled trial. Lancet. 1984;1(8390):1347.

145. Salvesen KA, Bakketeig LS, Eik-nes SH, et al. Routine ultrasonography in utero and school performance at age 8-9 years. Lancet. 1992;339(8785): 85-89. 146. Salvesen KA, Vatten LJ, Eik-Nes SH, et al. Routine ultrasonography in utero and subsequent handedness and neurological development. BMJ. 1993;307(6897):159-164. 147. Salvesen KA, Vatten LJ, Jacobsen G, et al. Routine ultrasonography in utero and subsequent vision and hearing at primary school age. Ultrasound Obstet Gynecol. 1992;2(4):243-244, 245-247. 148. Salvesen KA, Eik-Ness SH, Vatten LJ, et al. Routine ultrasound scanning in pregnancy [authors’ reply]. BMJ. 1993;307:1562. 149. Reissland N, Aydin E, Francis B, Exley K. Laterality of foetal self-touch in relation to maternal stress. Laterality. 2015;20(1):82-94. 150. Hepper PG. he developmental origins of laterality: fetal handedness. Dev Psychobiol. 2013;55(6):588-595. 151. Sidman RL, Rakic P. Neuronal migration, with special reference to developing human brain: a review. Brain Res. 1973;62(1):1-35. 152. Mole R. Possible hazards of imaging and Doppler ultrasound in obstetrics. Birth. 1986;13:Suppl:23-33 suppl. 153. Scheidt PC, Stanley F, Bryla DA. One-year follow-up of infants exposed to ultrasound in utero. Am J Obstet Gynecol. 1978;131(7): 743-748. 154. Salvesen K. Routine ultrasonography in utero and development in childhood. In: Tejani N, editor. Obstetrical events and developmental sequelae. 2nd ed. Boca Raton, Fla: CRC Press; 1994. 155. Stalberg K. Prenatal ultrasound and x-ray-potentially adverse efects on the CNS. Upsalla, Sweden: Upsalla Universitet; 2008. 156. Coyle I, Wayner MJ, Singer G. Behavioral teratogenesis: a critical evaluation. Pharmacol Biochem Behav. 1976;4(2):191-200. 157. McClintic AM, King BH, Webb SJ, Mourad PD. Mice exposed to diagnostic ultrasound in utero are less social and more active in social situations relative to controls. Autism Res. 2014;7(3):295-304. 158. Stalberg K, Haglund B, Axelsson O, et al. Prenatal ultrasound scanning and the risk of schizophrenia and other psychoses. Epidemiology. 2007;18(5):577-582. 159. Abramowicz JS. Ultrasound and autism: association, link, or coincidence? J Ultrasound Med. 2012;31(8):1261-1269. 160. Shu XO, Potter JD, Linet MS, et al. Diagnostic X-rays and ultrasound exposure and risk of childhood acute lymphoblastic leukemia by immunophenotype. Cancer Epidemiol Biomarkers Prev. 2002;11(2):177-185. 161. Naumburg E, Bellocco R, Cnattingius S, et al. Prenatal ultrasound examinations and risk of childhood leukaemia: case-control study. BMJ. 2000;320(7230):282-283. 162. Kinnier Wilson LM, Waterhouse JA. Obstetric ultrasound and childhood malignancies. Lancet. 1984;2(8410):997-999. 163. Bunin GR, Buckley JD, Boesel CP, et al. Risk factors for astrocytic glioma and primitive neuroectodermal tumor of the brain in young children: a report from the Children’s Cancer Group. Cancer Epidemiol Biomarkers Prev. 1994;3(3):197-204. 164. Sorahan T, Lancashire R, Stewart A, Peck I. Pregnancy ultrasound and childhood cancer: a second report from the Oxford Survey of Childhood Cancers. Br J Obstet Gynaecol. 1995;102(10):831-832. 165. Salvesen KA, Eik-Nes SH. Ultrasound during pregnancy and birthweight, childhood malignancies and neurological development. Ultrasound Med Biol. 1999;25(7):1025-1031. 166. Stalberg K, Haglund B, Axelsson O, et al. Prenatal ultrasound and the risk of childhood brain tumour and its subtypes. Br J Cancer. 2008;98(7): 1285-1287. 167. Sande RK, Matre K, Eide GE, Kiserud T. Ultrasound safety in early pregnancy: reduced energy setting does not compromise obstetric Doppler measurements. Ultrasound Obstet Gynecol. 2012;39(4):438-443. 168. Sande RK, Matre K, Eide GE, Kiserud T. he efects of reducing the thermal index for bone from 1.0 to 0.5 and 0.1 on common obstetric pulsed wave Doppler measurements in the second half of pregnancy. Acta Obstet Gynecol Scand. 2013;92(7):790-796. 169. ter Haar GR, Abramowicz JS, Akiyama I, et al. Do we need to restrict the use of Doppler ultrasound in the irst trimester of pregnancy? Ultrasound Med Biol. 2013;39(3):374-380.

CHAPTER 29

Bioeffects and Safety of Ultrasound in Obstetrics

170. Kossof G, Griiths KA, Garrett WJ, et al. hickness of tissues intervening between the transducer and fetus and models for fetal exposure calculations in transvaginal sonography. Ultrasound Med Biol. 1993;19(1):59-65. 171. Sheiner E, Shoham-Vardi I, Abramowicz JS. What do clinical users know regarding safety of ultrasound during pregnancy? J Ultrasound Med. 2007;26(3):319-325. 172. Marsal K. he output display standard: has it missed its target? Ultrasound Obstet Gynecol. 2005;25(3):211-214. 173. Piscaglia F, Tewelde AG, Righini R, et al. Knowledge of the bio-efects of ultrasound among physicians performing clinical ultrasonography: results of a survey conducted by the Italian Society for Ultrasound in Medicine and Biology (SIUMB). J Ultrasound. 2009;12:6-11. 174. Akhtar W, Arain MA, Ali A, et al. Ultrasound biosafety during pregnancy: what do operators know in the developing world? National survey indings from Pakistan. J Ultrasound Med. 2011;30(7):981-985. 175. Houston LE, Allsworth J, Macones GA. Ultrasound is safe… right? Resident and maternal-fetal medicine fellow knowledge regarding obstetric ultrasound safety. J Ultrasound Med. 2011;30(1):21-27. 176. Bagley J, homas K, DiGiacinto D. Safety practices of sonographers and their knowledge of the biologic efects of sonography. J Diag Med Sonography. 2011;27:252-261. 177. Bromley B, Spitz J, Fuchs K, hornburg LL. Do clinical practitioners seeking credentialing for nuchal translucency measurement demonstrate compliance with biosafety recommendations? Experience of the Nuchal Translucency Quality Review Program. J Ultrasound Med. 2014;33(7):1209-1214. 178. British Medical Ultrasound Society (BMUS) Safety Group. Guidelines for the safe use of diagnostic ultrasound equipment. Ultrasound. 2010;18: 52-59. 179. Lees C, Abramowicz JS, Brezinka C, et al. Ultrasound from conception to 10+0 weeks of gestation. London: Royal College of Obstetricians and Gynaecologists; 2015. Scientiic Impact Paper No. 49. 180. Abramowicz JS. Ultrasound in the irst trimester and earlier: how to keep it safe. In: Abramowicz JS, editor. First trimester ultrasound: a comprehensive guide. Cham. Switzerland: Springer; 2015. p. 1-19. 181. Abramowicz JS. Fetal Doppler: how to keep it safe? Clin Obstet Gynecol. 2010;53(4):842-850. 182. American Institute of Ultrasound in Medicine. AIUM oicial statement: Prudent use in pregnancy. 2012. Available from: http://www.aium.org/ oicialStatements/33. Accessed 26 December 2015. 183. American Institute of Ultrasound in Medicine. AIUM oicial statement: Keepsake fetal imaging. 2012. Available from: http://www.aium.org/ oicialStatements/31. Accessed 26 December 2015. 184. American Institute of Ultrasound in Medicine. AIUM oicial statement: As low as reasonably achievable (ALARA) principle. 2014. Available from: http://www.aium.org/oicialStatements/39. Accessed 26 December 2015. 185. American Institute of Ultrasound in Medicine. AIUM Statement on mammalian biological efects of heat. 2015. Available from: http://www.aium.org/ oicialStatements/17. Accessed 26 December 2015.

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186. British Medical Ultrasound Society. BMUS Statement on the safe use and potential hazards of diagnostic ultrasound. 2000, reconirmed 2012. Available from: https://www.bmus.org/static/uploads/resources/statement_on_the_ safe_use_and_potential_hazards_of_diagnostic_ultrasound.pdf. Accessed 26 December 2015. 187. BMUS. Guidelines for the safe use of diagnostic ultrasound equipment. Ultrasound. 2010;18:52-59. 188. British Medical Ultrasound Society Safety Group. BMUS Statement for the general public on the safety of medical ultrasound imaging. 2012. Available from: https://www.bmus.org/static/uploads/resources/Statement_for_the_ General_Public_on_the_Safety_of_Medical_Ultrasound_Imaging.pdf. Accessed 26 December 2015. 189. European Committee for Medical Ultrasound Safety of the European Federation of Societies for Ultrasound in Medicine and Biology. ECMUS Statement on the use of diagnostic ultrasound for producing souvenir images or recordings in pregnancy. 2012. Available from: https://www.bmus.org/ static/uploads/resources/ECMUS_Souvenir_Scanning.pdf. Accessed 26 December 2015. 190. European Committee for Medical Ultrasound Safety of the European Federation of Societies for Ultrasound in Medicine and Biology. ECMUS Guidelines for the safe use of Doppler ultrasound for clinical application. 2013. Available from: http://www.efsumb-portal.org/ep/article.php?id=50. Accessed 26 December 2015. 191. International Society for Ultrasound in Obstetrics and Gynecology. ISUOG safety statements, 2000-2015. Available from: http://www.isuog.org/ StandardsAndGuidelines/Statements+and+Guidelines/Safety+Statements/. Accessed 26 December 2015. 192. World Federation of Ultrasound in Medicine and Biology. WFUMB/ISUOG Statement on the safe use of Doppler ultrasound during 11-14 week scans (or earlier in pregnancy). 2011, reairmed 2015. Available from: http://www.wfumb.org/safety-statements/. Accessed 26 December 2015. 193. World Federation for Ultrasound in Medicine and Biology. WFUMB Symposium on Safety and Standardisation in Medical Ultrasound. Issues and recommendations regarding thermal mechanisms for biological efects of ultrasound. Hornbaek, Denmark, 30 August-1 September 1991. Ultrasound Med Biol. 1992;18(9):731-810. 194. Barnett SB. WFUMB Symposium on Safety of Ultrasound in Medicine. Conclusions and recommendations on thermal and non-thermal mechanisms for biological efects of ultrasound. Kloster-Banz, Germany, 14-19 April 1996. World Federation for Ultrasound in Medicine and Biology. Ultrasound Med Biol. 1998;24(Suppl. 1):i-xvi, S1-S58. 195. Health Canada. Guidelines for the safe use of diagnostic ultrasound: Canada Minister of Public Works and Government Services; 2001. 196. Abramowicz JS, Kossof G, Marsal K, Ter Haar G. Safety statement, 2000 (reconirmed 2003). International Society of Ultrasound in Obstetrics and Gynecology (ISUOG). Ultrasound Obstet Gynecol. 2003;21(1):100. 197. Barnett SB, Ter Haar GR, Ziskin MC, et al. International recommendations and guidelines for the safe use of diagnostic ultrasound in medicine. Ultrasound Med Biol. 2000;26(3):355-366.

CHAPTER

30

The First Trimester Elizabeth Lazarus and Deborah Levine

SUMMARY OF KEY POINTS • First-trimester development follows a predictable pattern on irst-trimester ultrasound. • Some ultrasound indings are deinitive for early pregnancy failure, whereas others are suggestive and require follow-up.

• Ultrasound is vital in the diagnosis of ectopic pregnancy in typical and atypical locations. • Gestational trophoblastic disease is composed of four entities, and ultrasound is helpful in their diagnosis and management.

CHAPTER OUTLINE MATERNAL PHYSIOLOGY AND EMBRYOLOGY SONOGRAPHIC APPEARANCE OF NORMAL INTRAUTERINE PREGNANCY Gestational Sac β-hCG and Early Pregnancy Ultrasound Yolk Sac Embryo and Amnion Embryonic Cardiac Activity Umbilical Cord and Cord Cyst ESTIMATION OF GESTATIONAL AGE Gestational Sac Size Crown-Rump Length EARLY PREGNANCY FAILURE Diagnostic Findings of Early Pregnancy Failure Crown-Rump Length 7 mm or Greater and No Heartbeat Gestational Sac Mean Sac Diameter 25 mm or Greater and No Embryo Worrisome Findings of Early Pregnancy Failure

T

Embryos With Crown-Rump Length Less Than 7 mm and No Heartbeat Gestational Sac With Mean Sac Diameter 16 to 24 mm and No Embryo Gestational Sac Appearance Small Mean Sac Diameter in Relationship to Crown-Rump Length Abnormally Large Amnion With Respect to Embryo Size Yolk Sac Size and Shape Embryonic Bradycardia Subchorionic Hemorrhage ECTOPIC PREGNANCY Clinical Presentation Sonographic Diagnosis Heterotopic Gestation Serum β-hCG Levels Speciic Sonographic Findings Nonspeciic Sonographic Findings Adnexal Mass Free Fluid Endometrium

he irst trimester of pregnancy is a period of rapid change that spans fertilization, formation of the blastocyst, implantation, gastrulation, neurulation, the embryonic period (weeks 6-10), and early fetal life.1 First-trimester sonographic diagnosis traditionally focused on evaluation of growth by serial examination to diferentiate normal from abnormal gestations. his has changed since the advent of transvaginal sonography (TVS), which afords enhanced resolution over transabdominal sonography (TAS), with earlier visualization of the gestational sac and its contents,2

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Implantation Sites Pregnancy of Unknown Location Management EVALUATION OF THE EMBRYO Normal Embryologic Findings Mimicking Pathology Rhombencephalon Physiologic Anterior Abdominal Wall Herniation Abnormal Embryos GESTATIONAL TROPHOBLASTIC DISEASE Hydatidiform Molar Pregnancy Complete Molar Pregnancy Partial Molar Pregnancy Coexistent Hydatidiform Mole and Normal Fetus Persistent Trophoblastic Neoplasia Invasive Mole Choriocarcinoma Placental-Site Trophoblastic Tumor Sonographic Features of Persistent Trophoblastic Neoplasia Diagnosis and Treatment CONCLUSION

earlier identiication of embryonic cardiac activity,3 and improved visualization of embryonic and fetal structures. Despite these technologic improvements, it is important to set clinically relevant and realistic goals for irst-trimester sonographic diagnosis. Most examinations are requested because the patient has vaginal bleeding or pain, or a palpable mass has been identiied on physical examination. Ultrasound in the irst trimester is oten requested to diagnose early pregnancy failure or an ectopic pregnancy.

CHAPTER 30 he goals of irst-trimester sonography include (1) visualization and localization of the gestational sac (intrauterine or ectopic pregnancy) and (2) early identiication of embryonic demise and other forms of nonviable gestation. It also seeks to identify those pregnancies that are at increased risk for early pregnancy failure. First-trimester ultrasound accurately dates the duration or menstrual/gestational age of the pregnancy and assists in early diagnosis of fetal abnormalities, including identiication of embryos more likely to be abnormal, based on secondary criteria (e.g., abnormal yolk sac). In multifetal pregnancies, irst-trimester ultrasound can be used to determine the number of embryos and the chorionicity and amnionicity. Current trends in ultrasound late in the irst trimester focus on nuchal translucency screening combined with maternal age and maternal serum screening to determine the risk of chromosomal abnormalities and structural anomalies. Associated with the increased emphasis on late irst-trimester ultrasound and irst-trimester screening, there is an opportunity to visualize fetal anomalies earlier than at the time of the standard 18- to 20-week scan. First-trimester diagnosis of speciic anomalies is discussed in the chapters covering those organ systems. As experience with early irst-trimester ultrasound evolves, reliable sonographic indicators of ectopic pregnancy and embryonic demise have been established.4-6 he accuracy of some sonographic signs used as indicators of the presence of a live embryo or of embryonic demise depends on the use of modern, high-resolution ultrasound equipment and the operator’s expertise. Published values in the literature based on data using highfrequency transducers cannot be applied to lower-resolution 5.0-MHz transducers.7,8 he TVS signs listed in this chapter assume the use of modern equipment with a transducer frequency of at least 7 to 8 MHz, with meticulous scanning technique. Transducers with frequencies of 10 MHz or higher can provide improved spatial resolution, identifying abnormal and normal features at even earlier points in pregnancy.9 Nyberg and Filly6 emphasize that experienced physicians who interpret ultrasound rarely rely on a single parameter and simultaneously consider multiple variables to create a diagnostic impression.

MATERNAL PHYSIOLOGY AND EMBRYOLOGY All dates presented in this chapter are in menstrual age or gestational age, in keeping with the radiologic and obstetric literature, rather than in embryologic age, as used by embryologists. his can be counted as follows: Gestational age = Conceptual age + 2 weeks Early in the menstrual cycle, the pituitary secretes rising levels of follicle-stimulating hormone (FSH) and luteinizing hormone (LH), which cause the growth of 4 to 12 primordial follicles into primary ovarian follicles10 (Fig. 30.1). When a luid-illed cavity or antrum forms in the follicle, it is referred to as a secondary follicle. he primary oocyte is of to one side of the follicle and surrounded by follicular cells or the cumulus oophorus. One follicle becomes dominant, bulges on the surface of the ovary,

The First Trimester

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and becomes a “mature follicle” or graaian follicle. It continues to enlarge until ovulation, with the remainder of the follicles becoming atretic. he developing follicles produce estrogen. he estrogen level remains relatively low until 4 days before ovulation, when the dominant or active follicle produces an estrogen surge, ater which an LH and prostaglandin surge results in ovulation. Ovulation follows the LH peak within 12 to 24 hours. Actual expulsion of the oocyte from the mature follicle is aided by several factors, including the intrafollicular pressure, possibly contraction of the smooth muscle in the theca externa stimulated by prostaglandins, and enzymatic digestion of the follicular wall.11 Ovulation occurs on approximately day 14 of the menstrual cycle with expulsion of the secondary oocyte from the surface of the ovary. In women with a menstrual cycle longer than 28 days, this ovulation occurs later, so that the secretory phase of the menstrual cycle remains at about 14 days. Ater ovulation, the follicle collapses to form the corpus luteum, which secretes progesterone and, to a lesser degree, estrogen. If a pregnancy does not occur, the corpus luteum involutes. In pregnancy, involution of the corpus luteum is prevented by human chorionic gonadotropin (hCG), which is produced by the outer layer of cells of the gestational or chorionic sac (syncytiotrophoblast). Before ovulation, endometrial proliferation occurs in response to estrogen secretion (Fig. 30.1). Ater ovulation, the endometrium becomes thickened, sot, and edematous under the inluence of progesterone.12 he glandular epithelium secretes a glycogen-rich luid. If pregnancy occurs, continued production of progesterone results in more marked hypertrophic changes in the endometrial cells and glands to provide nourishment to the blastocyst. hese hypertrophic changes are referred to as the decidual reaction and occur as a hormonal response regardless of the site of implantation, intrauterine or ectopic. Oocyte transport into the imbriated end of the fallopian tube occurs at ovulation as the secondary oocyte is expelled with the follicular luid and is “picked up” by the imbria. he sweeping movement of the imbria, the currents produced by the action of the cilia of the mucosal cells, and the gentle peristaltic waves from contractions of the fallopian musculature all draw the oocyte into the tube.13 he mechanism of sperm transport is regulated to maximize the chance of fertilization and ensure the most rigorous sperm will be available.14 From 200 to 600 million sperm and the ejaculate luid are deposited in the vaginal fornix during intercourse. Sperm must move through the cervical canal and its mucous plug, up the endometrial cavity, and down the fallopian tube to meet the awaiting oocyte within the distal third or ampullary portion of the fallopian tube. Sperm were thought to move primarily using their tails, although they travel at 2 to 3 mm per minute, which would take about 50 minutes to travel the 20 cm to their destination. Settlage et al.13 found motile sperm within the ampulla between 5 and 10 minutes ater deposition near the external cervical os. If inert particles such as radioactive macroaggregates or carbon particles are placed near the external os, they too will be picked up and transported up the uterus and down the tubes. Contractions of the inner layer of myometrium are believed to create a negative pressure strong enough to suck up particles and move them up the endometrial canal. hese contractions

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FIG. 30.1 Schematic Drawing of Interrelationships Among the Hypothalamus, Pituitary Gland, Ovaries, and Endometrial Lining. FSH, Follicle-stimulating hormone; LH, luteinizing hormone. (With permission from Moore KL. The developing human: clinically oriented embryology. 10th ed. Philadelphia: Elsevier; 2016.1)

CHAPTER 30

Posterior wall of uterus

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1051

Blastocysts Morula

Eight-cell stage

Four-cell stage

Two-cell stage Zygote

Follicle approaching maturity Secondary follicle Mature Growing follicle follicle Early primary Oocyte follicle

Fertilization

Oocyte in tube

Blood vessels Epithelium Corpus albicans Mature corpus luteum

Endometrium

Atretic (degenerating) follicle Atretic (degenerating) follicle

Released oocyte Ruptured follicle Connective tissue Developing corpus Coagulated blood luteum

FIG. 30.2 Diagram of Ovarian Cycle, Fertilization, and Human Development to the Blastocyst Stage. (With permission from Moore KL. The developing human: clinically oriented embryology. 10th ed. Philadelphia: Elsevier; 2016.1)

have been demonstrated in nonpregnant women and increase in strength and frequency to peak at 3.5 contractions per minute at ovulation.15 Fertilization occurs on or about day 14 as the mature ovum and sperm unite to form the zygote in the outer third of the fallopian tube (Fig. 30.2). Cellular division of the zygote occurs during transit through the fallopian tube. By the time the conceptus enters the uterus, about day 17, it is at the 12- to 15-cell stage (morula). By day 20, the conceptus has matured to the blastocyst stage. he blastocyst is a luid-illed cyst lined with trophoblastic cells that contain a cluster of cells at one side called the inner cell mass. On day 20, the blastocyst at the site of the inner cell mass burrows through the endometrial membrane into the hyperplastic endometrium, and implantation begins16 (Fig. 30.3A). Implantation is completed by day 23 as the endometrial membrane re-forms over the blastocyst (Fig. 30.3B). During implantation, the amniotic cavity forms in the inner cell mass. A bilaminar embryonic disk separates the amniotic cavity from the exocoelomic cavity. he primary (primitive) yolk sac forms

at about 23 days of gestational age as the blastocyst cavity becomes lined by the exocoelomic membrane and hypoblast. As the extraembryonic coelom forms, the primary yolk sac is pinched of and extruded, resulting in the formation of the secondary yolk sac (Fig. 30.4). Standard embryology texts indicate that the secondary yolk sac forms at approximately 27 to 28 days of menstrual age, when the mean diameter of the gestational sac is approximately 3 mm. It is the secondary yolk sac, rather than the primary yolk sac, that is visible with ultrasound. For the remainder of this chapter, the term yolk sac is used to refer to the secondary yolk sac. he extraembryonic coelom becomes the chorionic cavity. Later, because of diferential growth, the yolk sac comes to lie between the amnion and chorion. During week 4, there is rapid proliferation and diferentiation of the syncytiotrophoblast, forming primary chorionic villi. Traditional thinking that the syncytiotrophoblastic cells invade the maternal endometrial vessels, leaving maternal blood to bathe the trophoblastic ring, has been challenged. Hustin16 compared TVS to hysteroscopy of the placenta, chorionic villous sampling tissue, and

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A

B FIG. 30.3 Implantation of the Blastocyst Into Endometrium. Entire conceptus is approximately 0.1 mm at this stage. (A) Partially implanted blastocyst at approximately 22 days. (B) Almost completely implanted blastocyst at about 23 days. (With permission from Moore KL. The developing human: clinically oriented embryology. 10th ed. Philadelphia: Elsevier; 2016.1)

hysterectomy specimens with an early pregnancy in situ. Before 12 weeks, the intervillous space contains no blood, only clear luid, and on histologic examination, the villous tissue is separated from the maternal circulation by a continuous layer of trophoblastic cells. Only ater the third month does the trophoblastic shell become broken and the maternal circulation become continuous with the intervillous space. Furthermore, at weeks 8 and 9 of gestation, the trophoblastic shell forms plugs within the spiral arteries, allowing only iltered plasma to permeate the placenta.17 In two-thirds of abnormal pregnancies, the

trophoblastic shell is thinner and fragmented, and the trophoblastic invasion of the spiral arteries is reduced or absent.18 Vascularization of the placenta occurs at the beginning of the ith week. Oh et al.19 showed signiicant increases in sac size from 5 weeks onward in normal intrauterine pregnancy (IUP) versus pregnancy failure. he rationale for placental vascularization was based on early work by Folkman,20 who showed that tumors can grow to a size of 3 mm being nourished only by difusion. To exceed this size, cells must recruit host blood vessels, or the cells at the center will receive inadequate nutrition.

CHAPTER 30

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A

B

C

FIG. 30.4 Formation of Secondary Yolk Sac. (A) Approximately 26 days: formation of cavities within extraembryonic mesoderm. These cavities will enlarge to form extraembryonic coelom. (B) About 27 days and (C) 28 days: formation of secondary yolk sac with extrusion of primary yolk sac. Extraembryonic coelom will become chorionic cavity. (With permission from Moore KL. The developing human: clinically oriented embryology. 10th ed. Philadelphia: Elsevier; 2016.1)

Similarly, the rapidly growing embryonic implantation must be vascularized by the 3-mm stage that occurs at 5 weeks’ gestation. During the ith week, the embryo is converted by the process of gastrulation from a bilaminar disk to a trilaminar disk with the three primary germ cell layers: ectoderm, mesoderm, and endoderm. During gastrulation, the primitive streak and notochord form. he primitive streak gives rise to the mesenchyme, which forms the connective tissue of the embryo and stromal components of all glands. he formation of the neural plate and its closure to form the neural tube is referred to as neurulation. his process begins

in the ith week in the thoracic region and extends caudally and cranially, resulting in complete closure by the end of the sixth week (day 42). Failure of closure of the neural tube results in neural tube defects. During the ith week, two cardiac tubes (the primitive heart) develop from splanchnic mesodermal cells. By the end of the ith week, these tubes begin to pump into a primitive paired vascular system. By the end of the ith week, a vascular network develops in the chorionic villi that connect through the umbilical arteries and vein to the primitive embryonic vascular network. Essentially all internal and external structures appear in the adult form during the embryonic period, which ends at 10

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menstrual weeks. By the end of the sixth week, blood low is unidirectional, and by the end of the eighth week, the heart attains its deinitive form. he peripheral vascular system develops slightly later and is completed by the end of the tenth week. he primitive gut forms during week 6. he midgut herniates into the umbilical cord from week 8 through the end of week 12. he rectum separates from the urogenital sinus by the end of week 8, and the anal membrane perforates by the end of week 10. he metanephros, or primitive kidneys, ascend from the pelvis, starting at approximately week 8, but do not reach their adult position until week 11. Limbs are formed with separate ingers and toes. Almost all congenital malformations except abnormalities of the genitalia originate before or during the embryonic period. External genitalia are still in a sexless state at the end of week 10 and do not reach mature fetal form until the end of week 14. Early in the fetal period, body growth is rapid and head growth relatively slower, with the crown-rump length (CRL) doubling between weeks 11 and 14.

SONOGRAPHIC APPEARANCE OF NORMAL INTRAUTERINE PREGNANCY Gestational Sac Implantation usually occurs in the fundal region of the uterus between day 20 and day 23.21 In a study of early implantation sites in 21 patients, it was found that implantation occurs most frequently on the uterine wall ipsilateral to the ovulating ovary and least oten on the contralateral wall.21 In addition, in a study of predominant sleeping positions in the peri-implantation period, Magann et al.22 found that the 33% of women who slept prone were most likely to have a high or fundal implantation than those who slept on their back or side. he latter groups predominantly had implantations corresponding to their resting posture. At 23 days, the entire conceptus measures approximately 0.1 mm in diameter and cannot be imaged by TAS or TVS techniques. he earliest sonographic sign of an IUP was described by Yeh et al.,23 who identiied a focal echogenic zone of decidual thickening at the site of implantation at about 3 1 2 to 4 weeks of gestational age. his sign is nonspeciic and of limited diagnostic value. he irst reliable gray-scale evidence of an IUP is visualization of a small (1-2 mm luid collection surrounded by an echogenic rim) gestational sac within the thickened decidua. Yeh et al.23 originally identiied this sign, referred to as the intradecidual sign, which is seen at about 4.5 weeks’ gestation. An intradecidual gestational sac should be eccentrically located within the endometrium. It is important to ensure that the sac abuts the endometrial canal to distinguish an intrauterine gestational sac from a decidual cyst. he intradecidual sign was originally described on TAS,23 with a sensitivity of 92%, speciicity 100%, and overall accuracy of 93% for distinguishing between early IUP and ectopic pregnancy. Chiang et al.24 looked at this sign using TVS and found overall sensitivity of 60% to 68%, speciicity of 97% to 100%,

and overall accuracy of 67% to 73%, indicating that the sign, when present, is useful for diagnosing an IUP. When absent, it does not reliably exclude an IUP. It is usually possible to demonstrate an early IUP as a small intradecidual sac between 4 1 2 and 5 weeks’ gestational age using TVS (Figs. 30.5 and 30.6). Using a high-frequency (7.5-10 MHz) TVS, Oh et al.19 were able to identify a gestational sac in all 67 patients scanned between 28 and 42 days’ gestational age (mean sac diameter [MSD] between 28 and 35 days was 2.6 mm). he double-decidual sign (also called double decidual sac sign) was described by Bradley et al.25 and Nyberg et al.26 as a method for distinguishing between an early IUP and an endometrial luid collection of other origin, such as the pseudosac of an ectopic pregnancy. A well-deined double-decidual sign is an accurate predictor of the presence of an IUP. A vague or absent double-decidual sign should be considered nondiagnostic because it does not reliably exclude an IUP.27 he endometrium in the pregnant state is called the decidua capsularis, decidua vera, and decidua basalis. he doubledecidual sign is based on visualization of the gestational sac as an echogenic ring formed by the decidua capsularis and chorion laeve eccentrically located within the decidua vera (Fig. 30.6), forming two echogenic rings. he outer ring is formed by the echogenic endometrium of the lining of the uterus. he decidua basalis–chorion frondosum (future placenta) may also be visualized as an area of eccentric echogenic thickening. he double-decidual sign was initially described, and is considered most useful, on TAS. It can usually be identiied by about 5.5 to 6 weeks’ gestational age and is useful in establishing an intrauterine gestation prior to TAS ability to visualize the yolk sac. It is almost always resolvable by the time the gestational sac reaches 10 mm, at which point the yolk sac is typically visible by TVS, thus diminishing the usefulness of this inding.28 Parvey et al.29 found a double-decidual sign in only 53% of early pregnancies with no yolk sac or embryo present. hey also assessed visualization of the echogenic chorionic rim alone as a sign of IUP and found its presence in 64% of cases. It was more clearly deined in later pregnancies with a higher β-hCG level (mean, 16,082 mIU/mL) and thin, less clearly deined, or even absent in the earliest pregnancies. Using a higher-frequency 10-MHz transvaginal transducer to scan patients who had a positive pregnancy test and only a small (5.6 mm), and one yolk sac was irregular in contour. herefore in MCMA twins, a single, large, or normal-sized yolk sac with two live embryos can result in a normal twin delivery.

Embryo and Amnion Yolk Sac At 4 weeks’ menstrual age, the primary yolk sac begins to regress and the secondary yolk sac develops. he secondary yolk sac is the irst structure to be seen normally within the gestational sac. Using TAS, it is oten seen when the MSD is 10 to 15 mm and should typically be visualized by an MSD of 20 mm.42 TVS allows earlier and more detailed visualization of the yolk sac (Figs. 30.6 and 30.9), which is typically visualized by an MSD of 8 mm.28 However, the visualization of a yolk sac without an embryonic pole occurs only for a brief period of time. In patients being scanned for pregnancy of unknown viability, the MSD of 25 is used as the threshold, with need to visualize an embryo at this time. he demonstration of a yolk sac may be critical in diferentiating an early intrauterine gestational sac from a pseudosac.28 Although the double-decidual sign is not 100% speciic for presence of an IUP, the identiication of a yolk sac within the early gestational sac is diagnostic of IUP. he yolk sac plays an important role in human embryonic development.10 While the placental circulation is developing, the yolk sac plays a role in transfer of nutrients to the developing embryo in the third and fourth weeks. Angiogenesis occurs in the wall of the yolk sac in the ith week. he mesenchymal cells or angioblasts aggregate to form “blood islands”; a cavity forms within these islands, which fuse with others to form networks of endothelial channels.

Visualization of the amnion in the absence of an embryo usually occurs in intrauterine embryonic death as a result of resorption of the embryo45 (Fig. 30.12). Amniotic luid is a colorless, fetal dermal transudate; as the skin corniies and the kidneys begin to function, at about 11 weeks, it becomes pale yellow. he amnion becomes visible when the embryo has a CRL of 2 mm at 6 weeks. he cavity becomes almost spherical by about 7 weeks, likely a result of the more rapid increase in luid volume relative to the growth of the sac membrane to accommodate it. he actual rate of luid increase is more rapid ater about 9 weeks (Fig. 30.13), when urine is produced. Fluid accumulates at about 5 mL per day at 12 weeks. he amniotic cavity expands to ill the chorionic cavity completely by week 16. It is therefore normal to identify the amnion as a separate membrane or sac within the chorionic cavity before 16 weeks (Fig. 30.14). Occasionally, the amnion and chorionic membranes may fail to be juxtaposed at week 16 (so-called unfused amnion), and separation of these membranes may persist for a short time.46 Iatrogenic or spontaneous rupture of the amniotic membrane in the irst trimester is a rare occurrence and even more rarely results in the amniotic band sequence. his rupture may result in retraction of the amnion in part or in whole, up to the base of the umbilical cord where the amnion and chorion are adherent. More oten, the loating amniotic membranes do not adhere to the fetus, and no fetal anomalies occur.

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A

B

C

D

FIG. 30.9 Normal Yolk Sac. (A) Sagittal and (B) transverse TVS of the early IUP demonstrates the yolk sac at 5 weeks 5 days. (C) Yolk sac is seen separate from embryo (calipers) at 9 weeks. (D) At 11 weeks, yolk sac lies at edge of chorionic sac outside of early amnion.

ys

e

FIG. 30.10 Normal Embryo at 8 Weeks. TVS shows vitelline duct (thick arrow), yolk sac (ys), and embryo (e).

Embryonic Cardiac Activity Using TVS, an embryo with a CRL as small as 1 to 2 mm may be identiied immediately adjacent to the yolk sac (Fig. 30.15). In normal pregnancies the embryo can be identiied in gestational sacs as small as 10 mm and should always be identiied when

FIG. 30.11 Early Monochorionic Diamniotic (MCDA) Twins. Two separate yolk sacs are seen within a single chorion at 5 weeks 5 days. It is too early to visualize the two amnions.

the MSD is equal to or greater than 25 mm with optimal scanning parameters and high-resolution TVS.4,5 Embryologic data suggest the tubular heart begins to beat at 36 to 37 days’ gestational age.10 Cadkin and McAlpin47 described cardiac activity adjacent to the yolk sac before the embryo can

CHAPTER 30

A

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1059

B

FIG. 30.12 Abnormal Amnion. (A) TVS at 9 weeks demonstrates an empty amnion within the gestational sac. This pregnancy eventually failed. (B) Expanded amnion at 7 weeks. Note how the amnion is much larger than would be expected for an embryo (calipers) of this size. This pregnancy did not progress.

Umbilical Cord and Cord Cyst

FIG. 30.13 Normal 9-Week 4-Day Gestation. TVS shows the embryo (calipers) and the amnion (arrow) separate from the surrounding chorion.

be fully visualized at the end of the ith week. Ragavendra et al.48 placed a 12.5-MHz endoluminal catheter transducer into the endometrial canal adjacent to the gestational sac. hey identiied cardiac activity in an embryo with a CRL of 1.5 mm and resolved the two walls of the heart, seen only as a tube. Using TVS, cardiac activity is typically seen by the time an embryo is 2 mm in size, and is almost always seen by 5-mm CRL. However, for strict diagnosis of nonviable pregnancy the threshold is set at 7 mm CRL.4,5 Normal embryonic cardiac activity is greater than 100 beats per minute (bpm) (Video 30.1) when the embryo is less than 6.3 weeks and 120 bpm at or beyond 6.3 weeks.49 When embryonic cardiac activity is visualized and the rate is less than 100 bpm, then follow-up should be obtained. We have seen pregnancies with small embryos of 1–2 mm in size with heart rates of 80–99 bpm with normal follow-up (see Fig. 30.15).

he umbilical cord is formed at the end of the sixth week (CRL = 4.0 mm) as the amnion expands and envelops the connecting stalk, the yolk stalk, and the allantois. he cord contains two umbilical arteries, a single umbilical vein, the allantois, and yolk stalk (also called the omphalomesenteric duct or vitelline duct), all of which are embedded in Wharton jelly. he umbilical arteries arise from the internal iliac arteries and in the newborn become the superior vesical arteries and the medial umbilical ligaments. he umbilical vein carries oxygenated blood from the placenta to the fetus. he oxygenated blood is shunted through the ductus venosus into the inferior vena cava and the heart. he single let umbilical vein in the newborn becomes the ligamentum teres, which attaches to the let branch of the portal vein. he ductus venosus becomes the ligamentum venosum. he allantois is associated with bladder development and becomes the urachus and the median umbilical ligament. It extends into the proximal portion of the umbilical cord. he yolk stalk connects the primitive gut to the yolk sac. he paired vitelline arteries and veins accompany the stalk to provide blood supply to the yolk sac. he arteries arise from the dorsal aorta to supply initially the yolk sac, then the primitive gut. he arteries remain as the celiac axis, superior and inferior mesenteric arteries supplying the foregut, midgut, and hindgut, respectively. he vitelline veins drain directly into the sinus venosus of the heart. he right vein is later incorporated into the right hepatic vein. he portal vein is also formed by an anastomotic network of vitelline veins. he length of the umbilical cord has a close linear relationship with gestational age in normal pregnancies. Hill et al.50 found they could reliably measure the cord lengths in 53 embryos at 6 to 11 weeks’ gestational age. Also, the cord lengths in 60% of dead embryos were more than two standard deviations (2 SD) below the value for that expected gestational age. he width of the umbilical cord has also been measured sonographically, and Ghezzi et al.51 found a steady increase from 8 to 15 weeks. here was a signiicant correlation between cord

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B

FIG. 30.14 Normal 12-Week Gestation. (A) Surface rendering image from three-dimensional TVS shows the embryo within the amnion. (B) Two-dimensional TVS shows the amnion (arrow) approaching, but not fused with, the chorionic sac.

A

B

C

D

FIG. 30.15 Normal Embryo With Early Cardiac Activity. (A) Image shows 5-week 6-day embryo (calipers) adjacent to the yolk sac. (B) M-mode ultrasound shows a heart rate of 96 beats/min. (C) Two days later, the embryonic pole (calipers) has grown and (D) the heart rate has increased to 111 beats/min. See also Video 30.1.

CHAPTER 30 diameter and gestational age (r = 0.78; P < .001), CRL (r = 0.75; P < .001), and biparietal diameter (r = 0.81; P < .001) but no correlation with birth weight or placental weight. he cord diameter was signiicantly smaller by at least 2 SD in patients who developed preeclampsia or had a miscarriage. Cysts and pseudocysts within the cord have been described in the irst trimester.52 Cysts are usually seen in the eighth week and usually resolve by the 12th week. hey are singular, closer to the embryo/fetus than the placenta, with a mean size of 5.2 mm (Fig. 30.16). Cysts may originate from remnants of the allantois or omphalomesenteric duct and characteristically have an epithelial lining.53 It is hypothesized that the cyst is an amnion

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inclusion cyst that occurs as the amnion was enveloping the umbilical cord. In a series of 1159 consecutive patients scanned between 7 and 14 weeks, Ghezzi et al.54 found 24 cord cysts at a prevalence of 2.1%. Single cysts in the irst trimester were associated with a normal outcome and a healthy infant, whereas multiple or complex cysts were associated with an increased risk of miscarriage or aneuploidy. hus although umbilical cord cysts have been associated with chromosomal abnormalities if seen in the second and third trimesters, those seen in the irst trimester typically resolve and are not associated with poor outcome.

ESTIMATION OF GESTATIONAL AGE During the irst trimester, gestational age can be estimated sonographically with greater accuracy than at any other stage of pregnancy. As pregnancy progresses, biologic variation results in wider variation around the mean for all sonographic parameters at a given gestational age.

Gestational Sac Size

FIG. 30.16 Umbilical Cord Cyst at 10 Weeks. TVS shows a cyst (small arrow) arising from the cord (large arrow). On subsequent examination (not shown) the cyst was no longer seen.

he MSD ofers an opportunity to date an early pregnancy before the embryo can be visualized. he MSD is an average of the diameter of the sac, obtained by adding the anteroposterior and craniocaudad diameters on the sagittal view of the uterus to the transverse diameter obtained on the transverse view and dividing by three (Fig. 30.17). he gestational age can be predicted by MSD using the following formula: menstrual age in days = MSD in mm + 30.55 he MSD increases in size at a rate of 1.1 mm per day.56 If MSD is very small, about 2 mm, gestational age is 4 to 4 1 2 weeks, and MSD of about 5 mm is 5 weeks. At 5 1 2 weeks, a yolk sac appears (see Fig. 30.9A and B). At 6 weeks, an embryo irst appears adjacent to the yolk sac (see Fig. 30.15A). When the embryo is irst seen, cardiac activity is appreciated as a consistent licker40 (Fig. 30.15B and Video 30.1).

FIG. 30.17 Gestational Age Established by Mean Sac Diameter (MSD). Gestational age can be estimated measuring the sac in three dimensions. Average of three measurements is used to correlate with gestational age prior to visualization of the embryonic pole. MSD of 12 mm is consistent with gestational age of 6 weeks 0 days. However, these data are not used to formally establish pregnancy dating. Sonographic dating of the pregnancy is done with the crown-rump length when cardiac activity is present.

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PART IV

Crown-Rump Length Once the embryonic pole is visualized (just before 6 weeks), measurement of the CRL of the embryo is considered the most accurate method to date the pregnancy.57,58

EARLY PREGNANCY FAILURE One of the most important roles of ultrasound in the irst trimester is to identify early pregnancies that have failed or that are more likely to fail. Studies have demonstrated a 20% to 31% rate of early pregnancy loss ater implantation in normal healthy volunteers.59,60 Many pregnancies abort before the pregnancy is conirmed by either ultrasound or a chemical pregnancy test. Approximately 50% of miscarriage is caused by chromosomal abnormalities.61 Early pathologic studies of Hertig and Rock,60 also showed a high frequency of morphologic abnormalities in preimplantation embryos. Loss rates are increased with increased maternal age and prior history of early pregnancy failure.62 Although the etiology of irst-trimester pregnancy loss is still not fully understood, there are many known and suspected causes. In a study of 232 irst-trimester patients (normal, healthy women, positive urinary pregnancy test, and no vaginal bleeding) with TVS at the irst visit, Goldstein57 determined the incidence of subsequent pregnancy loss by following all to delivery or spontaneous abortion. his group had an overall pregnancy loss rate of 11.5% in the embryonic period, (i.e., 35) and low serum β-hCG ( 6 mm Calciied yolk sac Embryonic bradycardia Large subchorionic hemorrhage

Expanded amnion or empty amnion as evaluated by an experienced sonologist is diagnostic of miscarriage. If any uncertainty is present, then follow-up should be obtained. Findings are associated with miscarriage, but the size of the embryo and presence or absence of cardiac activity guides the diagnosis. Heart rate (HR) < 100 may be seen with 1- to 2-mm embryo and be a normal inding. In general, when HR is 10 mm) on prenatal sonography. J Ultrasound Med. 1997;16(11):731-734. 48. Ghai S, Fong KW, Toi A, et al. Prenatal US and MR imaging indings of lissencephaly: review of fetal cerebral sulcal development. Radiographics. 2006;26(2):389-405. 49. Quarello E, Stirnemann J, Ville Y, Guibaud L. Assessment of fetal sylvian issure operculization between 22 and 32 weeks: a subjective approach. Ultrasound Obstet Gynecol. 2008;32(1):44-49. 50. Toi A, Lister WS, Fong KW. How early are fetal cerebral sulci visible at prenatal ultrasound and what is the normal pattern of early fetal sulcal development? Ultrasound Obstet Gynecol. 2004;24(7):706-715. 51. Pashaj S, Merz E, Wellek S. Biometry of the fetal corpus callosum by threedimensional ultrasound. Ultrasound Obstet Gynecol. 2013;42(6): 691-698. 52. Rizzo G, Capponi A, Pietrolucci ME, et al. An algorithm based on OmniView technology to reconstruct sagittal and coronal planes of the fetal brain from volume datasets acquired by three-dimensional ultrasound. Ultrasound Obstet Gynecol. 2011;38(2):158-164. 53. Tonni G, Grisolia G, Sepulveda W. Second trimester fetal neurosonography: reconstructing cerebral midline anatomy and anomalies using a novel three-dimensional ultrasound technique. Prenat Diagn. 2014;34(1): 75-83. 54. Levine D, Barnes PD, Madsen JR, et al. Central nervous system abnormalities assessed with prenatal magnetic resonance imaging. Obstet Gynecol. 1999;94(6):1011-1019. 55. Pooh RK, Nagao Y, Pooh K. Fetal neuroimaging by transvaginal 3D ultrasound and MRI. Ultrasound Rev Obstet Gynecol. 2006;6:123-134. 56. Fong K, Chong K, Toi A, et al. Fetal ventriculomegaly secondary to isolated large choroid plexus cysts: prenatal indings and postnatal outcome. Prenat Diagn. 2011;31(4):395-400. 57. Van den Hof MC, Wilson RD. Fetal sot markers in obstetric ultrasound. J Obstet Gynaecol Can. 2005;27(6):592-636. 58. Ebrashy A, Kurjak A, Adra A, et al. Controversial ultrasound indings in mid trimester pregnancy. Evidence based approach. J Perinat Med. 2016;44(2):131-137. 59. Chapman T, Mahalingam S, Ishak GE, et al. Diagnostic imaging of posterior fossa anomalies in the fetus and neonate: part 1, normal anatomy and classiication of anomalies. Clin Imaging. 2015;39(1):1-8. 60. Gandoli Colleoni G, Contro E, et al. Prenatal diagnosis and outcome of fetal posterior fossa luid collections. Ultrasound Obstet Gynecol. 2012;39(6): 625-631. 61. Chen CY, Chen FH, Lee CC, et al. Sonographic characteristics of the cavum velum interpositum. AJNR Am J Neuroradiol. 1998;19(9):1631-1635. 62. Shah PS, Blaser S, Toi A, et al. Cavum veli interpositi: prenatal diagnosis and postnatal outcome. Prenat Diagn. 2005;25(7):539-542. 63. Eisenberg VH, Zalel Y, Hofmann C, et al. Prenatal diagnosis of cavum velum interpositum cysts: signiicance and outcome. Prenat Diagn. 2003; 23(10):779-783. 64. Saba L, Anzidei M, Raz E, et al. MR and CT of brain’s cava. J Neuroimaging. 2013;23(3):326-335. 65. Vergani P, Locatelli A, Piccoli MG, et al. Ultrasonographic diferential diagnosis of fetal intracranial interhemispheric cysts. Am J Obstet Gynecol. 1999;180(2 Pt 1):423-428. 66. Gaglioti P, Oberto M, Todros T. he signiicance of fetal ventriculomegaly: etiology, short- and long-term outcomes. Prenat Diagn. 2009;29(4): 381-388. 67. Tully HM, Dobyns WB. Infantile hydrocephalus: a review of epidemiology, classiication and causes. Eur J Med Genet. 2014;57(8):359-368. 68. Verhagen JM, Schrander-Stumpel CT, Krapels IP, et al. Congenital hydrocephalus in clinical practice: a genetic diagnostic approach. Eur J Med Genet. 2011;54(6):e542-e547.

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69. Guibaud L. Fetal cerebral ventricular measurement and ventriculomegaly: time for procedure standardization. Ultrasound Obstet Gynecol. 2009; 34(2):127-130. 70. Heiserman J, Filly RA, Goldstein RB. Efect of measurement errors on sonographic evaluation of ventriculomegaly. J Ultrasound Med. 1991; 10(3):121-124. 71. Melchiorre K, Bhide A, Gika AD, et al. Counseling in isolated mild fetal ventriculomegaly. Ultrasound Obstet Gynecol. 2009;34(2):212-224. 72. Farrell TA, Hertzberg BS, Kliewer MA, et al. Fetal lateral ventricles: reassessment of normal values for atrial diameter at US. Radiology. 1994; 193(2):409-411. 73. Filly RA, Goldstein RB. he fetal ventricular atrium: fourth down and 10 mm to go. Radiology. 1994;193(2):315-317. 74. Mahony BS, Nyberg DA, Hirsch JH, et al. Mild idiopathic lateral cerebral ventricular dilatation in utero: sonographic evaluation. Radiology. 1988;169(3):715-721. 75. Hertzberg BS, Lile R, Foosaner DE, et al. Choroid plexus–ventricular wall separation in fetuses with normal-sized cerebral ventricles at sonography: postnatal outcome. AJR Am J Roentgenol. 1994;163(2):405-410. 76. Pagani G, hilaganathan B, Prefumo F. Neurodevelopmental outcome in isolated mild fetal ventriculomegaly: systematic review and meta-analysis. Ultrasound Obstet Gynecol. 2014;44(3):254-260. 77. Weichert J, Hartge D, Krapp M, et al. Prevalence, characteristics and perinatal outcome of fetal ventriculomegaly in 29,000 pregnancies followed at a single institution. Fetal Diagn her. 2010;27(3):142-148. 78. Gaglioti P, Danelon D, Bontempo S, et al. Fetal cerebral ventriculomegaly: outcome in 176 cases. Ultrasound Obstet Gynecol. 2005;25(4):372-377. 79. D’Addario V, Pinto V, Di Cagno L, Pintucci A. Sonographic diagnosis of fetal cerebral ventriculomegaly: an update. J Matern Fetal Neonatal Med. 2007;20(1):7-14. 80. Vintzileos AM, Ingardia CJ, Nochimson DJ. Congenital hydrocephalus: a review and protocol for perinatal management. Obstet Gynecol. 1983;62(5): 539-549. 81. Lee JE, Gleeson JG. Cilia in the nervous system: linking cilia function and neurodevelopmental disorders. Curr Opin Neurol. 2011;24(2): 98-105. 82. McAllister JP 2nd. Pathophysiology of congenital and neonatal hydrocephalus. Semin Fetal Neonatal Med. 2012;17(5):285-294. 83. Monteagudo A, Timor-Tritsch IE. Moomjy M. Nomograms of the fetal lateral ventricles using transvaginal sonography. J Ultrasound Med. 1993;12(5):265-269. 84. Garel C, Fetal MRI. what is the future? Ultrasound Obstet Gynecol. 2008;31(2):123-128. 85. Morris JE, Rickard S, Paley MN, et al. he value of in-utero magnetic resonance imaging in ultrasound diagnosed foetal isolated cerebral ventriculomegaly. Clin Radiol. 2007;62(2):140-144. 86. Stroustrup Smith A, Levine D, et al. Magnetic resonance imaging of the kinked fetal brain stem: a sign of severe dysgenesis. J Ultrasound Med. 2005;24(12):1697-1709. 87. Bafero GM, Crovetto F, Fabietti I, et al. Prenatal ultrasound predictors of postnatal major cerebral abnormalities in fetuses with apparently isolated mild ventriculomegaly. Prenat Diagn. 2015;35(8):783-788. 88. Laskin MD, Kingdom J, Toi A, et al. Perinatal and neurodevelopmental outcome with isolated fetal ventriculomegaly: a systematic review. J Matern Fetal Neonatal Med. 2005;18(5):289-298. 89. Sadan S, Malinger G, Schweiger A, et al. Neuropsychological outcome of children with asymmetric ventricles or unilateral mild ventriculomegaly identiied in utero. BJOG. 2007;114(5):596-602. 90. Uher BF, Golden JA. Neuronal migration defects of the cerebral cortex: a destination debacle. Clin Genet. 2000;58(1):16-24. 91. Barkovich AJ, Guerrini R, Kuzniecky RI, et al. A developmental and genetic classiication for malformations of cortical development: update 2012. Brain. 2012;135(Pt 5):1348-1369. 92. Sarnat HB, Flores-Sarnat L. Integrative classiication of morphology and molecular genetics in central nervous system malformations. Am J Med Genet A. 2004;126a(4):386-392. 93. van der Knaap MS, Valk J. Classiication of congenital abnormalities of the CNS. AJNR Am J Neuroradiol. 1988;9(2):315-326.

94. Greene ND, Copp AJ. Neural tube defects. Annu Rev Neurosci. 2014;37:221-242. 95. Goldstein RB, Filly RA. Prenatal diagnosis of anencephaly: spectrum of sonographic appearances and distinction from the amniotic band syndromex. AJR Am J Roentgenol. 1988;151:547-550. 96. Naidich TP, Griiths PD, Rosenbloom L. Central nervous system injury in utero: selected entities. Pediatr Radiol. 2015;45(Suppl. 3):S454-S462. 97. Sepulveda W, Corral E, Ayala C, et al. Chromosomal abnormalities in fetuses with open neural tube defects: prenatal identiication with ultrasound. Ultrasound Obstet Gynecol. 2004;23(4):352-356. 98. Caici D, Sepulveda W. First-trimester echogenic amniotic luid in the acrania-anencephaly sequence. J Ultrasound Med. 2003;22(10): 1075-1079. 99. Engels AC, Joyeux L, Brantner C, et al. Sonographic detection of central nervous system defects in the irst trimester of pregnancy. Prenat Diagn. 2016;36(3):266-273. 100. Chen CP, Chang TY, Lin YH, Wang W. Prenatal sonographic diagnosis of acrania associated with amniotic bands. J Clin Ultrasound. 2004;32(5): 256-260. 101. Goldstein RB, LaPidus AS, Filly RA. Fetal cephaloceles: diagnosis with US. Radiology. 1991;180(3):803-808. 102. Kasprian GJ, Paldino MJ, Mehollin-Ray AR, et al. Prenatal imaging of occipital encephaloceles. Fetal Diagn her. 2015;37(3):241-248. 103. Hoving EW. Nasal encephaloceles. Childs Nerv Syst. 2000;16(10-11): 702-706. 104. Moron FE, Morriss MC, Jones JJ, Hunter JV. Lumps and bumps on the head in children: use of CT and MR imaging in solving the clinical diagnostic dilemma. Radiographics. 2004;24(6):1655-1674. 105. Hunt JA, Hobar PC. Common craniofacial anomalies: facial clets and encephaloceles. Plast Reconstr Surg. 2003;112(2):606-615. 106. Tirumandas M, Sharma A, Gbenimacho I, et al. Nasal encephaloceles: a review of etiology, pathophysiology, clinical presentations, diagnosis, treatment, and complications. Childs Nerv Syst. 2013;29(5):739-744. 107. Chen CP. Syndromes, disorders and maternal risk factors associated with neural tube defects (I). Taiwan J Obstet Gynecol. 2008;47(1):1-9. 108. Copp AJ, Stanier P, Greene ND. Neural tube defects: recent advances, unsolved questions, and controversies. Lancet Neurol. 2013;12(8): 799-810. 109. Chen CP. Syndromes, disorders and maternal risk factors associated with neural tube defects (V). Taiwan J Obstet Gynecol. 2008;47(3): 259-266. 110. Brunelle F, Baraton J, Renier D, et al. Intracranial venous anomalies associated with atretic cephalocoeles. Pediatr Radiol. 2000;30(11):743-747. 111. Siverino RO, Guarrera V, Attina G, et al. Parietal atretic cephalocele: associated cerebral anomalies identiied by CT and MR imaging. Neuroradiol J. 2015;28(2):217-221. 112. Bannister CM, Russell SA, Rimmer S, et al. Can prognostic indicators be identiied in a fetus with an encephalocele? Eur J Pediatr Surg. 2000;10(Suppl. 1):20-23. 113. Bui CJ, Tubbs RS, Shannon CN, et al. Institutional experience with cranial vault encephaloceles. J Neurosurg. 2007;107(1 Suppl.):22-25. 114. Tissir F, Qu Y, Montcouquiol M, et al. Lack of cadherins Celsr2 and Celsr3 impairs ependymal ciliogenesis, leading to fatal hydrocephalus. Nat Neurosci. 2010;13(6):700-707. 115. Waters AM, Beales PL. Ciliopathies: an expanding disease spectrum. Pediatr Nephrol. 2011;26(7):1039-1056. 116. Brancati F, Dallapiccola B, Valente EM. Joubert syndrome and related disorders. Orphanet J Rare Dis. 2010;5:20. 117. Pugash D, Oh T, Godwin K, et al. Sonographic ‘molar tooth’ sign in the diagnosis of Joubert syndrome. Ultrasound Obstet Gynecol. 2011;38(5): 598-602. 118. Chen CP. Meckel syndrome: genetics, perinatal indings, and diferential diagnosis. Taiwan J Obstet Gynecol. 2007;46(1):9-14. 119. Aguirre-Pascual E, Epelman M, Johnson AM, et al. Prenatal MRI evaluation of limb-body wall complex. Pediatr Radiol. 2014;44(11):1412-1420. 120. Daltro P, Fricke BL, Kline-Fath BM, et al. Prenatal MRI of congenital abdominal and chest wall defects. AJR Am J Roentgenol. 2005;184(3): 1010-1016.

CHAPTER 34 121. Iqbal CW, Derderian SC, Cheng Y, et al. Amniotic band syndrome: a single-institutional experience. Fetal Diagn her. 2015;37(1):1-5. 122. D’Addario V, Rossi AC, Pinto V, et al. Comparison of six sonographic signs in the prenatal diagnosis of spina biida. J Perinat Med. 2008;36(4): 330-334. 123. Chen CP. Syndromes, disorders and maternal risk factors associated with neural tube defects (III). Taiwan J Obstet Gynecol. 2008;47(2):131-140. 124. hompson DN. Postnatal management and outcome for neural tube defects including spina biida and encephalocoeles. Prenat Diagn. 2009;29(4): 412-419. 125. Kawamura T, Morioka T, Nishio S, et al. Cerebral abnormalities in lumbosacral neural tube closure defect: MR imaging evaluation. Childs Nerv Syst. 2001;17(7):405-410. 126. McLone DG, Dias MS. he Chiari II malformation: cause and impact. Childs Nerv Syst. 2003;19(7-8):540-550. 127. Miller E, Widjaja E, Blaser S, et al. he old and the new: supratentorial MR indings in Chiari II malformation. Childs Nerv Syst. 2008;24(5): 563-575. 128. Stoll C, Dott B, Alembik Y, Roth MP. Associated malformations among infants with neural tube defects. Am J Med Genet A. 2011;155A(3): 565-568. 129. Nielsen LA, Maroun LL, Broholm H, et al. Neural tube defects and associated anomalies in a fetal and perinatal autopsy series. APMIS. 2006;114(4): 239-246. 130. Bahlmann F, Reinhard I, Schramm T, et al. Cranial and cerebral signs in the diagnosis of spina biida between 18 and 22 weeks of gestation: a German multicentre study. Prenat Diagn. 2015;35(3):228-235. 131. Bredaki FE, Poon LC, Birdir C, et al. First-trimester screening for neural tube defects using alpha-fetoprotein. Fetal Diagn her. 2012;31(2): 109-114. 132. Campbell J, Gilbert WM, Nicolaides KH, Campbell S. Ultrasound screening for spina biida: cranial and cerebellar signs in a high-risk population. Obstet Gynecol. 1987;70(2):247-250. 133. Ball RH, Filly RA, Goldstein RB, Callen PW. he lemon sign: not a speciic indicator of meningomyelocele. J Ultrasound Med. 1993;12(3):131-134. 134. Barkovich AJ, Gressens P, Evrard P. Formation, maturation, and disorders of brain neocortex. AJNR Am J Neuroradiol. 1992;13(2):423-446. 135. Callen AL, Filly RA. Supratentorial abnormalities in the Chiari II malformation, I: the ventricular “point.”. J Ultrasound Med. 2008;27(1):33-38. 136. Bernard JP, Cuckle HS, Stirnemann JJ, et al. Screening for fetal spina biida by ultrasound examination in the irst trimester of pregnancy using fetal biparietal diameter. Am J Obstet Gynecol. 2012;207(4):306 e1-306 e5. 137. Buisson O, De Keersmaecker B, Senat MV, et al. Sonographic diagnosis of spina biida at 12 weeks: heading towards indirect signs. Ultrasound Obstet Gynecol. 2002;19(3):290-292. 138. Chaoui R, Benoit B, Heling KS, et al. Prospective detection of open spina biida at 11-13 weeks by assessing intracranial translucency and posterior brain. Ultrasound Obstet Gynecol. 2011;38(6):722-726. 139. Chaoui R, Nicolaides KH. From nuchal translucency to intracranial translucency: towards the early detection of spina biida. Ultrasound Obstet Gynecol. 2010;35(2):133-138. 140. Chen FC, Gerhardt J, Entezami M, et al. Detection of spina biida by irst trimester screening—results of the prospective multicenter Berlin IT-Study. Ultraschall Med. 2017;38(2):151-157. 141. Finn M, Sutton D, Atkinson S, et al. he aqueduct of Sylvius: a sonographic landmark for neural tube defects in the irst trimester. Ultrasound Obstet Gynecol. 2011;38(6):640-645. 142. Kappou D, Papastefanou I, Pilalis A, et al. Towards detecting open spina biida in the irst trimester: the examination of the posterior brain. Fetal Diagn her. 2015;37(4):294-300. 143. Lachmann R, Chaoui R, Moratalla J, et al. Posterior brain in fetuses with open spina biida at 11 to 13 weeks. Prenat Diagn. 2011;31(1):103-106. 144. Lachmann R, Picciarelli G, Moratalla J, et al. Frontomaxillary facial angle in fetuses with spina biida at 11-13 weeks’ gestation. Ultrasound Obstet Gynecol. 2010;36(3):268-271. 145. Simon EG, Arthuis CJ, Haddad G, et al. Biparietal/transverse abdominal diameter ratio 97% of cases). his cranial lesion consists of variable degrees of displacement of the cerebellar vermis, fourth ventricle, and medulla oblongata through the foramen magnum into the upper cervical canal and is usually easier to identify than the spinal lesion between 16 and 24 weeks’ gestation. In transaxial scans through the posterior fossa, Chiari II malformation is manifest as a deformation of the cerebellar shape (banana sign) and nonvisualization of the cisterna magna. Cranial malformations may signal the sonographer that a detailed study of the spine is required to search for spina biida.

Anatomic Landmarks Used to Establish Level of Bony Defect • T12 corresponds to the medial ends of the most caudal ribs. • L5-S1 lies at the superior margin of the iliac wing.28 • S4 is the most caudal vertebral body ossiication center in the second trimester.65 • S5 is the most caudal vertebral body ossiication center in the third trimester.65 Thoracic (T), lumbar (L), and sacral (S) vertebrae.

CHAPTER 35

The Fetal Spine

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5 L

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FIG. 35.13 Myeloschisis. (A) Posterior transaxial scan shows splaying of the lumbar laminae (arrows) away from midline. Only a thin membrane (M) overlies the spinal defect posteriorly. (B) Posterior transaxial scan of the specimen after delivery shows in more detail the splaying of the laminae (arrows) away from midline and the membrane (M) covering the defect. (C) Lateral transaxial scan of specimen shows increased distance between the pedicles (curved arrows) and mild lateral angulation of the pedicles away from their expected positions (straight arrow, ossiied centrum). (D) Lateral longitudinal scan of specimen shows the progressive enlargement of the interpedicular distances in the lumbar spine, indicative of spina biida. Ossiied pedicles (straight arrows); iliac wing (curved arrow). (E) Posterior longitudinal scan of specimen shows abrupt truncation of the soft tissues of the fetal back (long arrow) at the site of the open neural tube defect; short arrow, spinal cord. (F) Radiograph of specimen shows divergence of the laminae (L) away from midline instead of the normal course, which is toward midline. (G) Photograph of myeloschisis defect of the thoracolumbar spine shows exposed, disorganized neural tissue within the defect. (H) Three-dimensional scan of another fetus at 19 weeks, as viewed from the posterior aspect of the fetus. Note the abnormal divergence of the pedicles in the lumbar spine (arrows, 12th rib level; 5, level L5). (I) Three-dimensional scan of a different fetus at 21 weeks, as viewed from the posterior aspect of the fetus. Note the divergence of the lumbar pedicles and the splaying of the laminae (L) away from the midline. (I courtesy of Siemens Ultrasound.)

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SC

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FIG. 35.14 Spina Biida With Myelomeningocele, 17 Weeks’ Gestation Specimen. (A) Posterior transaxial scan of the midlumbar spine shows the splaying of the laminae (curved arrows) and the myelomeningocele sac (short arrows). (B) Posterior longitudinal scan of the thoracolumbar area shows the myelomeningocele sac (short arrows) and disorganized neural tissue (long arrows) within it; SC, spinal cord. (C) Radiograph shows the interpedicular distances in the lumbar spine are widened and the laminae are splayed laterally (arrows). (D) Lateral transaxial scan in a different fetus shows the myelomeningocele sac (S) containing linear echoes representing neural tissue and the splayed laminae/pedicles complex (L, arrows).

Spinal dysraphism allows a leak of cerebrospinal luid from the spinal canal into the amniotic luid, which causes low intracranial pressure early in pregnancy. Low intracranial pressure induces a smaller-than-normal posterior fossa compartment. he cerebellum then grows into this abnormally small space, which leads to obliteration of the cisterna magna, compression

of the cerebellar hemispheres, herniation of the cerebellar tonsils into the cervical spinal canal, and related abnormalities such as ventriculomegaly. Ventriculomegaly is usually mild in the second trimester and worsens postpartum ater repair of the spinal defect. Ventriculomegaly is seen in 44% to 86% of fetuses with spina biida.71,72 he most common single cause of ventriculomegaly is

A

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FIG. 35.15 Skin-Covered Myelomeningocele. (A) Endovaginal posterior transaxial scan shows a myelomeningocele sac covered by a thick wall (arrowheads). Echogenic material passes through the spina biida defect into the myelomeningocele sac. Endocervical canal (arrows). (B) Endovaginal color Doppler posterior transaxial scan demonstrates a blood vessel protruding from the spinal canal into the myelomeningocele sac. (C) Endovaginal posterior longitudinal scan shows the myelomeningocele sac covered by a thick wall (arrowheads). (D) Neonatal picture shows the focal skin-covered lumbar myelomeningocele. The bluish tinge within the sac is a blood vessel detected by endovaginal color Doppler in B. (E) and (F) Longitudinal and posterior transaxial scans of a different fetus at 19 weeks’ gestational age demonstrate a small posterior cyst containing neural elements (calipers) covered by skin protruding through the splayed laminae. No intracranial abnormalities were demonstrated.

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A

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F F

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FIG. 35.16 Lumbar Meningocele, 34 Weeks’ Gestation. (A) Posterior transaxial sonogram demonstrates a luid-illed sac (short arrows) along the fetal back. There is a small defect in the neural arch (long arrow). (B) Posterior longitudinal sonogram shows the wall of the meningocele (short arrows) and the focal spina biida defect in the posterior neural arch (long arrow). (C) Posterior longitudinal and (D) posterior transaxial sonograms demonstrate abnormally posterior thoracic spinal cord (arrows) in the nondependent portion of the spinal canal. Cerebrospinal luid (F) is between the anterior aspect of the spinal cord and the anterior wall of the spinal canal.

spina biida, although only 30% to 40% of fetuses with enlarged ventricles actually have spina biida. On ultrasound, the Chiari II malformation manifests as obliteration of the cisterna magna.73,74 he compression of the cerebellum changes its shape, giving the banana sign.71,75 In two diferent series, obliteration of the cisterna magna was noted in 22 of 23 cases with spina biida

at 16 to 27 weeks’ gestation74 and in 18 of 20 cases at 24 weeks and earlier.74 Concave deformity of the fetal frontal bones in the second trimester is called the lemon sign.76 Various authors have shown that 85% of fetuses with spina biida before 24 weeks’ gestation have the lemon sign.72,77-79 In practice, the lemon sign can be

CHAPTER 35 diicult to portray unequivocally. he lemon sign spontaneously resolves in the third trimester.78 In addition, it is seen in 1% of normal fetuses.77,78 he lemon sign should prompt detailed examination of the posterior fossa, to search for obliteration of the cisterna magna and for the banana sign, and the fetal spine, for direct evidence of spina biida.

Associated Noncranial Abnormalities Foot deformities, primarily clubfoot, and dislocation of the hips are frequently associated with spina biida.80 hese abnormalities are caused by imbalanced muscular actions resulting from peripheral nerve involvement with the NTD. In fetuses with open spina biida, 24% demonstrate additional morphologic abnormalities on second-trimester sonography, such as renal abnormalities, choroid plexus cysts, cardiac ventricular septal defect, omphalocele, and intrauterine growth restriction.58

Sonographic Signs of Spina Biida Nonvisualization of cisterna magna Deformation of cerebellum (banana sign) Concave frontal bones (lemon sign) Dilation of the lateral ventricles Chiari II malformation (97%) Biparietal diameter lower than expected

Prognosis It is diicult to predict the long-term prognosis in a fetus with an identiied myelomeningocele. However, the outcome is better for low lesions (lower lumbar or sacral), closed defects, and those with minimal or no hydrocephalus and no compression of the hindbrain from Chiari II malformation.55,66,75,81 In more than 880 patients82 of live deliveries with spina biida, about 85% survived past age 10, and 2% died in the neonatal period. Of the survivors, about 50% had some type of learning disability. About 25% of survivors had an intelligence quotient (IQ) above 100, with about 75% above 80. About 33% of survivors developed symptoms and signs related to pressure on the hindbrain and brainstem (e.g., pain, weakness, and spasticity in arms), and some required cervical laminectomy to relieve the pressure. Wong and Paulozzi83 found 5-year survival rates of 82.7% for 1979-1983, 88.5% for 1984-1988, and 91.0% for 1989-1994. Determining prognosis for survival for current newborns is more diicult because of medical and surgical advances since studies describing patients born in the 1960s, 1970s, and 1980s.2 Beyond survival, multiple impairments may afect the individual, including motor dysfunction, bladder and bowel dysfunction, and intellectual impairment.2 Degree of muscle dysfunction is deined by the highest level of the open NTD, not by the number of involved vertebrae or the size of the overlying sac. When the lesion is thoracic, the legs are without muscle function, and when it is upper lumbar (L1-L2), useful leg function is minimal. When the upper level is L3-L5, the prognosis for longterm walking and the need for assistive devices are diicult to predict. hose with sacral defects will usually be able to walk well but with imperfect gait. Almost all people with spina biida,

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including those with sacral defects, will have some degree of bowel and bladder dysfunction. It is very diicult to predict the ultimate level of intellectual functioning. In general, those who do not require ventricular shunting have much better outcomes for intellectual functioning. In those requiring shunts, the average IQ is approximately 80, which is low-normal range.84 he rate of profound intellectual impairment (IQ < 20) in those with shunts is 5%, usually related to medical complications such as shunt infections and Chiari II efects (e.g., apnea, hypoxia).

Fetal Surgery for Myelomeningocele he irst fetal surgery for repair of myelomeningocele was performed in 1997. A formal clinical trial was performed from 2003 to 2010, with early termination of the study due to positive fetal results (decreased hindbrain herniation/need for shunt and improved spinal level of function). However, families and clinicians must evaluate the potential for improved function for the child against the risks of fetal/maternal surgical morbidity, most commonly preterm delivery and uterine dehiscence.85 Fetal myelomeningocele is a nonlethal entity; in utero surgery for repair of myelomeningocele is potentially lethal.86 Although myelomeningocele is a primary embryologic disorder, neurologic damage is also secondary to progressive in utero damage to the exposed spinal cord. he development of techniques to close open NTDs before birth has generated great interest and hope for fetal interventions and outcomes. Prior to the 2003 trial, preliminary observations from two centers suggested that improvements may occur not in spinal cord function as originally postulated87 but in the extent of the hindbrain herniation and the frequency that shunting is required to control hydrocephalus. In a report of 25 patients who underwent intrauterine myelomeningocele repair at Vanderbilt University, no improvement in leg function resulted from the surgery, but there was a substantially reduced incidence of moderate to severe hindbrain herniation (4% vs. 50%) and a moderate reduction in the incidence of shunt-dependent hydrocephalus (58% vs. 92%).88 he number of U.S. centers is limited to prevent the uncontrolled proliferation of new centers ofering this complex multidisciplinary procedure.89 Prospective parents electing surgery90 should weigh the potential beneits against the potential risks.90-93

MYELOCYSTOCELE Myelocystocele is an uncommon form of spinal dysraphism. here is dilation of the central canal of the spinal cord. he central canal herniates posteriorly through the spinal cord and through the posterior neural arch to form an exterior sac. here may be no associated spina biida lesion. he sac is composed of three layers, from inner to outer: the hydromyelia sac, which is lined by spinal canal ependyma; the meningeal layer, which is contiguous with the meninges around the spinal cord; and the skin. he luid within the inner sac is continuous with the luid of the central canal of the spinal cord; the luid between the hydromyelia sac and the meningeal layer is continuous with the subarachnoid luid.

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Myelocystocele may occur at any level of the spine and is oten associated with Chiari II malformation.94-96 Prenatal and postnatal sonography demonstrates a “cyst within a cyst” appearance (Fig. 35.17). Splaying of the laminae and pedicles may or may not be present. he prognosis for a myelocystocele is worse than for a simple meningocele; infants with a simple meningocele may remain normal neurologically ater surgical repair. he prognosis with myelocystocele is worse because there is usually some degree of associated myelodysplasia (i.e., dysplasia of spinal cord). Although neurologic function is normal in the immediate postoperative period, neurologic deicits oten become apparent later in life. A terminal myelocystocele occurs at the spinal cord termination. he central canal of the spinal cord herniates with overlying

arachnoid and cerebrospinal luid through a defect in posterior spinal elements and presents as a skin-covered mass along the posterior aspect of the lumbosacral area. here may be associated maldevelopment of the lower spine, pelvis, genitalia, bowel, bladder, kidneys, and abdominal wall. MRI provides the best imaging evaluation of the morphologic abnormalities ater birth.97-99

DIASTEMATOMYELIA Diastematomyelia, also termed split-cord malformation, is a partial or complete sagittal clet in the spinal cord, the distal conus of the cord, or ilum terminale. Diastematomyelia is characterized by a sagittal osseous or ibrous septum in the spinal

C H C

A

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C

C

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FIG. 35.17 Myelocystocele. (A) Coronal sonogram of thoracic spine at 18 weeks’ gestation demonstrates a double-walled cystic mass (arrows) with inner cystic component (C) arising from the upper thoracic area. (B) Axial sonogram of the fetal chest 1 week later demonstrates a double-walled cystic mass (arrows) arising along the posterior aspect of the fetal chest; H, fetal heart. The inner cystic component (C) is slightly smaller and lattened compared to the irst scan. No abnormality was noted in the ossiied neural arch. (C) Sonogram of the specimen demonstrates the double-walled cystic mass (white arrows) arising from the posterior thorax with a hypoechoic tract (black arrows) extending from the posterior aspect of the spinal cord (curved arrow) toward the central cystic component (C) of the posterior mass. (D) CT scan of the specimen after injection of water-soluble contrast material into the cyst demonstrates contrast within the cyst (C) and within a sinus tract (short arrows), leading to the spinal cord (long arrow).

Continued

CHAPTER 35

The Fetal Spine

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S C C

C

E

F W

S

G

W

S M CC

C W

E

M

H FIG. 35.17, cont’d (E) Lateral view of the posterior cystic thoracic mass (C). (F) Sagittal magnetic resonance scan demonstrates the cystic mass along the upper thoracic area, with the small sinus tract (arrows) extending from the posterior aspect of the spinal cord (S) toward the cystic mass (C). (G) Gross pathologic specimen demonstrates the collapsed cyst (C) in contiguity with the cervical portion of the spinal cord (S). (H) Histologic section shows abnormal channel (arrows) communicating with the posterior aspect of the spinal cord (S), as well as defect in the posterior spinal cord (arrowheads) communicating with the central canal (CC) of the spinal cord. C, Central cystic component of posterior mass (M); E, ependymal lining of central cyst, which communicates with central canal of spinal cord; W, outer wall of cystic mass.

cord.100,101 his may be associated with a spina biida defect and hydromyelia (dilation of central canal of spinal cord) but may occur in the absence of overt spina biida.102 Diastematomyelia may also be associated with segmental anomalies of the vertebral bodies or visceral malformations such as horseshoe or ectopic kidney, utero-ovarian malformation, and anorectal malformation. If the spinal canal is traversed by a bony septum or spur, the septum will appear as an abnormal hyperechoic focus,103-105 which is best demonstrated in the posterior transaxial and lateral longitudinal scan planes (Fig. 35.18). When diastematomyelia is not associated with other spinal anomalies, the prognosis is favorable. In seven of eight cases reported by Has et al.,106 the defects had normal amniotic AFP and AChE levels and were considered isolated. heir review of the literature showed 26 cases diagnosed prenatally, 12 of which had no associated abnormality and had a favorable prognosis.

SCOLIOSIS AND KYPHOSIS Kyphosis is exaggerated curvature of the spine in the sagittal plane. Scoliosis is lateral curvature of the spine in the coronal

plane. Kyphosis and scoliosis may be positional and nonpathologic or permanent based on an underlying structural abnormality, such as hemivertebrae, butterly vertebrae, and block vertebrae. Pathologic kyphosis and scoliosis are oten associated with spina biida or ventral abdominal wall defects.107 Less common associations include limb–body wall complex, amniotic band syndrome, arthrogryposis, skeletal dysplasias, VACTERL association (vertebral abnormalities, anal atresia, cardiac abnormalities, tracheoesophageal istula, renal agenesis, and limb defects),108,109 and caudal regression syndrome. Mild scoliosis may be caused by a hemivertebra (Fig. 35.19).106,109 he posterior longitudinal scan is the best view to assess for kyphosis; the lateral longitudinal plane is the best to assess for scoliosis (Fig. 35.19). Because oligohydramnios can cause positional curvature in the fetal spine, a conident diagnosis of pathologic kyphosis or scoliosis should be made only if the curvature is severe. Possible associated anomalies must then be sought because prognosis depends on the coexistent anomalies. A hemivertebra represents underdevelopment or nondevelopment of one-half of a vertebral body; that is, one of the two early

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FIG. 35.18 Diastematomyelia. (A) Coronal and (B) axial sonograms of the spine demonstrate two hyperechoic foci (arrows) caused by the bony septum within the spinal canal with intact skin along the fetal back. (C) Anteroposterior radiograph and (D) CT scan demonstrate a bony septum (arrows) within the central portion of the spinal canal. (E) Diplomyelia and tethered cord. Posterior transaxial sonogram of another fetus shows cord in the nondependent portion of the spinal canal with luid (F) interposed between the cord and anterior margin of the spinal canal. The anterior aspect of the cord has a bilobed shape instead of a smooth, circular arc with bilateral central canal echoes (arrows).

A

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FIG. 35.19 Kyphosis. (A) Sagittal scan of the spine demonstrates a focal kyphosis at the thoracolumbar junction. (B) Three-dimensional image of the same patient demonstrates a left upper lumbar hemivertebra as the cause of the kyphosis.

CHAPTER 35 chondriication centers is deicient. he remaining ossiication center is displaced laterally with respect to the vertebrae above and below it, leading to a short-segment mild scoliosis. he abnormalities can be detected prenatally and may be best portrayed with 3D ultrasound.31-34 Fetuses with an isolated

a

Vertebral abnormalities, anal atresia, cardiac abnormalities, tracheoesophageal istula, renal agenesis, and limb defects.

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hemivertebra have an excellent prognosis, whereas those with other fetal anomalies (e.g., Potter syndrome; cardiac, intestinal, intracranial, and limb anomalies) have a poor prognosis.110 he presence of associated anomalies reduces the survival rate to approximately 50%. If oligohydramnios is also present, the mortality rate approaches 100%.111

Causes of Scoliosis or Kyphosis Hemivertebrae Butterly vertebrae Block vertebrae Spina biida Ventral abdominal wall defects Limb–body wall complex Amniotic band syndrome Arthrogryposis Skeletal dysplasias VACTERLa association Caudal regression syndrome

The Fetal Spine

SACRAL AGENESIS Sacral agenesis is an uncommon fetal abnormality that may be present in conditions such as caudal regression sequence, sirenomelia sequence, cloacal exstrophy sequence, and the VACTERL association. he caudal regression sequence (caudal regression syndrome) and the sirenomelia sequence are thought to be separate pathologic entities.112,113

CAUDAL REGRESSION In caudal regression or dysplasia, abnormalities of the lower spine and limbs occur, including sacral agenesis, lumbar spine deiciency, and leg anomalies such as femoral hypoplasia (Fig. 35.20). Defects of the neural tube and the genitourinary,

B

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FIG. 35.20 Caudal Regression. (A) Sagittal sonogram of spine at 21 weeks shows abrupt termination of ossiied vertebral bodies. (B) Transverse view of pelvis with legs in long axis shows lack of ossiied pelvic bones and atrophic musculature about the lower extremities. (C) Transverse color Doppler image at level of bladder shows lack of ossiied pelvic bones. (D) In a different fetal specimen, radiograph shows abrupt termination (arrows) of the lumbar spine and absence of the sacrum. The pelvic bones are small and deformed.

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F

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FIG. 35.21 Sirenomelia. (A) Sagittal view of fetus at 12 weeks’ gestation shows unusual angulation of lower extremity. (B) Long-axis view of a single lower extremity. (C) In a different fetus, radiograph shows single femur (F) and single tibia (T). Note the segmented defects in the vertebrae of the thoracic and lumbar spine (arrows).

gastrointestinal, and cardiac systems are common. Occurrence is sporadic; caudal regression is more common in infants of mothers with diabetes mellitus. he cause has not been established. Sonography can demonstrate absence of the sacrum and shortened femurs. he legs can be lexed and abducted at the hips, and there may be clubfoot. Sonography may detect associated urinary anomalies (renal agenesis, cystic dysplasia, caliectasis) and gastrointestinal abnormalities (e.g., duodenal atresia).114 he prognosis depends on the severity and extent of the skeletal abnormalities and associated anomalies. In sacral agenesis with no internal organ involvement, there are usually deicits in the legs and deicient control of bladder and bowel functions. In infants with internal organ involvement, the prognosis is related to these defects.

SIRENOMELIA Sirenomelia sequence is a rare disorder in which the legs are fused and the feet are deformed or absent115 (Fig. 35.21). he cause is probably an aberrant fetal artery that branches from the upper abdominal aorta and passes into the umbilical cord to the placenta.116 Arterial blood low bypasses the lower fetal body. he distal abdominal aorta, the aorta’s distal branches, and subtended structures are small and underdeveloped. his leads to malformations of spine, legs, kidneys, gut, and genitalia. Normally the umbilical arteries, which arise from the fetal iliac arteries, carry blood from the fetus into the umbilical cord and then into the placenta. At sonography, there is advanced oligohydramnios because of reduced or absent renal function. he legs are fused, or there is a single leg. he feet are absent, or there may be a single foot. here may be sacral agenesis, deiciency of the lower lumbar spine, and thoracic anomalies. hese indings may be diicult to appreciate because of the advanced oligohydramnios or anhydramnios.112 he prolonged anhydramnios causes pulmonary hypoplasia, which is usually fatal. he risk of recurrence is the same as in the general population.

SACROCOCCYGEAL TERATOMA Fetal teratomas may arise from the sacrum or coccyx, from other midline structures from the level of the brain to the coccyx, or from the gonads.117 Sacrococcygeal teratomas arise from the pluripotent cells of Hensen node located anterior to the coccyx. Sacrococcygeal teratomas contain all three germ layers (ectoderm, mesoderm, and endoderm) and thus may contain elements of many tissues, including neural, respiratory, and gastrointestinal. Sacrococcygeal tumor is rare (1 : 35,000 births)118 but is the most common tumor among neonates. Females are afected four times more frequently than males. Sacrococcygeal teratomas are classiied into four types118: type I, tumor predominantly external with only minimal presacral involvement; type II, tumor presenting externally but with signiicant intrapelvic extension; type III, tumor apparent externally but with predominant pelvic mass and extension into the abdomen; type IV, tumor presacral with no external presentation (Fig. 35.22).117

Types of Sacrococcygeal Teratomas Type I (47%): external mass predominant Type II (34%): external mass with signiicant internal component Type III (9%): internal mass predominant, with smaller external component Type IV (10%): presacral mass only

At birth, 75% of sacrococcygeal teratomas are benign, 12% are immature, and 13% are malignant. Because malignant potential increases with the age of the infant, surgery must be performed shortly ater birth. Sonography usually demonstrates a mass in the rump or buttocks area adjacent to the spine119 (Video 35.6). Most teratomas (85%) are either solid or mixed (solid and cystic); 15% are mostly cystic, which is a benign sign. Calciications are frequently present.

CHAPTER 35

The Fetal Spine

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B S

SCT

SCT SCT

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FIG. 35.22 Sacrococcygeal Teratoma. (A) Sagittal sonogram shows type II sacrococcygeal teratoma (SCT) that is predominantly external but has a substantial intrapelvic component. The tumor extends up to level L5 and displaces the fetal urinary bladder (B) anteriorly. Note the calciications (arrows) within the tumor. (B) T2-weighted sagittal magnetic resonance image demonstrates the extent and internal structure of the sacrococcygeal tumor (SCT); S, stomach. (C) Lateral radiograph in a different neonate. (A and B courtesy of Drs. Fong, Pantazi, and Toi, Mt. Sinai Hospital, Toronto.)

Large masses may displace and distort neighboring structures, such as the rectum and urinary bladder (see Fig. 35.22). Compression of the distal ureters may cause hydronephrosis. Larger solid tumors may develop substantial arteriovenous shunting, causing fetal cardiac failure and hydrops.120 he development of hydrops in the presence of a sacrococcygeal teratoma carries a poor prognosis.120-124

than 4.5 cm diameter, cesarean section may be considered because of the risk of dystocia and hemorrhage during vaginal delivery. In utero surgery for arteriovenous shunting has been described for treatment of fetal hydrops from congestive heart failure in early pregnancy ( 20% LHR, Lung-to-head ratio; LiTR, liver to fetal thoracic volume ratio; MRI, magnetic resonance imaging; o/e, observed-to-expected; PPLV, percent predicted lung volume; TFLV, total fetal lung volume.

Prenatal pulmonary artery measurements at the hila at the level of the four-chamber view have been performed.211-214 Measuring the main right and let pulmonary artery and comparing with normals via an observed-to-expected ratio shows a reduction in values in fetuses with CDH and pulmonary hypoplasia. Doppler wave forms have been useful in deining the most severe CDH cases. Increased pulmonary artery pulsatility index (>1) and peak early diastolic reversed low in the main pulmonary artery (>3.5) relect high resistance in pulmonary vascular bed with preferential low through the ductus arteriosus and are correlated with poor lung growth.215,216 Other tests utilized in CDH include a hyperoxygenation test for pulmonary vascular reactivity at 31 to 36 weeks’ gestation, in which reactivity (20% reduction in pulmonary artery pretest pulsatility index) suggests a good outcome,217,218 and assessment of fractional moving blood volume because a decrease in this fraction is correlated with decreased lung growth and an increased intrapulmonary artery impedance in CDH.219-223 Patients with fetuses with CDH generally undergo extensive prenatal imaging and counseling. Follow-up ultrasound examinations should be performed to assess fetal well-being, amniotic luid levels, lung volume, and changes in mediastinal shit that could result in hemodynamic changes.

Other Hernias and Eventration In bilateral hernias the falciform ligament is drawn into the hernia.224,225 Mediastinal shit is variable, but typically the heart is displaced anteriorly and superiorly. Features of both right- and let-sided CDH are present. Pericardial hernias result from failure of the retrosternal portion of the septum transversum to close the communication between the pericardial and peritoneal cavities.226 he liver may herniate into the pericardial sac.171,225 Pericardial efusion results from mass efect on the heart and obstruction of venous return or from mechanical irritation of membranes.227 Because the diferential diagnosis of a pericardial mass includes pericardial tumors such as teratoma, it is important to recognize the liver as part of the hernial sac contents by identifying the hepatic vessels in the mass.219,228 In diaphragmatic eventration the intact diaphragm is displaced cephalad at the weakened muscular portion, without communication between the abdominal and thoracic cavities229 (Fig. 36.15). Diaphragmatic eventration is associated with a lower

CHAPTER 36

Right

The Fetal Chest

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perinatal mortality rate compared to CDH and may not require surgical repair. hus it is crucial to make the distinction between the two diagnoses to provide appropriate counseling.

Associated Anomalies CDH may be an isolated defect or may be associated with other structural, chromosomal, or syndromal anomalies. Associated anomalies are present in 25% to 55% of cases. Congenital heart disease is the most common association (20%), with hemodynamically signiicant heart disease in 11% of cases.230-232 Because of the high rate of associated cardiac abnormalities, formal fetal echocardiography is indicated in fetuses with CDH.

B

FIG. 36.15 Eventration of the Hemidiaphragm. (A) Transverse view of the thorax demonstrates the stomach in the thorax with mild mediastinal shift. (B) Coronal and (C) sagittal T2-weighted MRI shows the high position of stomach with intact diaphragm.

Associated central nervous system anomalies are second in frequency of associated structural abnormalities in fetuses with CDH; these anomalies include anencephaly, ventriculomegaly, and neural tube defects.191 Chromosomal abnormalities occur in 10% to 20% of antenatally detected CDH, the most common being trisomy 18.192,193 Chromosomal abnormalities are most common when CDH is present in association with other structural abnormalities. Given the high association with aneuploidy, chromosomal assessment is typically performed. Associated syndromes include Fryn, Beckwith-Wiedemann, Simpson-Golabi-Behmel, Brachmann–de Lange, and Perlman.195

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TABLE 36.5 Sample Studies of Predictors of Survival in Left-Sided Congenital Diaphragmatic Hernia Imaging Findings

Sign/ Value

Liver position208

Liver up Liver down 1

1.5 MoM)

MCV of parents to check for thalassemia ( 1.5 MoM or hydropic), unless the pregnancy is at a gestational age when risks associated with delivery are considered to be less than those associated with the procedure.203 If it is anticipated that the fetus may require transfusion (e.g., parvovirus infection with elevated MCA Doppler velocity), it is prudent to have crossmatched blood and platelets ready to avoid the risks with a second procedure. PUBS is usually performed in a setting that allows maternal sedation and intervention for fetal distress ater 24 weeks, most oten an operating room for labor and delivery. he patient is prepped and sterilely draped and the uterus displaced slightly to the let with appropriate maternal wedging. he ultrasound transducer is draped with a sterile sheath to allow guidance on the sterile ield. he patient is oten given conscious sedation for comfort and to minimize maternal movement during the procedure. Local anesthetic with lidocaine may be used for patient comfort. Ultrasound guidance may be provided by a second

C

F P

FIG. 41.28 Cordocentesis. Transverse ultrasound image shows needle (arrows) traversing placenta (P) and entering placental cord insertion. Note loop of umbilical cord (C) and fetus (F).

provider or by the operator using a freehand technique. A 20- to 22-gauge needle is typically used, and most oten the umbilical vein is targeted at the placental cord insertion (Fig. 41.28). Other approaches include the umbilical vein at the fetal cord insertion or a free loop of cord. he needle position is conirmed by obtaining a blood specimen, ultrasound observation of the needle in the vein, and sonographic streaming within the umbilical vein ater injection of saline. Heparinized syringes are used for fetal blood sampling, and values for hemoglobin/hematocrit, platelets, and mean corpuscular volume (MCV) are obtained. he fetal MCV (which should be >100 µm3) is higher than the maternal value and can help conirm fetal origin of the blood sample. Depending on the insertion site and indication for cordocentesis, fetal paralysis can be considered with vecuronium (0.1 mg/kg estimated fetal weight)204 or atracurium besylate (0.4 mg/kg estimated fetal weight).205 Fetal cardiac activity is documented throughout the procedure. he fetal hematocrit is checked to determine the amount of transfusion needed (Hct < 30% is 2.5th centile >20 weeks). To limit the amount of luid being transfused into the relatively small circulatory capacity of the fetus, packed RBCs (type O negative; Hct > 90%) are given. he goal is to transfuse to Hct of 40 mL/dL. Successful treatment of anemia with intravascular blood transfusion has been reported as early as 13 weeks’ gestation.145 When performing PUBS it is important to have a team involved that includes genetic counselors (regarding the underlying cause of anemia), laboratory medicine professionals (to check the MCV and have packed RBCs available), and maternal fetal medicine specialists as well as individuals familiar with guidance for procedures with ultrasound. When PUBS is not possible, particularly at early gestational age when the umbilical cord is small and diicult to safely

CHAPTER 41

Fetal Hydrops

1435

sampling or amniocentesis (Fig. 41.30). his can be both diagnostic (e.g., lymphocyte count in chylothorax or for rapid karyotype) and occasionally therapeutic. Simultaneous sampling does not increase the overall procedure risk.

Postnatal Investigations Ater birth, the placenta should be sent for pathologic analysis, and a skeletal survey may be helpful. A geneticist may see the neonate to provide additional input. In cases of death, detailed autopsy and placental examination, correlated with antenatal indings, is the best way to determine the cause of nonimmune hydrops.210,211 Further investigations may be prompted by additional physical indings at autopsy.212 If a metabolic condition is suspected as the cause of hydrops, inclusion bodies can be sought on microscopy. In some series the cause of hydrops was identiied in only 40% to 50% of patients without autopsy,135 versus 80% to 90% ater postmortem examination.210,213

FETAL WELFARE ASSESSMENT IN NONIMMUNE HYDROPS FIG. 41.29 Fetal Blood Sampling in Intrahepatic Portion of Umbilical Vein. Arrows point to the position of the 20-gauge needle in the intrahepatic portion of the umbilical vein.

instrument, intraperitoneal, intrahepatic (Fig. 41.29), or intracardiac transfusion can be performed.206

Fetal Transfusion If fetal transfusion is required, T-connector tubing is oten employed for ease of transfusion. he volume to be transfused can be calculated by using the following formula207: Volume transfused (mL) = Volume fetoplacental unit (mL)  Hematocrit final − Hematocrit initial  ×  Hematocrit transfused blood  he fetoplacental volume can be estimated as 1.046 + fetal weight in grams × 0.14.207 Either maternal cells or donated O-negative, washed, leukocyte-reduced blood is used for transfusion. Maternal cells may be consumed less rapidly than anonymous donation, but timing and pregnancy-associated anemia limit its use.208 A posttransfusion sample is obtained to evaluate the efects of the procedure. Future transfusions are scheduled based on fetal Doppler assessment26 or by estimating a 0.7% decrease in the hematocrit per day and scheduling transfusion for estimated hematocrits of 20 to 22 mL/dL.209 If the cordocentesis or transfusion is being performed for reasons other than Rh(D) isoimmunization, in a Rh(D)-negative mother, RhoGAM should be administered ater the procedure.

Cavity Aspiration he clinician can usually advance the needle easily into the fetal chest, abdomen, or amniotic luid at the time of fetal blood

Noninvasive ultrasound techniques for fetal well-being assessment in pregnancies complicated by nonimmune hydrops include biophysical assessment, pulsed Doppler velocimetry of umbilical and regional fetal vessels, and functional cardiac assessment. Fetal Doppler evaluation may give some indication of anemia, cardiac failure, and well-being.25 Umbilical vein and intrahepatic vein pulsations, or ductus venosus a-wave reversal, represent cardiac diastolic dysfunction and have been correlated with poor perinatal outcomes.214

OBSTETRIC PROGNOSIS he overall mortality rate among fetuses with nonimmune hydrops is approximately 70%,31 with mortality in cases of structural abnormalities not amenable to therapy as high as 100%. In a series of 100 cases of nonimmune hydrops, 74 were thought to have a nontreatable cause, and none of these resulted in a live birth; of 26 with a treatable cause, 18 resulted in a live birth and were alive at 1 year of age.31 Gestational age at diagnosis of hydrops has been used to predict outcome. A 10-year review of 82 cases presenting ater 20 weeks135 reported an overall mortality rate of 87%, and those diagnosed ater 24 weeks were more likely to be idiopathic or related to cardiothoracic abnormalities. Spontaneous resolution of hydrops has been reported in fetuses with normal chromosomes diagnosed before 24 weeks. Although the overall prognosis for fetal hydrops has improved in recent years, most series are small with a mixture of causes and thus are diicult to compare. Some improvement in outcome over earlier reports is attributable to the growing number of cases that are amenable to in utero therapy. Unfortunately, many cases still represent a terminal process. Earlier identiication and referral, thorough evaluation, and fetal therapy in appropriate cases are the cornerstone to further improvements in prognosis. Obtaining the best diagnosis is helpful in counseling about recurrence risks.

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Maternal Complications (Mirror Syndrome) Maternal complications may occur in association with fetal hydrops. Hypoproteinemia, edema, weight gain, hypertension, oliguria, and preeclampsia may develop.215 his association has been termed mirror syndrome because edema in the pregnant patient mirrors that of the hydropic fetus.34,216,217 he syndrome has been described in conjunction with hydrops of various causes.215,218,219 Perinatal mortality and morbidity rates are high. Maternal outcome can be improved by delivery of the fetus and placenta or by fetal intervention to treat the cause of the hydrops.217,220-222 If hydrops cannot be cured, delivery may limit the risk of maternal complications.35,222 Espinoza et al.223 recently suggested the high plasma concentrations of soluble vascular endothelial growth factor receptor 1 (sVEGFR-1) is implicated in the pathophysiology of mirror syndrome. Hypoxia of the villous trophoblast in cases of villous edema leads to increased production and release of sVEGFR-1

B

FIG. 41.30 Drainage of Ascites in Fetus at 26 Weeks With Lymphatic Duct Dysplasia. (A) Transverse view of fetal abdomen shows ascites with omentum (arrows) outlined by ascitic luid. (B) and (C) Images during draining procedure show the needle in the amniotic luid (B) and ascitic luid (C).

and other antiangiogenic factors into the maternal circulation. Excessive concentrations of these products may be responsible for maternal edema in mirror syndrome.

Delivery Mode and location of delivery are based on obstetric factors, taking into account the underlying prognosis.224 Uterine overdistention in severe polyhydramnios carries the risks of placental abruption and cord prolapse ater membrane rupture and postpartum hemorrhage from uterine atony. Prematurity secondary to polyhydramnios is a major contributing factor to the poor outcome of some neonates. herapeutic amniocentesis before induction of labor may be considered in cases with massive polyhydramnios to decrease the risk of malpresentation or cord prolapse. Indomethacin has also been used to decrease the amniotic luid volume.225 his drug should be used with caution ater 32 weeks’ gestation because of the potential for ductal constriction.

CHAPTER 41

Predelivery Aspiration Procedures Fetal luid collections may be drained under ultrasound guidance just before delivery to assist with neonatal resuscitation. his is particularly relevant if large fetal pleural efusions are present.115 Massive ascites may also be drained to prevent abdominal dystocia (when vaginal birth is planned) and aid in fetal breathing when ascites has caused elevation of the diaphragms.

Postnatal Outcome Because of the high incidence of in utero demise, the cause of hydrops in utero is diferent from that with a live neonate. In a review of 30 cases of hydrops diagnosed between 10 and 14 weeks of pregnancy, all pregnancies with nonimmune hydrops resulted in abortion, intrauterine fetal death, or pregnancy termination.136 A 2007 national database review of live-born neonates with hydrops found heart problems (13.7%), abnormalities in heart rate (10.4%), TTTS (9%), congenital anomalies (8.7%), chromosomal abnormalities (7.5%), congenital viral infections (6.7%), isoimmunization (4.5%), and congenital chylothorax (3.2%).226 Mortality rates were highest among neonates with congenital anomalies (57.7%) and lowest among those with congenital chylothorax (5.9%), and a cause could not be determined in 26%. Factors associated independently with death were younger gestational age, low 5-minute Apgar score, and high levels of support needed the irst day ater birth.226 his study reported a 36% death rate before discharge or transfer to another hospital. he severity of hydrops and birth gestational age of the infant are the key determinants for survival. his is important because delivering a fetus early to treat worsening hydrops may not improve survival. Data are limited regarding long-term outcome of children surviving ater hydrops. In one series, 13 in 19 (68%) children surviving beyond 1 year of age were normal; two had mild developmental delay at 1 year of age; one 8-year-old child was mentally retarded; and three (16%) had severe psychomotor impairment with marked growth failure.227 Haverkamp et al.228 found that 86% of patients had normal psychomotor development, 86% showed normal neurologic status, 7% had minor neurologic dysfunction, and 4% had spastic cerebral paresis.

CONCLUSION Hydrops represents a terminal stage for many conditions, the vast majority of which are fetal in origin. he onset of hydrops signiies fetal decompensation. Immune causes can be successfully treated in utero, as can an increasing number of nonimmune causes. Whereas in the past, nonimmune hydrops carried virtually 100% mortality, this is no longer the case. A team approach using obstetric imagers, maternal fetal medicine specialists, neonatologists, and geneticists can help to decide which cases are suitable for therapeutic intervention. A comprehensive approach must be taken to the investigation of hydrops, both for the management of the index case and for future counseling. Cornerstones of this investigation are detailed ultrasound, including echocardiography, fetal karyotyping, and other

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survival of Hb Bart’s hydrops syndrome leads to new aspects for counselling of alpha-thalassaemic traits. Eur J Pediatr. 1999;158(3):217-220. Kempe A, Rosing B, Berg C, et al. First-trimester treatment of fetal anemia secondary to parvovirus B19 infection. Ultrasound Obstet Gynecol. 2007; 29(2):226-228. Perkins RP. Hydrops fetalis and stillbirth in a male glucose-6-phosphate dehydrogenase-deicient fetus possibly due to maternal ingestion of sulisoxazole; a case report. Am J Obstet Gynecol. 1971;111(3):379-381. Lallemand AV, Doco-Fenzy M, Gaillard DA. Investigation of nonimmune hydrops fetalis: multidisciplinary studies are necessary for diagnosis—review of 94 cases. Pediatr Dev Pathol. 1999;2(5):432-439. Rodriguez MM, Chaves F, Romaguera RL, et al. Value of autopsy in nonimmune hydrops fetalis: series of 51 stillborn fetuses. Pediatr Dev Pathol. 2002;5(4):365-374. Barron SD, Pass RF. Infectious causes of hydrops fetalis. Semin Perinatol. 1995;19(6):493-501. Porter HJ, Quantrill AM, Fleming KA. B19 parvovirus infection of myocardial cells. Lancet. 1988;1(8584):535-536. Naides SJ, Weiner CP. Antenatal diagnosis and palliative treatment of non-immune hydrops fetalis secondary to fetal parvovirus B19 infection. Prenat Diagn. 1989;9(2):105-114. Morey AL, Keeling JW, Porter HJ, Fleming KA. Clinical and histopathological features of parvovirus B19 infection in the human fetus. Br J Obstet Gynaecol. 1992;99(7):566-574. Oyer CE, Ongcapin EH, Ni J, et al. Fatal intrauterine adenoviral endomyocarditis with aortic and pulmonary valve stenosis: diagnosis by polymerase chain reaction. Hum Pathol. 2000;31(11):1433-1435. Bates Jr HR. Coxsackie virus B3 calciic pancarditis and hydrops fetalis. Am J Obstet Gynecol. 1970;106(4):629-630. von Kaisenberg CS, Jonat W. Fetal parvovirus B19 infection. Ultrasound Obstet Gynecol. 2001;18(3):280-288. Gray ES, Davidson RJ, Anand A. Human parvovirus and fetal anaemia. Lancet. 1987;1(8542):1144. Miller E, Fairley CK, Cohen BJ, Seng C. Immediate and long term outcome of human parvovirus B19 infection in pregnancy. Br J Obstet Gynaecol. 1998;105(2):174-178. Bhal PS, Davies NJ, Westmoreland D, Jones A. Spontaneous resolution of non-immune hydrops fetalis secondary to transplacental parvovirus B19 infection. Ultrasound Obstet Gynecol. 1996;7(1):55-57. Pryde PG, Nugent CE, Pridjian G, et al. Spontaneous resolution of nonimmune hydrops fetalis secondary to human parvovirus B19 infection. Obstet Gynecol. 1992;79(5 Pt 2):859-861. Humphrey W, Magoon M, O’Shaughnessy R. Severe nonimmune hydrops secondary to parvovirus B-19 infection: spontaneous reversal in utero and survival of a term infant. Obstet Gynecol. 1991;78(5 Pt 2): 900-902. Cossart YE, Field AM, Cant B, Widdows D. Parvovirus-like particles in human sera. Lancet. 1975;1(7898):72-73. Kovacs BW, Carlson DE, Shahbahrami B, Platt LD. Prenatal diagnosis of human parvovirus B19 in nonimmune hydrops fetalis by polymerase chain reaction. Am J Obstet Gynecol. 1992;167(2):461-466. Nagel HT, de Haan TR, Vandenbussche FP, et al. Long-term outcome ater fetal transfusion for hydrops associated with parvovirus B19 infection. Obstet Gynecol. 2007;109(1):42-47. Dembinski J, Haverkamp F, Maara H, et al. Neurodevelopmental outcome ater intrauterine red cell transfusion for parvovirus B19-induced fetal hydrops. BJOG. 2002;109(11):1232-1234. De Jong EP, Lindenburg IT, van Klink JM, et al. Intrauterine transfusion for parvovirus B19 infection: long-term neurodevelopmental outcome. Am J Obstet Gynecol. 2012;206(3):204.e1-204.e5. Dafos F, Forestier F, Capella-Pavlovsky M, et al. Prenatal management of 746 pregnancies at risk for congenital toxoplasmosis. N Engl J Med. 1988;318(5):271-275. Friedman S, Ford-Jones LE, Toi A, et al. Congenital toxoplasmosis: prenatal diagnosis, treatment and postnatal outcome. Prenat Diagn. 1999; 19(4):330-333. Zornes SL, Anderson PG, Lott RL. Congenital toxoplasmosis in an infant with hydrops fetalis. South Med J. 1988;81(3):391-393.

CHAPTER 41 169. Inoue T, Matsumura N, Fukuoka M, et al. Severe congenital cytomegalovirus infection with fetal hydrops in a cytomegalovirus-seropositive healthy woman. Eur J Obstet Gynecol Reprod Biol. 2001;95(2):184-186. 170. Revello MG, Gerna G. Diagnosis and management of human cytomegalovirus infection in the mother, fetus, and newborn infant. Clin Microbiol Rev. 2002;15(4):680-715. 171. Negishi H, Yamada H, Hirayama E, et al. Intraperitoneal administration of cytomegalovirus hyperimmunoglobulin to the cytomegalovirus-infected fetus. J Perinatol. 1998;18(6 Pt 1):466-469. 172. Barton JR, horpe Jr EM, Shaver DC, et al. Nonimmune hydrops fetalis associated with maternal infection with syphilis. Am J Obstet Gynecol. 1992;167(1):56-58. 173. Harger JH, Ernest JM, hurnau GR, et al. Frequency of congenital varicella syndrome in a prospective cohort of 347 pregnant women. Obstet Gynecol. 2002;100(2):260-265. 174. Anderson MS, Abzug MJ. Hydrops fetalis: an unusual presentation of intrauterine herpes simplex virus infection. Pediatr Infect Dis J. 1999; 18(9):837-839. 175. Ashshi AM, Cooper RJ, Klapper PE, et al. Detection of human herpes virus 6 DNA in fetal hydrops. Lancet. 2000;355(9214):1519-1520. 176. Ranucci-Weiss D, Uerpairojkit B, Bowles N, et al. Intrauterine adenoviral infection associated with fetal non-immune hydrops. Prenat Diagn. 1998; 18(2):182-185. 177. Schroter B, Chaoui R, Meisel H, Bollmann R. [Maternal hepatitis B infection as the cause of nonimmunologic hydrops fetalis]. Z Geburtshilfe Neonatol. 1999;203(1):36-38. 178. Jauniaux E, Van Maldergem L, De Munter C, et al. Nonimmune hydrops fetalis associated with genetic abnormalities. Obstet Gynecol. 1990;75(3 Pt 2):568-572. 179. Wraith JE. Lysosomal disorders. Semin Neonatol. 2002;7(1):75-83. 180. Ravindranath Y, Paglia DE, Warrier I, et al. Glucose phosphate isomerase deiciency as a cause of hydrops fetalis. N Engl J Med. 1987;316(5): 258-561. 181. Gilsanz F, Vega MA, Gomez-Castillo E, et al. Fetal anaemia due to pyruvate kinase deiciency. Arch Dis Child. 1993;69(5 Spec No):523-524. 182. Rotig A, Cormier V, Blanche S, et al. Pearson’s marrow-pancreas syndrome. A multisystem mitochondrial disorder in infancy. J Clin Invest. 1990;86(5): 1601-1608. 183. Fayon M, Lamireau T, Bioulac-Sage P, et al. Fatal neonatal liver failure and mitochondrial cytopathy: an observation with antenatal ascites. Gastroenterology. 1992;103(4):1332-1335. 184. de Koning TJ, Toet M, Dorland L, et al. Recurrent nonimmune hydrops fetalis associated with carbohydrate-deicient glycoprotein syndrome. J Inherit Metab Dis. 1998;21(6):681-682. 185. Alegria A, Martins E, Dias M, et al. Glycogen storage disease type IV presenting as hydrops fetalis. J Inherit Metab Dis. 1999;22(3):330-332. 186. Knisely AS, Mieli-Vergani G, Whitington PF. Neonatal hemochromatosis. Gastroenterol Clin North Am. 2003;32(3):877-889, vi-vii. 187. Kessel I, Makhoul IR, Sujov P. Congenital hypothyroidism and nonimmune hydrops fetalis: associated? Pediatrics. 1999;103(1):E9. 188. Stulberg RA, Davies GA. Maternal thyrotoxicosis and fetal nonimmune hydrops. Obstet Gynecol. 2000;95(6 Pt 2):1036. 189. Pratt L, Digiosia J, Swenson JN, et al. Reversible fetal hydrops associated with indomethacin use. Obstet Gynecol. 1997;90(4 Pt 2):676-678. 190. Adler SP, Manganello AM, Koch WC, et al. Risk of human parvovirus B19 infections among school and hospital employees during endemic periods. J Infect Dis. 1993;168(2):361-368. 191. Saltzman DH, Frigoletto FD, Harlow BL, et al. Sonographic evaluation of hydrops fetalis. Obstet Gynecol. 1989;74(1):106-111. 192. Teoh TG, Ryan G, Johnson J, Winsor EJ. he role of fetal karyotyping from unconventional sources. Am J Obstet Gynecol. 1996;175(4 Pt 1): 873-877. 193. Cheong Leung W, Chitayat D, Seaward G, et al. Role of amniotic luid interphase luorescence in situ hybridization (FISH) analysis in patient management. Prenat Diagn. 2001;21(4):327-332. 194. Soma H, Yamada K, Osawa H, et al. Identiication of Gaucher cells in the chorionic villi associated with recurrent hydrops fetalis. Placenta. 2000;21(4): 412-416.

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195. Galjaard H. Fetal diagnosis of inborn errors of metabolism. Baillieres Clin Obstet Gynaecol. 1987;1(3):547-567. 196. Van Kamp IL, Klumper FJ, Oepkes D, et al. Complications of intrauterine intravascular transfusion for fetal anemia due to maternal red-cell alloimmunization. Am J Obstet Gynecol. 2005;192(1):171-177. 197. Tongsong T, Wanapirak C, Kunavikatikul C, et al. Fetal loss rate associated with cordocentesis at midgestation. Am J Obstet Gynecol. 2001;184(4): 719-723. 198. Tongsong T, Wanapirak C, Kunavikatikul C, et al. Cordocentesis at 16-24 weeks of gestation: experience of 1,320 cases. Prenat Diagn. 2000;20(3): 224-228. 199. Weiner CP, Okamura K. Diagnostic fetal blood sampling-technique related losses. Fetal Diagn her. 1996;11(3):169-175. 200. Ghidini A, Sepulveda W, Lockwood CJ, Romero R. Complications of fetal blood sampling. Am J Obstet Gynecol. 1993;168(5):1339-1344. 201. Liao C, Wei J, Li Q, et al. Eicacy and safety of cordocentesis for prenatal diagnosis. Int J Gynaecol Obstet. 2006;93(1):13-17. 202. Pasman SA, Claes L, Lewi L, et al. Intrauterine transfusion for fetal anemia due to red blood cell alloimmunization: 14 years experience in Leuven. Facts Views Vis Obgyn. 2015;7(2):129-136. 203. Mari G, Norton ME, Stone J, et al. Society for Maternal-Fetal Medicine (SMFM) Clinical Guideline #8: the fetus at risk for anemia—diagnosis and management. Am J Obstet Gynecol. 2015;212(6):697-710. 204. Dafos F, Forestier F, Mac Aleese J, et al. Fetal curarization for prenatal magnetic resonance imaging. Prenat Diagn. 1988;8(4):312-314. 205. Bernstein HH, Chitkara U, Plosker H, et al. Use of atracurium besylate to arrest fetal activity during intrauterine intravascular transfusions. Obstet Gynecol. 1988;72(5):813-816. 206. Yinon Y, Visser J, Kelly EN, et al. Early intrauterine transfusion in severe red blood cell alloimmunization. Ultrasound Obstet Gynecol. 2010;36(5):601-606. 207. Mandelbrot L, Dafos F, Forestier F, et al. Assessment of fetal blood volume for computer-assisted management of in utero transfusion. Fetal her. 1988; 3(1-2):60-66. 208. el-Azeem SA, Samuels P, Rose RL, et al. he efect of the source of transfused blood on the rate of consumption of transfused red blood cells in pregnancies afected by red blood cell alloimmunization. Am J Obstet Gynecol. 1997;177(4):753-757. 209. Mari G, Zimmermann R, Moise Jr KJ, Deter RL. Correlation between middle cerebral artery peak systolic velocity and fetal hemoglobin ater 2 previous intrauterine transfusions. Am J Obstet Gynecol. 2005;193(3 Pt 2): 1117-1120. 210. Ruiz Villaespesa A, Suarez Mier MP, Lopez Ferrer P, et al. Nonimmunologic hydrops fetalis: an etiopathogenetic approach through the postmortem study of 59 patients. Am J Med Genet. 1990;35(2):274-279. 211. Knisely AS. he pathologist and the hydropic placenta, fetus, or infant. Semin Perinatol. 1995;19(6):525-531. 212. Steiner RD. Hydrops fetalis: role of the geneticist. Semin Perinatol. 1995;19(6):516-524. 213. Santolaya J, Alley D, Jafe R, Warsof SL. Antenatal classiication of hydrops fetalis. Obstet Gynecol. 1992;79(2):256-259. 214. Gudmundsson S, Huhta JC, Wood DC, et al. Venous Doppler ultrasonography in the fetus with nonimmune hydrops. Am J Obstet Gynecol. 1991; 164(1 Pt 1):33-37. 215. Kaiser IH. Ballantyne and triple edema. Am J Obstet Gynecol. 1971;110(1):115-120. 216. Kumar B, Nazaretian SP, Ryan AJ, Simpson I. Mirror syndrome: a rare entity. Pathology. 2007;39(3):373-375. 217. Vidaef AC, Pschirrer ER, Mastrobattista JM, et al. Mirror syndrome. A case report. J Reprod Med. 2002;47(9):770-774. 218. Ordorica SA, Marks F, Frieden FJ, et al. Aneurysm of the vein of Galen: a new cause for Ballantyne syndrome. Am J Obstet Gynecol. 1990; 162(5):1166-1167. 219. Dorman SL, Cardwell MS. Ballantyne syndrome caused by a large placental chorioangioma. Am J Obstet Gynecol. 1995;173(5):1632-1633. 220. Livingston JC, Malik KM, Crombleholme TM, et al. Mirror syndrome: a novel approach to therapy with fetal peritoneal-amniotic shunt. Obstet Gynecol. 2007;110(2 Pt 2):540-543.

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221. Duthie SJ, Walkinshaw SA. Parvovirus associated fetal hydrops: reversal of pregnancy induced proteinuric hypertension by in utero fetal transfusion. Br J Obstet Gynaecol. 1995;102(12):1011-1013. 222. Heyborne KD, Chism DM. Reversal of Ballantyne syndrome by selective second-trimester fetal termination. A case report. J Reprod Med. 2000; 45(4):360-362. 223. Espinoza J, Romero R, Nien JK, et al. A role of the anti-angiogenic factor sVEGFR-1 in the ‘mirror syndrome’ (Ballantyne’s syndrome). J Matern Fetal Neonatal Med. 2006;19(10):607-613. 224. McCurdy Jr CM, Seeds JW. Route of delivery of infants with congenital anomalies. Clin Perinatol. 1993;20(1):81-106. 225. Kirshon B, Mari G, Moise Jr KJ. Indomethacin therapy in the treatment of symptomatic polyhydramnios. Obstet Gynecol. 1990;75(2):202-205. 226. Abrams ME, Meredith KS, Kinnard P, Clark RH. Hydrops fetalis: a retrospective review of cases reported to a large national database and identiication of risk factors associated with death. Pediatrics. 2007;120(1):84-89. 227. Nakayama H, Kukita J, Hikino S, et al. Long-term outcome of 51 liveborn neonates with non-immune hydrops fetalis. Acta Paediatr. 1999; 88(1):24-28. 228. Haverkamp F, Noeker M, Gerresheim G, Fahnenstich H. Good prognosis for psychomotor development in survivors with nonimmune hydrops fetalis. BJOG. 2000;107(2):282-284. 229. Mari G, Abuhamad AZ, Cosmi E, et al. Middle cerebral artery peak systolic velocity: technique and variability. J Ultrasound Med. 2005;24(4): 425-430.

230. Machin GA. Hydrops revisited: literature review of 1,414 cases published in the 1980s. Am J Med Genet. 1989;34(3):366-390. 231. Santo S, Mansour S, hilaganathan B, et al. Prenatal diagnosis of non-immune hydrops fetalis: what do we tell the parents? Prenat Diagn. 2011;31(2): 186-195. 232. Center for Disease Control (CDC). Risks associated with human parvovirum B19 infection. MMWR Morb Mortal Wkly Rep. 1989;38(6):81-88, 93-97. 233. Dijkmans AC, de Jong EP, Dijkmans BA, et al. Parvovirus B19 in pregnancy: prenatal diagnosis and management of fetal complications. Curr Opin Obstet Gynecol. 2012;24(2):95-101. 234. Cavoretto P, Molina F, Poggi S, et al. Prenatal diagnosis and outcome of echogenic fetal lung lesions. Ultrasound Obstet Gynecol. 2008;32(6): 769-783. 235. Wilson RD, Baxter JK, Johnson MP, et al. horacoamniotic shunts: fetal treatment of pleural efusions and congenital cystic adenomatoid malformations. Fetal Diagn her. 2004;19(5):413-420. 236. Loh KC, Jelin E, Hirose S, et al. Microcystic congenital pulmonary airway malformation with hydrops fetalis: steroids vs open fetal resection. J Pediatr Surg. 2012;47(1):36-39. 237. Society for Maternal-Fetal Medicine, Simpson LL. Twin-twin transfusion syndrome. Am J Obstet Gynecol. 2013;208(1):3-18.

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Fetal Measurements: Normal and Abnormal Fetal Growth and Assessment of Fetal Well-Being Carol B. Benson and Peter M. Doubilet

SUMMARY OF KEY POINTS • Accurate assignment of gestational age to a pregnancy is important for several reasons, including timing of screening tests for aneuploidy, monitoring fetal growth and diagnosing growth disturbances, and scheduling of delivery by elective induction or cesarean. • If a woman has more than one sonogram during her pregnancy, the pregnancy should not be redated after the irst scan; instead, the gestational age at the time of subsequent scans is the age at initial scan plus the time elapsed since that scan. • In the irst trimester, dating by sonographic indings or mean sac diameter prior to 6.0 weeks’ gestation has an accuracy of ±0.5 weeks, while dating by crown-rump length at 6.0 weeks or later has an accuracy of ±0.7 weeks. • Sonographic dating in the second and third trimesters has an accuracy of ±1.2 weeks at 14 to 20 weeks, ±1.9 weeks

•

•

•

•

at 20 to 26 weeks, ±3.1 to 3.4 weeks at 26 to 32 weeks, and ±3.5 to 3.8 after 32 weeks. Fetal weight is estimated using a formula that incorporates measurements of the fetal head, abdomen, and femur and has an accuracy (95% conidence range) of ±15% to 18%. Estimated fetal weight should be assessed in relation to gestational age to determine whether the fetus is appropriate in size for gestational age. If a fetus is diagnosed as small-for-gestational-age, with an estimated fetal weight less than 10th percentile for gestational age, an attempt should be made to determine the cause through evaluation of both mother and fetus. When a fetus is suspected of being growth restricted, antenatal surveillance with biophysical proiles and fetal Doppler can guide management and improve outcome.

CHAPTER OUTLINE GESTATIONAL AGE DETERMINATION First Trimester Second and Third Trimesters Fetal Head Measurements Femur Length Abdominal Circumference Composite Formulas Gestational Age Estimation by Ultrasound: Most Accurate Approach at Each Stage of Pregnancy

S

WEIGHT ESTIMATION AND ASSESSMENT Estimation of Fetal Weight Recommended Approach Weight Assessment in Relation to Gestational Age FETAL GROWTH ABNORMALITIES The Large Fetus General Population Diabetic Mothers

onographic measurements of the fetus provide information about fetal age and growth. hese data are used to assign gestational age, estimate fetal weight, and diagnose growth disturbances. As discussed in other chapters, fetal measurements are also used in the diagnosis of a number of fetal anomalies, such as skeletal dysplasias1 and microcephaly.2 Each of these abnormalities can be diagnosed or suspected on the basis of measurements that deviate from the “normal for dates.”

The Small-for-Gestational-Age Fetus and Fetal Growth Restriction ASSESSMENT OF FETAL WELL-BEING Biophysical Proile Fetal Doppler Umbilical Artery Doppler Ductus Venosus Doppler Middle Cerebral Artery Doppler Summary of Fetal Doppler

It is important to begin by deining the various terms used in the evaluation of the age of a pregnancy. he true measure of a pregnancy’s age is the number of days since conception, termed conceptual age. Historically, however, pregnancies were dated by the number of days since the irst day of the last menstrual period (LMP), termed menstrual age, because for most of human history it was unknown when conception occurred. In women with regular 28-day cycles, menstrual age

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is 2 weeks more than conceptual age, because conception occurs approximately 2 weeks ater the LMP in such women. Currently, the term most oten used to date pregnancies is gestational age, which is similar to menstrual age and is deined as follows: Gestational age = Conceptual age + 2 weeks In women with 28-day cycles, gestational age and menstrual age are equal. In women with longer cycles, gestational age is less than menstrual age; the opposite holds in women with shorter cycles. Accurate knowledge of gestational age is important for a number of reasons. he timing of screening tests in the irst trimester, such as nuchal translucency measurement and maternal cell free fetal DNA analysis,3,4 genetic amniocentesis in the second trimester, and elective induction or cesarean delivery in the third trimester are all based on the gestational age. he diferentiation between term and preterm labor and the characterization of a fetus as “postdates” depend on gestational age. Knowledge of the gestational age can be critical in distinguishing normal from pathologic fetal development. Midgut herniation, for example, is normal up to 11 to 12 weeks of gestation5 but signiies omphalocele thereater. he normal size of a variety of fetal body parts depends on gestational age, as do levels of maternal serum alpha-fetoprotein,6 human chorionic gonadotropin,7 and estriol.8 When a fetal anomaly is detected prenatally, the maternal choices and obstetric management are signiicantly inluenced by gestational age. Estimation of the fetal weight, on its own and in relation to the gestational age, can inluence obstetric management decisions concerning the timing and route of delivery. A fetus growing poorly may beneit from close monitoring of fetal well-being to determine if early delivery is indicated. Such a fetus may be inadequately supplied by its placenta with oxygen and nutrients and, therefore, may do better in the care of a neonatologist than in utero. When a fetus is large, cesarean may be the preferred route of delivery, particularly in pregnancies complicated by maternal diabetes. In view of these considerations, fetal measurements should be a component of every complete obstetric sonogram.9 he well-being of the fetus at risk for perinatal morbidity and mortality, such as a growth-restricted fetus, can be monitored by ultrasound using the biophysical proile and Doppler. Abnormalities and changes in any of these surveillance tests may guide decisions about timing of delivery.10,11

GESTATIONAL AGE DETERMINATION Clinical dating of a pregnancy is usually based on the patient’s recollection of the irst day of her LMP and on physical examination of uterine size. Unfortunately, both of these methods are imprecise, leading to inaccuracies in gestational age assignment. Dating by LMP (menstrual age) may be inaccurate because of variability in length of menstrual cycles, faulty memory,12,13 recent exposure to oral contraceptives, or bleeding during early pregnancy.14 Determining gestational age from the palpated dimension of the uterus may be afected by uterine ibroids, multiple pregnancy, and maternal body habitus.

Clinical dating is accurate only if either of the following two conditions apply: (1) the patient is a good historian with regular menstrual cycles, and the uterine size correlates closely with LMP; or (2) information is available specifying the time of conception, such as a basal body temperature chart or pregnancy achieved via assisted reproductive technologies in women treated for infertility. Ultrasound provides an alternative and, in many cases, superior approach to gestational age estimation. Sonographic age estimation is based on sonographic indings or measurements taken during the ultrasound examination. Because biologic variability in the size of fetuses increases as pregnancy progresses, the accuracy of sonographic age estimates declines as pregnancy proceeds.15-28 hus, if a woman has more than one sonogram during a pregnancy, the pregnancy should never be redated ater the irst scan. he decision as to whether to use clinical dating or sonographic dating at the time of the irst scan is not well established for all pregnancies. In some cases, though, the decision is clear-cut: pregnancies achieved via in vitro fertilization should be dated based on the embryo transfer dates, and naturally conceived pregnancies in women with irregular menstrual cycles or with poor recollection of their LMP should be dated based on sonographic criteria. In other situations, however, particularly for pregnancies conceived naturally in women with regular cycles and good recollection of LMP, there are two reasonable alternatives. he irst approach is to date the pregnancy based on LMP whenever the ages based on LMP and sonography are close to one another: within 5 days up to 8.9 weeks; within 7 days from 9.0 weeks to 15.9 weeks; within 10 days from 16.0 weeks to 21.9 weeks; within 14 days from 22.0 weeks to 27.9 weeks; and within 21 days from 28.0 weeks onward.16 An alternative approach is to use sonographic dating routinely up to 24 weeks and the LMP thereater, if the LMP is clearly recalled and within 21 days of sonographic dating.15 Whichever approach is used, it is important to know what sonographic criteria are available for gestational age estimation and which are the most accurate at each stage of pregnancy.

First Trimester Sonographic indings and measurements allow highly accurate dating from 5 weeks’ gestation until the end of the irst trimester. he earliest sign of an intrauterine pregnancy is identiication of a gestational sac in the uterine cavity. his appears as a round or oval luid collection within the uterine cavity irst seen on transvaginal sonography at approximately 5 weeks’ gestation.29 In some cases, the early gestational sac is surrounded by one or two echogenic rings, formed by the proliferating chorionic villi and the deeper layer of the decidua vera.30,31 hese rings are not consistently present, however, and any round or oval luid collection in the mid uterus of a woman with a positive pregnancy test is highly likely to be a gestational sac32 (Fig. 42.1). From 5 to 6 weeks’ gestation, two methods can be used to assign gestational age by ultrasound: (1) measurement of mean sac diameter (MSD) or (2) sonographic identiication of gestational sac contents. he MSD is calculated as the average of the anteroposterior diameter, the transverse diameter, and the longitudinal diameter. It increases from 2 mm at 5 weeks to

CHAPTER 42

FIG. 42.1 Gestational Sac. At 5.0 weeks’ gestation, gestational sac (arrow) appears as a small, intrauterine luid collection.

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FIG. 42.2 Yolk Sac. Gestational sac contains yolk sac (arrow) on transvaginal sonogram at 5.5 weeks’ gestation. No embryo is seen. SAG ML, Sagittal midline.

TABLE 42.1 Gestational Dating by Mean Sac Diameter (MSD) in the Early First Trimester MSD (mm) 2 3 4 5 6 7 8 9 10

Gestational Age (Weeks) 5.0 5.1 5.2 5.4 5.5 5.6 5.7 5.9 6.0

95% Conidence interval = ±0.5 week. Values from Daya S, Wood S, Ward S, et al. Early pregnancy assessment with transvaginal ultrasound scanning. CMAJ. 1991; 144(4):441-446.33

10 mm at 6 weeks,33 a growth pattern that can be used to assign gestational age during this period (Table 42.1). he second method, based on the sonographic indings within the gestational sac, is best done by transvaginal sonography and relies on the observation that, on average, the gestational sac is irst identiiable at 5.0 weeks, the yolk sac at 5.5 weeks (Fig. 42.2), and the embryo and embryonic heartbeat at 6.0 weeks34 (Fig. 42.3, Video 42.1). he timing of these milestones is subject to minimal variability, with a 95% conidence range of approximately 0.5 weeks.31 Gestational age can be assigned based on these milestones (Table 42.2). From 6 weeks until the end of the irst trimester, gestational age correlates closely with the crown-rump length (CRL) of the embryo or fetus.35,36 he term embryo is commonly used up to 10 weeks’ gestation, and the term fetus applies thereater.37 he CRL is the length of the embryo or fetus from the top of its head to the bottom of its torso. It is measured as the longest dimension of the embryo, excluding the yolk sac and extremities. From 9 or 10 weeks onward, the CRL measurements are most accurate

FIG. 42.3 Embryonic Heartbeat. Transvaginal sonogram and M-mode at 6 weeks demonstrate cardiac activity originating from tiny embryo (arrow) adjacent to the yolk sac. See also Video 42.1.

if taken with the fetus in neutral position38 (Fig. 42.4). he CRL can be used to assign gestational age accurately up to 14 weeks because there is little biologic variability in fetal length up until that age39 (Table 42.3). Ater that point, the CRL of the longer, more developed fetus becomes less reliable. At this later stage, the CRL is afected by the fetal position, measuring shorter in a fetus whose spine is lexed and longer in a fetus whose spine is extended.

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TABLE 42.2 Gestational Dating by Ultrasound in the First Trimester Sonographic Finding

Gestational Age (Weeks)

Gestational sac, no yolk sac, embryo, or heartbeat Gestational sac with yolk sac, no embryo or heartbeat Gestational sac with heartbeat and embryo ) = 1.4787 − 0.003343 AC × FL + BPD2 + 0.0458 AC + 0.158 FL FORMULA 2a Log10 (EFW >) = 1.1134 + 0.05845 AC − 0.000604 AC2 − 0.007365 BPD2 + BPD2 + 0.00595 BPD × AC + 0.1694 BPD FORMULA 3a Log10 (EFW) = 1.3598 + 0.051 AC + 0.01844 FL − 0.0037 AC × FL a

Formulas from Hadlock FP, Harrist RB, Sharman RS, et al. Estimation of fetal weight with the use of head, body, and femur measurements—a prospective study. Am J Obstet Gynecol. 1985;151(3):333-337.26 AC, Abdominal circumference (cm); BPD, biparietal diameter (cm); EFW, estimated fetal weight, in grams (g); FL, femur length (cm); OFD, occipitofrontal diameter (cm).

of gestational age (Table 42.10), several of which appear in the literature.71-76 here is some debate about a number of aspects of fetal weight assessment in relation to gestational age. Should a weight table or chart based on neonatal weights or on estimated fetal weights be used? Should the table or chart be derived solely from pregnancies of low-risk mothers? Should “population norms” or “customized norms” be used? Most weight norms (tables or charts) are derived from large data sets of neonatal birth weights from babies born at a known gestational age.71-76 At least one chart, on the other hand, was produced using estimated fetal weights instead of neonatal birth weights.77,78 A rationale for the latter is that several studies have shown that fetuses that deliver preterm are smaller, on average, than those of the same gestational age that remain in utero.79-83 Babies born preterm thus represent an abnormal group with a negatively skewed weight distribution. his supports the argument that fetuses should be compared to fetuses, not to babies.84 A large international study, INTERGROWTH-21st, used another approach to produce weight norms derived from a healthy population.85,86 Although it is based on birth weights rather than

TABLE 42.10 Fetal Weight Percentiles in the Third Trimester WEIGHT PERCENTILES (GRAMS) Gestational Age (Weeks)

10th

50th

90th

25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43

490 568 660 765 884 1020 1171 1338 1519 1714 1919 2129 2340 2544 2735 2904 3042 3142 3195

660 760 875 1005 1153 1319 1502 1702 1918 2146 2383 2622 2859 3083 3288 3462 3597 3685 3717

889 1016 1160 1322 1504 1706 1928 2167 2421 2687 2959 3230 3493 3736 3952 4127 4254 4322 4324

With permission from Doubilet PM, Benson CB, Nadel AS, Ringer SA. Improved birth weight table for neonates developed from gestations dated by early ultrasonography. J Ultrasound Med. 1997;16(4):241-249.71

fetal weights, the study population used to generate these norms consists of babies born at or beyond 33 weeks to mothers with no known pregnancy-related risk factors. he INTERGROWTH21st norms, however, are of limited use for assessing fetal weight in relation to gestational age, because they do not cover the period prior to 33 weeks’ gestation. Perhaps the biggest controversy in weight assessment is whether the estimated weight of a fetus should be compared to norms from the overall population or to customized norms87-91 derived from a subgroup of fetuses similar to that fetus. For example, if an African-American fetus has an estimated weight of 1200 g at 30 weeks’ gestation, should the weight percentile be determined from overall population norms or from African-American norms? In that example, the population-based percentile would be lower than the customized percentile, because African-American fetuses and neonates are smaller, on average, than those in the general population.92 Although there are proponents of customized norms,93-95 a major concern with this approach is that it can do harm by inadvertently normalizing the weight of a fetus who is small on a pathologic basis.96,97 his viewpoint is supported by the fact that at least some population groups with small babies have elevated rates of postnatal complications98 and by the INTERGROWTH-21st inding that neonates of healthy mothers do not difer in size based on ethnic background.99 Overall, our recommended approach is to use population norms. Although it would theoretically be preferable to use norms

FETAL GROWTH ABNORMALITIES The Large Fetus he large-for-gestational-age (LGA) neonate (or fetus) is deined as one whose weight is above the 90th percentile for gestational age.71,103-105 Macrosomia, a related entity, is most oten deined on the basis of a weight above 4000 g; other weight cutofs (4100 g, 4500 g) are sometimes used.74,76-80,106 hese growth disturbances occur with diferent frequencies and are associated with diferent morbidities and mortalities in diabetic mothers as compared to the general population. herefore these two patient populations are considered separately.

General Population About 10% of all infants have birth weights above the 90th percentile for gestational age and are considered LGA infants.

5.0 4.5 4.0 3.5 3.0 2.5 2.0 1.5 1.0 0.5

A

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99th percentile 90th percentile 50th percentile 10th percentile 1st percentile

25

30 35 Gestational age (wks)

25

30 35 Gestational age (wks)

40

100 90 80 EFW percentile

derived from estimated fetal weights,77,78 norms derived from birth weights are better established and are based on larger study populations.71-76 he weight gain between two ultrasound examinations can be estimated as the diference between the two estimated weights. Adequacy of weight gain can be assessed by comparing this diference to established normal fetal growth rate as a function of gestational age. INTERGROWTH-21st data indicate that median fetal weight gain per week decreases progressively from 33 weeks of gestation onward, with a maximum rate of 270 g per week at 33 weeks, down to 100 g per week at 41 weeks.86 Other older growth tables suggest that weight gain may increase until 36 weeks, then decline steadily thereater.71,72 he longer the time is between scans, the more accurate the sonographic estimate of interval weight gain will be. When two scans are performed within 1 week of each other, weight gain cannot be determined reliably, because weight prediction is too imprecise to detect small changes in growth. Furthermore, estimating weight too close to the time of the prior scan could raise unnecessary concern by a spurious inding that the fetus has grown subnormally or even lost weight. hus there is little or no value in computing an estimated weight at the time of the second scan 1 week ater the irst. Instead, it is recommended that fetal weight gain only be assessed ater an interval of at least 2 weeks’ duration.10,11 When several examinations have been performed, fetal growth can be depicted graphically by means of a trend plot or growth curve. One form of growth curve plots the estimated fetal weight versus gestational age, with the curve for the fetus being examined superimposed on lines depicting the 1st, 10th, 50th, 90th, and 99th percentiles (Fig. 42.10A). An alternative mode of display plots the estimated fetal weight percentile versus gestational age (Fig. 42.10B). In this latter format, the graph for a normally growing fetus will be a horizontal line, indicating maintenance of a particular weight percentile throughout gestation. A down sloping line suggests subnormal growth rate. Calculation of weight percentiles and plotting of growth curves are most easily accomplished by computer, using an obstetric ultrasound sotware package that performs these tasks.100-102 Alternatively, similar results can be achieved by means of a calculator and manual plotting of data.

EFW (kg)

CHAPTER 42

70 60 50 40 30 20 10 0

B

40

FIG. 42.10 Fetal Growth Curves. (A) Estimated fetal weight plotted against gestational age, superimposed on 1st, 10th, 50th, 90th, and 99th percentile curves. The fetus depicted here has a normal growth pattern, with estimated fetal weights between the 50th and 90th percentile over four sonograms. (B) Estimated fetal weight (EFW) percentile against gestational age.

Of all newborns, 8% to 10% have birth weights over 4000 g and thus are classiied as “macrosomic,” and 2% weigh over 4500 g.104,106-109 hese rates, however, vary considerably among diferent patient subgroups, depending on presence or absence of risk factors. Risk factors for LGA and macrosomia include maternal obesity, history of a previous LGA infant, prolonged pregnancy (>40 weeks), excess pregnancy weight gain, multiparity, and advanced maternal age.103,104,107,110-112 Large fetuses have an increased incidence of perinatal morbidity and mortality, in large part because of obstetric complications. Shoulder dystocia, fractures, and facial and brachial plexus palsies occur more frequently as a result of traumatic delivery.106,110,113,114 he incidence of perinatal asphyxia, meconium aspiration, neonatal hypoglycemia, and other metabolic complications is signiicantly increased in these pregnancies.103,106,107,110 he most straightforward approach to diagnosing fetal LGA and macrosomia is to use the estimated fetal weight computed from sonographic measurements. An estimated weight above the 90th percentile for gestational age suggests LGA, and a weight estimate above 4000 g suggests macrosomia. Although weight estimation is somewhat less accurate in large than in average-sized fetuses,62,115 this approach has been demonstrated to be moderately good for diagnosing LGA and macrosomia. It has a positive

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predictive value (PPV) of up to 51% for LGA and 67% for macrosomia. Other proposed sonographic parameters have lower sensitivity or lower PPV than the estimated fetal weight62,103,106,116-124 (Table 42.11).

Diabetic Mothers Fetuses of insulin-dependent and gestational diabetic mothers are exposed to high levels of glucose throughout pregnancy and, as a result, produce excess insulin. his leads to overgrowth of the fetal trunk and abdominal organs, while the head and brain grow at a normal rate.104,105 herefore these fetuses tend to have diferent body proportions than fetuses of nondiabetic mothers. Sonographic measurements of fetuses of diabetic mothers demonstrate accelerated growth of the fetal thorax and abdomen beginning between 28 and 32 weeks’ gestation.104,105,125 An LGA weight occurs in 25% to 42% and macrosomia in 10% to 50% of infants of diabetic mothers.104,105,126 As many as 12% of infants of mothers with diabetes weigh more than 4500 g at birth. Perinatal complications are more frequent in macrosomic fetuses of diabetic mothers than in those of nondiabetic mothers.109,113,114,127,128 Shoulder dystocia, for example, occurs in 31% of macrosomic fetuses of diabetic mothers and only 3% to 10% of macrosomic fetuses of nondiabetic mothers.110,113 Many sonographic parameters, involving a variety of measurements, formulas, and ratios, have been proposed for diagnosing LGA and macrosomia in the fetus of the diabetic mother117,129-131 (Table 42.12). As a group, these have higher sensitivities and PPVs than sonographic criteria in the general population, in part because of the higher prevalence of large fetuses in diabetic mothers. As in the general population, the most straightforward approach to diagnosing LGA and macrosomia in the fetuses of diabetic mothers is by means of the sonographically estimated

fetal weight.68,117,129,132,133 A fetus whose estimated weight falls above the 90th percentile for gestational age has a 74% likelihood of being LGA, versus 19% if the estimated weight lies below the 90th percentile.129 A weight estimate above 4000 g is associated with a 77% chance of macrosomia, and one above 4500 g with an 86% chance. he chance of macrosomia is only 16% when the weight estimate is less than 4000 g.68 hus, if vaginal delivery is believed to be contraindicated for the macrosomic fetuses of diabetic mothers, the estimated fetal weight should be considered when selecting the route of delivery.

The Small-for-Gestational-Age Fetus and Fetal Growth Restriction Fetuses are termed small for gestational age (SGA) if their estimated weights are below the 10th percentile for gestational age. SGA fetuses are a heterogeneous group and can be subdivided into constitutionally small fetuses (e.g., those with small parents) and fetuses whose small size is due to a pathologic process.

Small-for-Gestational-Age Fetuses: Causes CONSTITUTIONALLY SMALL PATHOLOGICALLY SMALL Placenta Mediated Primary placental Maternal Fetal Aneuploidy Malformations Infections

TABLE 42.11 Sonographic Criteria for Large-for-Gestational Age (LGA) and Macrosomia in the General Population: Performance Characteristics PREDICTIVE VALUES (%)a

(%) Sensitivity

Speciicity

Positive

Negative

CRITERIA TO PREDICT LGAa Elevated AD-BPD115 Low FL/AC103,115 Elevated AFV119,123 Elevated ponderal index103,115 High EFW103,123 Elevated growth score103 Elevated AFV, high EFW123

46 24-75 12-17 13-15 20-74 14 11

79 44-93 92-98 85-98 93-96 91 99

19 13-26 19-35 13-36 6-51 10 54

93 92-94 91 91-94 88-94 90 99

CRITERIA TO PREDICT MACROSOMIA Elevated FL121 Elevated AC121 High EFW63,124,121 Elevated BPD121

24 53 11-65 29

96 94 89-96 98

52 63 38-67 71

88 89 83-91 92

a Predictive values for criteria for LGA computed using Bayes’ theorem,112 assuming an LGA prevalence rate of 10%. AC, Abdominal circumference; AD, abdominal diameter; AFV, amniotic luid volume; BPD, biparietal diameter; EFW, estimated fetal weight; FL, femur length; FL/AC, femur length to abdominal circumference ratio. With permission from Doubilet PM, Benson CB. Fetal growth disturbances. Semin Roentgenol. 1990;25(4):309-316.117

CHAPTER 42 As a group, SGA fetuses have a poor prognosis, with increased perinatal morbidity and mortality rates. heir mortality rate is four to eight times that of non-SGA fetuses.134-136 Half of surviving SGA fetuses have serious short- or long-term morbidity, including meconium aspiration, pneumonia, and metabolic disorders.134,137-139 he risk, however, is dependent on the cause of the small size. Constitutionally small fetuses carry no elevated risk, unlike those who are small because of a pathologic condition. Furthermore, the potential to improve outcome by appropriate management of pathologically small fetuses varies depending on causation. For example, when the small size is caused by placental insuficiency, early delivery may improve outcome, but this intervention is unlikely to afect outcome in chromosomally abnormal fetuses. he term fetal growth restriction (FGR), also called intrauterine growth restriction, is used diferently by diferent authors. Some use FGR and SGA synonymously, considering all fetuses below the 10th percentile for gestational age to be growth restricted. Others use FGR to refer to pathologically small fetuses. Terminology aside, determination of the cause(s) of small fetal size is oten diicult, so that all SGA fetuses should be classiied as suspected FGR.140 he approach to SGA or FGR involves three steps: (1) diagnosis: identify small fetuses; (2) classiication: attempt to determine the cause of the small size; (3) management: institute monitoring and decide on timing of delivery. he most direct approach to identifying SGA fetuses is to diagnose SGA if the estimated fetal weight falls below the 10th percentile for the best estimate of gestational age. Several other criteria for diagnosing SGA or FGR have been proposed, including sonographic measurements and ratios,141 as well as a multiparameter scoring system.142,143 None of the individual parameters

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has a high PPV,141 and the performance characteristics of the scoring system143 are not good enough to make up for its complexity and cumbersome nature. hus the straightforward approach of using the estimated fetal weight percentile is the preferred method for diagnosing SGA fetuses. Once SGA has been diagnosed, an attempt should be made to determine its cause through evaluation of both the mother and the fetus. Maternal assessment should include physical examination and blood tests, directed toward diagnosis of hypertension, renal disease, and other maternal conditions that can cause FGR. Fetal assessment begins with a careful sonographic examination, looking especially for indings suggestive of a chromosomal or viral cause (e.g., holoprosencephaly, clenched hands, rocker-bottom feet, intracranial calciications). If such a inding is present, amniocentesis or umbilical blood sampling can conirm the diagnosis of a chromosomal abnormality. A viral cause of FGR may also be diagnosed by these procedures, in some cases.144 Growth-restricted fetuses, other than those with a lethal condition, such as trisomy 13 or 18, should be carefully monitored for the remainder of the pregnancy. he monitoring is typically performed at weekly or semiweekly intervals. Sonographic features to be followed include amniotic luid volume, biophysical proile score, estimated fetal weight percentile, and fetal Doppler. A worsening trend in one or more of these features should prompt consideration of early delivery.

ASSESSMENT OF FETAL WELL-BEING It has been shown that when a fetus is suspected of being growth restricted or having another condition that could afect the

TABLE 42.12 Sonographic Criteria for Large-for-Gestational Age (LGA) and Macrosomia in Diabetic Mothers: Performance Characteristics (%)

PREDICTIVE VALUES (%)

Sensitivity

Speciicity

Positive

Negative

CRITERIA TO PREDICT LGAa Elevated HC129 Elevated AC/BPD130 High EFW129 Elevated BPD129 Elevated AC105,127,129 Elevated AC growth105 Low FL/AC105,130 Elevated AC, high EFW129

50 83 78 13 71-88 84 58-79 72

80 60 78 86 81-85 85 75-80 71

64 71 74 75 56-78 79 68-83 89

70 75 81 57 81-96 89 75-76 89

CRITERIA TO PREDICT MACROSOMIA Elevated AC127 Low FL/AC131 Elevated TD-BPD126 High EFW68

84 48-64 87 48

78 60-74 72 95

41 36-42 61 77

96 80-83 92 84

a Predicted values for criteria for LGA computed using Bayes theorem,112 assuming an LGA prevalence rate of 10%. AC, Abdominal circumference; AC/BPD, abdominal circumference to biparietal diameter ratio; BPD, biparietal diameter; EFW, estimated fetal weight; FL, femur length; FL/AC, femur length to abdominal circumference ratio; HC, head circumference; TD, thoracic diameter. With permission from Doubilet PM, Benson CB. Fetal growth disturbances. Semin Roentgenol. 1990;25(4):309-316.117

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Fetal and Placental Risk Factors Associated With Fetal Growth Restriction

Maternal Risk Factors Associated With Fetal Growth Restriction

FETAL FACTORS Chromosomal Abnormalities Trisomy 13, 18, 21 Monosomy (45,XO) Deletions Uniparental disomy Conined placental mosaicism

GENETIC/CONSTITUTIONAL NUTRITION/STARVATION Inlammatory bowel disease Ileojejunal bypass Chronic pancreatitis Low prepregnancy weight Poor pregnancy weight gain, second and third trimesters

Congenital Malformations Absence of fetal pancreas Anencephaly Diaphragmatic hernia Omphalocele Gastroschisis Renal agenesis/dysplasia Multiple malformations

HYPOXIC Severe lung disease Cyanotic heart disease Sickle cell anemia

Multiple Gestations Monochorionic twins One fetus with malformations Twin-to-twin transfusion Discordant twins Triplets PLACENTAL FACTORS Abnormal trophoblastic invasion Multiple placental infarctions (chronic abruption) Umbilical-placental vascular anomalies Abnormal cord insertion (velamentous cord insertion) Placenta previa Circumvallate placenta Chorioangiomata With permission from Lin C. Current concepts of fetal growth restriction: part I. Causes, classiication, and pathophysiology. Obstet Gynecol. 1998;92(6):1044-1055.135

oxygenation or nutrition to the fetus, antenatal surveillance can improve the outcome for these fetuses. Surveillance of such a fetus includes serial ultrasounds to monitor fetal growth, perform biophysical proiles (BPPs), and measure Doppler parameters. Nonstress tests (NSTs) are also used to monitor fetal well-being. he nature and frequency of monitoring tests depends on the apparent severity of fetal compromise.10,11

VASCULAR Chronic hypertension Preeclampsia Collagen vascular disease Type 1 diabetes mellitus RENAL Glomerulonephritis Lipoid nephritis Arteriolar nephrosclerosis Renal transplantation ANTIPHOSPHOLIPID ANTIBODIES ENVIRONMENT AND DRUGS High altitude Emotional stress Physical stress Cigarette smoking Alcohol abuse Substance abuse (heroin, cocaine) Therapeutic drugs Antimetabolites Anticonvulsants Anticoagulants POOR OBSTETRIC HISTORY Previous stillbirths Recurrent aborters Previous birth of growth-restricted fetus Previous preterm births With permission from Lin C. Current concepts of fetal growth restriction: part I. Causes, classiication, and pathophysiology. Obstet Gynecol. 1998;92(6):1044-1055.135

Biophysical Proile he BPP, introduced in the 1980s, is a noninvasive test of fetal well-being based on four ultrasound parameters and the NST. he four ultrasound parameters are (1) fetal movement, (2) fetal tone, (3) fetal breathing movements, and (4) amniotic luid volume (Table 42.13, Fig. 42.11, Videos 42.2 and 42.3). Each parameter receives 2 points if the fetus meets criteria and 0 points if it does not. hus a perfect score for the ultrasound portion of the BPP is 8 out of 8, with 2 points given for each of the four parameters.145,146 he parameters were chosen to assess both the acute and the chronic state of the fetus, with acute parameters being fetal tone, movement, and breathing movements, and amniotic

luid volume being a chronic marker of fetal well-being.145 Studies have shown that the BPP is reliable and reproducible, and that scores of 8 out of 8 are associated with a low rate of stillbirths and low rate of fetal asphyxia within 1 week of testing.11,145,147-150 Lower scores, those below 6 out of 8, are associated with increased risk for fetal asphyxia, low cord pH, cerebral palsy, and stillbirth. he lower the score is, the higher the risk of perinatal compromise will be.11,145,148 he BPP exam is performed within 30 minutes. If a fetus does not meet criteria for a parameter within the 30-minute time period, that parameter is given a score of 0. he BPP score

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TABLE 42.13 Biophysical Proile Parameters for 30-Minute Ultrasound Examination Parameter

2 Points Given

0 Points Given

Fetal movement

At least 3 discrete body or limb movements At least 1 episode of extension and lexion of extremity or spine At least 30 seconds of continuous, rhythmic breathing movements Single pocket at least 1 cm across and 2 cm in vertical

Less than 3 discrete body or limb movements No episode of extension and lexion of extremity or spine No episode of continuous breathing movement for 30 seconds No pocket 1 cm across and 2 cm in vertical

Fetal tone Fetal breathing movement Amniotic luid volume

With permission from Manning FA, Platt LD, Sipos L. Antepartum fetal evaluation: development of a fetal biophysical proile. Am J Obstet Gynecol. 1980;136(6):787-795.146

A

C

B

FIG. 42.11 Ultrasound Parameters for the Biophysical Proile. (A) Sonogram of amniotic luid pocket measuring 5.8 cm in vertical and more than 1 cm across, an adequate amount to earn 2 points for amniotic luid for the biophysical proile. (B) Fetal breathing motion is identiied by observing the diaphragm (arrow) of the fetus in longitudinal view to detect rhythmic inspiratory and expiratory movements. Two points are given if the fetus has 30 seconds of continuous breathing movements during the 30-minute exam. (C) Three-dimensional sonogram of fetus in curled position. In the biophysical proile, points for fetal movement are given if the fetus has at least three movements of the body or extremities in the 30-minute period and points are given for tone if there is at least one episode of lexion and extension. See also Videos 42.2 and 42.3.

is reported as the number of points earned over the total for the study, which is 8 for an ultrasound BPP without NST. When a score of less than 8 out of 8 is given, the parameter or parameters for which no points were given should also be reported. For example, if a fetus has normal amniotic luid volume with a

pocket of luid more than 2 cm vertical and 1 cm wide, demonstrates adequate fetal movement and tone to obtain 2 points for each, but does not demonstrate fetal breathing movement during the 30-minute exam, that BPP would be reported as 6 out of 8 with 2 points deducted for lack of fetal breathing movement. In

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most cases, the BPP does not require a full 30 minutes of sonographic evaluation, because, given the short sleep cycles of the fetus, it typically meets criteria in less than that time, sometimes as short as 5 minutes.145 he BPP as a test of fetal well-being has several limitations. First, the test is less reliable in the severely premature fetus because of lack of brain maturity and should not be administered before 24 weeks’ gestation.145 Second, the biophysical state of the fetus is afected by administration of corticosteroids, which may cause depression of fetal breathing and movement for a few days ater treatment.151-155 his latter limitation must be kept in mind when using the BPP to guide management decisions shortly ater steroid treatment.145

Fetal Doppler Doppler parameters of a number of vessels, including the umbilical artery, umbilical vein, ductus venosus, middle cerebral artery, aortic isthmus, and uterine artery in the mother, have been studied to determine if Doppler parameters can be used to predict outcome and direct management.140,156-160 Among vessels studied, umbilical artery Doppler has been shown to be the most useful for monitoring fetuses at risk for compromise, particularly those with suspected FGR.11,140,148,156,160,161 When umbilical artery Doppler is incorporated into surveillance of fetuses with suspected growth restriction, overall outcome is improved, with fewer unnecessary interventions, inductions of labor, cesarean deliveries, and perinatal deaths. 10,148,160-162 Although umbilical artery Doppler has been shown to improve outcome in fetuses with suspected growth restriction and in mothers with preeclampsia or hypertension, routine screening with umbilical artery Doppler in low-risk pregnancies is not recommended, because it has not resulted in improved outcome in this patient population.140,161 Although some advocate adding middle cerebral artery and/or ductus venosus Doppler to the evaluation of fetuses with suspected growth restriction and abnormal umbilical artery Doppler,161,163-165 studies have not yet shown improved outcomes when these additional Doppler studies are performed.10,11,140,148,160

Umbilical Artery Doppler Umbilical artery Doppler is used to assess fetal well-being ater 24 weeks’ gestation for those fetuses with suspected growth restriction or in mothers with preeclampsia or hypertension.140,148,156,160,161 To obtain a waveform, the Doppler gate is placed on a free loop of umbilical cord, away from the placental and fetal cord insertions and in the absence of fetal breathing movements. he ratio of peak systolic to end-diastolic velocity is calculated (S/D ratio). Flow in the umbilical artery is normally low resistance, with an S/D ratio of less than 3.5 up to 28 weeks’ gestation and less than 3.0 thereater166 (Fig. 42.12A). With signiicant placental dysfunction, resistance in the placenta increases and low in the umbilical artery demonstrates diminished diastolic low, with an S/D ratio above the normal range (Fig. 42.12B). In such cases, the risk of fetal compromise and perinatal mortality is increased. he risk of fetal compromise is increased further when end-diastolic low in the umbilical artery is absent

(Fig. 42.12C), and is highest when end-diastolic low is reversed (Fig. 42.12D). In particular, the risk of perinatal mortality within 1 week of diagnosing reversed end-diastolic low in the umbilical artery of a growth-restricted fetus is so high, close to 50%, that delivery is generally recommended, regardless of the gestational age.10,11,140,156,167-170

Ductus Venosus Doppler he ductus venosus is the short vessel connecting the umbilical vein near its junction with the let portal vein directly to the inferior vena cava. his allows shunting of umbilical venous blood directly to the heart, bypassing the liver. Normal low in the ductus venosus is antegrade, toward the heart, throughout the cardiac cycle (Fig. 42.13A). Studies have shown that absent or reversed low (Fig. 42.13B) in the ductus venosus at any time during the cardiac cycle is a sign of cardiovascular instability and is associated with increased morbidity and mortality rates in growth-restricted fetuses.10,11,140,148,150,160 However, these same studies demonstrate poor sensitivities and speciicities, and, therefore, the value of ductus venosus Doppler for directing the management of growth-restricted fetuses has not been established.11,140,148,160 Middle Cerebral Artery Doppler Doppler of the middle cerebral artery (MCA) provides information about low resistance in the fetal brain. For optimal interrogation of the MCA, the Doppler gate should be placed on the middle cerebral artery in the proximal third of the vessel, close to its origin from the circle of Willis. If peak systolic velocity is being measured, the Doppler angle must be zero or angle correction must be used. Normally, low in the MCA is high resistance, with low diastolic low (Fig. 42.14A). In the compromised fetus, vessels in the brain vasodilate, a response called “brain sparing,” leading to decreased resistance to blood low and increased diastolic low in the MCA. his “brain-sparing” efect can be measured by calculating the resistive index (RI) of the MCA waveform. he RI is considered abnormal when it is less than the ith percentile for gestational age 148,159,160 (Fig. 42.14B). An abnormal RI in the MCA is associated with perinatal mortality and morbidity, including acidosis at birth, low 5-minute Apgars, and neonatal intracranial hemorrhage.148,159 However, the published studies are inconsistent, and an abnormal MCA Doppler is a poor predictor of adverse outcome in preterm infants. here is no convincing evidence that the use of MCA Doppler for guiding management of growth-restricted fetuses improves outcome.10,148,160,171 Some have advocated using the MCA Doppler in conjunction with umbilical artery Doppler to improve the identiication of fetuses at risk for poor outcome. In particular, some have recommended comparing the RI or pulsatility index (PI) in the MCA to the corresponding RI or PI in the umbilical artery in a ratio called the “cerebroplacental ratio” (Fig. 42.15): Cerebroplacental ratio Middle cerebral artery pulsatility index = Umbilical artery pulsatility index

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A

C

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B

D

FIG. 42.12 Umbilical Artery Doppler. (A) Color and spectral Doppler of umbilical artery demonstrating normal low with systolic to diastolic ratio (S/D) normal at 2.13. (B) Sonogram of term fetus showing Doppler gate on umbilical artery and spectral waveform with elevated S/D of 4.15 due to diminished diastolic low. (C) Sonogram showing Doppler gate on umbilical artery and spectral waveform below demonstrating absent end-diastolic low (arrows). (D) Color and spectral Doppler demonstrating reversed end-diastolic low (arrows).

A

B

FIG. 42.13 Ductus Venosus Doppler. (A) Color and spectral Doppler of the ductus venosus demonstrating normal low, toward the heart throughout the cardiac cycle. (B) Color and spectral Doppler of the ductus venosus demonstrating reversed low (arrows) during part of the cardiac cycle, an abnormal inding.

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A

B

FIG. 42.14 Middle Cerebral Artery Doppler. (A) Color and spectral Doppler of normal fetal middle cerebral artery with normal resistive index (RI) of 0.89. (B) Color and spectral Doppler of abnormal fetal middle cerebral artery demonstrating abnormally low resistive index (RI) of 0.64 (arrow) as a result of elevated diastolic low.

A

B

FIG. 42.15 Cerebroplacental Ratio. Normal cerebroplacental ratio of 1.49, calculated by taking the ratio of A, the resistive index in the middle cerebral artery (0.85) to B, the resistive index in the umbilical artery (0.57).

he cerebroplacental ratio is abnormal if it is less than 1.0.161,163 his ratio takes into account the decreased MCA resistance with “brain sparing” and vasodilation and increased umbilical artery resistance from increased placental resistance associated with placental dysfunction. An abnormal cerebroplacental ratio is associated with increased fetal distress in labor, low cord pH, and high neonatal intensive care admissions.10,140,159,160,163,172 However, the utility of this ratio in the surveillance of the growthrestricted fetus has not been well established.

Summary of Fetal Doppler To date, the only Doppler surveillance study that has been shown to improve outcome in growth-restricted fetuses is umbilical artery Doppler. Although ductus venosus and MCA Doppler have been shown to demonstrate changes with fetal compromise, their use in guiding management of high-risk pregnancies with FGR has not been proven.

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159. Cruz-Martinez R, Figueras F, Hernandez-Andrade E, et al. Changes in myocardial performance index and aortic isthmus and ductus venosus Doppler in term, small-for-gestational age fetuses with normal umbilical artery pulsatility index. Ultrasound Obstet Gynecol. 2011;38(4):400-405. 160. Mone F, McAulife FM, Ong S. he clinical application of Doppler ultrasound in obstetrics. Obstet Gynaecol. 2014;17(1):13-19. 161. Copel JA, Bahtiyar MO. A practical approach to fetal growth restriction. Obstet Gynecol. 2014;123(5):1057-1069. 162. Alirevic Z, Stampalija T, Gyte GML. Fetal and umbilical Doppler ultrasound in high-risk pregnancies. Cochrane Database Syst Rev. 2013;(11):CD007529. 163. DeVore GR. he importance of the cerebroplacental ratio in the evaluation of fetal well-being in SGA and AGA fetuses. Am J Obstet Gynecol. 2015;213(1):5-15. 164. Baschat AA. Venous Doppler for fetal assessment. UpToDate. 2015. 165. Cruz-Martinez R, Tenorio V, Padilla N, et al. Risk of ultrasound-detected neonatal brain abnormalities in intrauterine growth-restricted fetuses born between 28 and 34 weeks’ gestation: relationship with gestational age at birth and fetal Doppler parameters. Ultrasound Obstet Gynecol. 2015;46(4):452-459. 166. Acharya G, Wilsgaard T, Berntsen GKR, et al. Reference ranges for serial measurements of umbilical artery Doppler indices in the second half of pregnancy. Am J Obstet Gynecol. 2005;192(3):937-944.

167. Karsdorp VHM, van Vugt JMG, van Geijn HP, et al. Clinical signiicance of absent or reversed end diastolic velocity waveforms in umbilical artery. Lancet. 1994;344(8938):1664-1668. 168. Valcamonico A, Danti L, Frusca T, et al. Absent end-diastolic velocity in umbilical artery: risk of neonatal morbidity and brain damage. Am J Obstet Gynecol. 1994;170(3):796-801. 169. Ertan AK, He JP, Tanriverdi HA, et al. Comparison of perinatal outcome in fetuses with reverse or absent enddiastolic low in the umbilical artery and/or fetal descending aorta. J Perinat Med. 2003;31(4):307-312. 170. Gerber S, Hohlfeld P, Viquerat F, et al. Intrauterine growth restriction and absent or reverse end-diastolic blood low in umbilical artery (Doppler class II or III): a retrospective study of short- and long-term fetal morbidity and mortality. Eur J Obstet Gynecol Reprod Biol. 2006;126(1):20-26. 171. Fieni S, Gramellini D, Piantelli G. Lack of normalization of middle cerebral artery low velocity prior to fetal death before the 30th week of gestation: a report of three cases. Ultrasound Obstet Gynecol. 2004;24(4):474-476. 172. Figueras F, Savchev S, Triunfo S, et al. An integrated model with classiication criteria to predict small-for-gestational-age fetuses at risk of adverse perinatal outcome. Ultrasound Obstet Gynecol. 2015;45(3):279-285.

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Sonographic Evaluation of the Placenta Thomas D. Shipp

SUMMARY OF KEY POINTS • The placenta undergoes tremendous development within the irst half of pregnancy yet continues to mature and develop during the gestation. • A placenta that lies near or over the internal cervical os is common early in gestation, yet most of these will resolve by the end of pregnancy. Ultrasound, especially transvaginal sonography, is instrumental to determine placental position. • Placenta accreta is increasingly common and ultrasound is vital for its identiication, especially in patients at high risk for its development. Sonographic indings most important for identifying placenta accreta are placental lacunae, loss of the placental-myometrial hypoechoic space, abnormalities of the uterine-bladder interface, and color Doppler abnormalities. • Placental infarctions are commonly identiied within the placenta, especially in patients at high risk for their

development (e.g., those who have preeclampsia, maternal vascular disease, or thrombophilia). • Abnormalities of placental shape are common, as are differences in location of the placental umbilical cord insertion. • The presence of a vasa previa is associated with increased perinatal morbidity and mortality rates. Vasa previa should be evaluated for all gravidas, especially for those with an increased risk of its development. • Those parturients with abnormal postpartum bleeding should be evaluated for the presence of retained products of conception. Echogenic endometrial masses in these patients strongly suggest the presence of retained products of conception.

CHAPTER OUTLINE PLACENTAL DEVELOPMENT Placental Appearance Placental Size Placental Vascularity and Doppler Ultrasound Amnion-Chorion Separation Elastography PLACENTA PREVIA PLACENTA ACCRETA PLACENTAL ABRUPTION PLACENTAL INFARCTION PLACENTAL MASSES

T

MESENCHYMAL DYSPLASIA OF THE PLACENTA MOLAR GESTATIONS MORPHOLOGIC PLACENTAL ABNORMALITIES Circumvallate Placenta Succenturiate Lobe Bilobed Placenta UMBILICAL CORD Size and Appearance Insertion Into the Placenta

he use of ultrasound to evaluate the placenta is routine among the majority of pregnant American women because they have at least one ultrasound examination during pregnancy. A wide range of pregnancy complications result from abnormal placental development, including preeclampsia, intrauterine growth restriction (IUGR), and abruption. Other placental and umbilical cord abnormalities, such as placenta previa, placenta accreta/increta/percreta, or vasa previa, may cause major maternal and fetal complications, especially if not recognized antenatally. Timely recognition of these abnormalities can lead to improved management of pregnancy and delivery. hus careful examination

Velamentous and Marginal Cord Insertions Vasa Previa PLACENTA DURING LABOR AND POSTPARTUM Third Stage of Labor Retained Products of Conception CONCLUSION

of the placenta by ultrasound can contribute directly to enhanced patient care and improved outcomes.

PLACENTAL DEVELOPMENT he early developing embryo is surrounded by amnion and chorion. Villi cover the entire surface of the chorion up to about 8 weeks of gestation (Fig. 43.1). he villi, which are the basic structures of the placenta, initially form by 4 or 5 weeks’ gestation. he villi next to the decidua capsularis degenerate, forming the chorion laeve. he villi contiguous with the decidua basalis

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Decidual vessel Maternal decidua

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FIG. 43.1 Human Placenta Microarchitecture. Fetal derivatives in the placenta consist of fetal vessels and placental cotyledons (villi). Villi consist of fetal vessels surrounded by cytotrophoblast cells (CT). Covering the cytotrophoblast cells is a multinucleated cellular layer called the syncytiotrophoblast (ST). Anchoring villi are in direct contact with the maternal uterine lining, called the decidua. The decidua is traversed by maternal vasculature. Blood from these vessels empties into the intervillous space and bathes the placental villi. Note that maternal and fetal blood vessels are separated by trophoblast, villous stroma, and fetal vascular endothelium. Cytotrophoblast cells from anchoring villi can change into an invasive phenotype called extravillous cytotrophoblast cells (EVT). EVT invade deeply into the maternal decidua. Some EVT, called endovascular trophoblast cells (ET), embed within the walls of the maternal vasculature. (With permission from Comiskey M, Warner CM, Schust DJ. MHC molecules of the preimplantation embryo and trophoblast. In: Mor G, editor. Immunology of pregnancy. Austin/New York: Landes Bioscience, 2006.)

become the chorion frondosum and later the placenta. he fetal side of the placenta consists of the chorionic plate and chorionic villi. he maternal side consists of the decidua basalis, which opens up into large cisterns, the intervillous spaces. he fetal villi are immersed in maternal blood located in the intervillous spaces. Anchoring villi develop from the chorionic plate.1 hese attach to the decidua basalis, holding the placenta in place.2,3 By the end of pregnancy, the villi have a surface area of 12 to 14 square meters.4 his type of placentation, seen in humans and some rodents, is termed hemochorial placentation.

Placental Appearance Sonographically, the placenta in the irst and second trimesters is slightly more echogenic than the surrounding myometrium (Fig. 43.2A). he attachment site, or base of the placenta, should be clearly delineated from the underlying myometrium. he edges of the placenta usually have a small sinus, the marginal sinus of the placenta (Fig. 43.2B), where intervillous blood drains into the maternal venous circulation. his area should not be confused with a placental separation. Placental lakes (venous lakes, at least 2 × 2 cm) occur in up to 5% of pregnancies5-10 (Fig. 43.2C, Video 43.1). hey represent areas of intervillous spaces devoid of placental villous trees and are seen as hypoechoic structures within the placenta. Moving blood low can be seen in these areas. hey may have irregular shapes or a narrow, cletlike appearance and may change in appearance over the gestation. Large placental lakes (>5 cm in largest dimension) have been associated with IUGR.10 As the placenta matures, areas of echogenicity within the placenta are visualized (Fig. 43.2D and E). In cases of placental infarction, there may be hypoechoic lesions with echogenic borders.

Placental Size he placenta typically has a round shape with a central umbilical cord insertion, but variability in the shape of the placenta is quite common.11 Placental length is approximately six times its maximal width at 18 to 20 weeks’ gestation. he mean thickness of the placenta in millimeters in the irst half of pregnancy closely approximates the gestational age in weeks.12 If the placenta thickness is greater than 4 cm (40 mm) before 24 weeks, an abnormality should be suspected. hese abnormalities include ischemic-thrombotic damage, intraplacental hemorrhage, chorioangioma, and fetal hydrops13 (Fig. 43.3, Video 43.2). Given the variable shape of the placenta, calculating a placental volume from two-dimensional (2D) imaging can be complicated. Multiplanar volume calculation involves sequential sections of the placenta at intervals such as 1.0 mm. he margins are manually traced, and a volume is calculated.14 Most current studies appraising the use of three-dimensional (3D) sonography have used the VOCAL (Virtual Organ Computer-aided AnaLysis) method,14 in which the 3D volume in question is rotated and the area of interest traced at its margin, ater which a volume is calculated (Fig. 43.4). Placental volume approximation in the irst trimester holds promise as an important part of early pregnancy evaluation. Uterine artery Doppler analysis provides limited information regarding IUGR and the efects of maternal hypertension, but it is insuicient as a sole indicator of trophoblast invasion, in part because it is typically performed late in the second trimester. Small placental volumes in the irst trimester presage abnormal uterine artery perfusion.15 Uterine artery Doppler ultrasound combined with assessment of placental volume may identify pregnant women at risk for hypertension, abruption, or IUGR.16,17 First-trimester placental volumes correlate with both placental

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FIG. 43.2 Normal Appearance of Placenta. (A) At 18 weeks, note the uniformly echogenic appearance of the placenta. (B) Note marginal sinus of placenta (arrow), a circumferential venous drainage point into the maternal uterine veins that should not be mistaken for placental separation. (C) Placental lake (arrow) at 20 weeks. See also Video 43.1. (D) Placenta at 32 weeks’ gestation. Note the diffuse placental calciications. (E) Placenta at 39 weeks’ gestation with deined linear calciications outlining the placental cotyledons. Note the increasing echogenicity in the placenta as it matures.

weight and birth weight, but they have not been shown to predict the development of preeclampsia.18,19 he irst-trimester placental volume quotient (placental volume/crown-rump length) is low for aneuploid fetuses, with 53% having a quotient less than 10th percentile.20 For twins, the placental volume is 83%, and for triplets 76%, that of singletons, for a given gestational age.21 he placenta dramatically increases in size until approximately 15 to 17 weeks’ gestation. From this point, there is a fourfold increase in placental size until delivery, whereas over this same time period the fetus has a 50-fold increase in size.22 Midtrimester placental volume is associated with maternal nutritional status, birth weight, and pregnancy outcome.23-27

Placental Vascularity and Doppler Ultrasound

FIG. 43.3 Thick Placenta in Fetal Hydrops. The calipers indicate how one would measure the thickness of the placenta. Note the ascites (arrow). See also Video 43.2 for thick placenta in fetus with villitis.

he human placenta is a discoidal, villous, hemochorial structure. Nutrients are exchanged over many villi. Surrounding the villi are the intervillous spaces, which are bathed in maternal blood. he villi are sproutlike projections from the chorionic plate into the intervillous space. he villi are directly connected to the fetal vascular system, whereas the maternal blood emanates from the developing spiral arteries to the intervillous spaces to contact

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FIG. 43.4 Three-Dimensional Assessment of Placental Volume in Second Trimester.

Umbilical vein

Fetal circulation

Umbilical arteries

Amniochorionic membrane

Decidua parietalis Chorion

Chorionic plate

Intervillous space Main stem villus

Amnion

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FIG. 43.5 Schematic Drawing of Placental Vasculature.

directly the trophoblasts of the villi28 (Fig. 43.5). Maternal blood low of the intervillous space depends on low from the spiral arteries. Maternal vascular disease (e.g., hypertension) can directly afect the pregnancy by limiting this blood low.29 Intervillous blood low begins early in the irst trimester.30-32 Color Doppler ultrasound has been used to detect this intervillous and spiral artery low by 12 weeks’ gestation, but the low, if any, that occurs before this time is not well understood.33 Before 12 weeks, the presence of intervillous blood low by gray-scale imaging may indicate failed pregnancy.34 Color and power Doppler sonography have been used to identify blood low in intraplacental villous arteries.35 A decrease

in the number of detectable intraplacental villous arteries is associated with IUGR.36 hree-dimensional power Doppler ultrasound provides a better appreciation of placental vascularity and pathophysiology by assessing placental low and documenting the amount of low in a given area. Because of its low variability between sampling sites in varied parts of the placenta, 3D imaging may have a future role in assessing low in high-risk pregnancies (e.g., hypertension, IUGR).37 Recent work by multiple researchers has shown that 3D placental vascularization indices are lower for those with preeclampsia,19 are not aided by the inclusion of pregnancy-associated plasma protein A (PAPP-A) and uterine artery Doppler indices,38 and may be improved with the addition

CHAPTER 43 of 3D placental volume and computer analysis of placental calciication.39 How well these indices can be used for the prediction of preeclampsia requires further investigation. First-trimester 3D power Doppler placental indices are unable to diferentiate between those destined to have growth restriction as compared to normally grown fetuses.40 Recent work in an animal model, however, demonstrating discrimination of maternal and fetal blood low in the microvasculature of the placenta may allow further insights into placental blood low and its efects on placental function.41

Amnion-Chorion Separation he amnion normally “fuses” with the chorion early in the second trimester. Failure of the amnion and chorion to fuse ater 17 weeks is a rare complication of pregnancy, associated with multiple abnormalities. Previous amniocentesis is a risk factor for amnionchorion separation.42 Associated factors may include IUGR, preterm delivery, oligohydramnios, placental abruption, and Down syndrome43 (Fig. 43.6).

Elastography A preliminary report has attempted to diferentiate subchorionic hematoma from placenta previa using elastography.44 More rigorous evaluations have shown that the use of both shear wave and strain elastography of the placenta was diferent between normal pregnancies and those that developed preeclampsia.45,46 his exciting novel area of placental research ofers much promise for the future.

PLACENTA PREVIA he term placenta previa refers to a placenta that is “previous” to the fetus in the birth canal. he incidence at delivery is approximately 0.5% of all pregnancies.47 Bleeding in the second and third trimesters is the hallmark of placenta previa. his bleeding can be life threatening to the mother and fetus. With antenatal detection, expectant management and cesarean delivery,

FIG. 43.6 Chorioamniotic Separation in Second Trimester. Amnion (short arrow) is separated from the chorion (long arrow).

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both maternal and perinatal mortality rates have decreased over the past 40 years.48,49 Accurate diagnosis of placenta previa is vital to improve the outcome for mother and neonate. he diferentiation of placental position has historically been performed by digital assessment of the lower uterine segment and placenta through the cervix. Using this potentially hazardous method of evaluation, placental position was classiied as complete placenta previa, partial placenta previa, incomplete placenta previa, marginal placenta previa, low-lying placenta, and placenta distant from the internal cervical os. hese classiications do not directly apply to the ultrasound examination of placental position relative to the cervix. he use of ultrasound to evaluate the position of the placenta in the uterus has both improved knowledge of the placenta within the uterus and simpliied terminology with respect to placental position (Fig. 43.7). Complete placenta previa describes the situation in which the internal cervical os is totally covered by the placenta. Some diferentiate those placentas that have a portion of placental substance that extends over the internal cervical os from those that are centrally placed over the cervix, a so-called central placenta previa. Marginal placenta previa denotes placental tissue at the edge of, or encroaching on, the internal cervical os. A low placenta is one in which the placental edge is within 2 cm, but not covering any portion, of the internal cervical os. he terms incomplete placenta previa and partial placenta previa have no place in the current sonographic assessment of placental position and should be used only by a clinician performing a digital examination when a “double setup” is necessary to determine where the leading edge of the placenta lies. Transabdominal scanning can be used to visualize the internal cervical os and to determine the relation of the placenta to the cervix in most cases. Factors that can adversely afect the visualization of the cervix include prior abdominal surgery, obesity, deep or low position of the fetal head or presenting part, overilled or underilled maternal bladder, or uterine contractions. Transvaginal sonography (TVS) is safe50 and accurate in depicting the internal cervical os. he proximity of the cervix to the vaginal probe allows higher-frequency probes to be used, with better resolution and thus better visualization of the internal cervical os. With improved resolution, clinicians can accurately determine the position of the leading placental edge to the internal cervical os. he use of TVS has been shown to change the assessment of the placental location in 25% of cases when the placenta is within 2 cm of the internal cervical os, as identiied with transabdominal sonography.51 A leading placental edge greater than 2 cm from the internal cervical os is associated with vaginal delivery, and distances less than 2 cm are associated with bleeding, potentially leading to cesarean delivery.52,53 Although placenta previa can occur in nulliparas, risk factors include number of prior cesarean deliveries (odds ratio: 4.5 for one; 44.9 for four54), increasing parity independent of number of prior cesarean deliveries,55 and increasing maternal age.56 Early in the second trimester, the placenta occupies a relatively large portion of the uterine cavity and oten is positioned near the cervix. As the uterus grows, a lesser proportion of placentas are located near the internal cervical os. his relative change in placental position is best understood by the placental migration

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FIG. 43.7 Placental Position. (A)-(D) Transabdominal sonography (TAS) and (E)-(H) transvaginal sonography (TVS) can be used to determine placental position with respect to the internal os (arrows). If the position is unclear with TAS, TVS should be used. (A) and (E) Complete central placenta previa. (B) and (F) Complete posterior placenta previa. (C) and (G) Marginal placenta previa. (D) and (H) Low placenta. The calipers show the distance from the internal cervical os to the leading placental edge.

theory.57 his theory of “dynamic placentation” suggests that as the uterus develops, the placenta is “drawn away” from the internal cervical os. It is unclear whether the primary mechanism is disproportionate development of the lower uterine segment so that the placenta, although it does not detach from the uterine wall, comes to lie more distant from the internal cervical os. his theory would also be consistent with complete central placenta previas that do not resolve at a rate approaching that of other low-lying placentas, because the expansion of the lower uterine segment would not lead to the resolution of this type of placenta previa. If the placenta overlaps the cervix by less than 2 cm at the end of the second trimester, more than 88% of patients deliver vaginally.58 A rate of migration (in the second and third trimesters) away from the internal os of 3.0 to 5.4 mm per week is also associated with vaginal delivery, whereas a placental-internal os distance of less than 2 cm or a pattern of migration of 0.3 to 0.6 mm weekly are associated with interventional cesarean delivery and a higher rate of peripartum complications.58,59 he prediction of a placenta previa at delivery is best when the placenta overlaps the internal cervical os by 1.4 cm at 10 to 16 weeks’ gestation,60 or 2 cm at 20 to 23 weeks’ gestation.61 Mustafa et al.62 demonstrated that if the placenta overlaps by 2.3 cm at 11 to 14 weeks, the probability of a placenta previa at term is 8%, with a sensitivity of 83% and a speciicity of 86%.62 Aside from a complete central placenta previa, given the current data, it is still diicult to predict precisely which patients will have resolution of their low placenta; therefore further ultrasound examinations are required to assess placental position if a low

placenta is identiied early in gestation. In a large retrospective study, if the placenta was low (5 mm from a straight line connecting the external and internal os), the cervical length can be either traced or the sum of two straight lines that follow the curve can be used.21,28 Using these standard criteria, the interobserver coeicient of variation can be improved to 3.3%.27 TVS is superior to the TAS technique. Higher-frequency transducers and closer proximity to the structures studied allow for better resolution. Potential complications of TVS include an increased risk of bleeding in the presence of placenta previa,

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induction of uterine activity in women with cervical shortening caused by cervical stimulation, and chorioamnionitis in the presence of ruptured membranes. However, increased risk of chorioamnionitis or neonatal sepsis with TVS ater preterm premature rupture of membranes (PPROM) has not been demonstrated.29,30 TVS has also been deemed safe to use in patients with placenta previa with no increased risk for bleeding; however, caution is advised to ensure that the probe is always carefully inserted under real-time visualization.31 To date, TVS assessment of cervical length by three-dimensional sonography has been limited to the development of a normal distribution curve of cervical length through gestation. Overall, mean cervical length appears to be longer than the measurement by traditional two-dimensional scanning. However, there is to be high intra/interobserver variability.32 Currently, there are no reported studies of the relationship between three-dimensional TVS and SPTB prediction.

Technical Limitations and Pitfalls As mentioned previously, one limitation of TAS, especially in advanced gestation, is that the cervix may be obscured by the presenting part, in particular with a cephalic presentation. In addition, a short cervix or empty bladder may reduce the quality of the measurement obtained, whereas a full bladder may artiicially elongate the cervix. here are a number of technical limitations and pitfalls associated with TVS of the cervix. Large maternal body habitus can limit visualization. Bowel gas can obscure visualization. A lower uterine segment myometrial contraction, immediately superior to the cervix, may result in a pseudoelongation of the cervix (Fig. 44.6). he classic tips to recognize this appearance is the artiicially elongated length of the cervix (>5 cm), the thicker diameter of the “cervix” at the proximal extent, which actually incorporates the lower uterine muscle so that it appears thicker than at the external os. he thickness of the internal and external cervical os should be similar. Lower uterine segment contractions are transient and rarely persist beyond 15 minutes. A second pitfall associated with the lower uterine segment contraction has been termed “pseudodilation” of the cervix. It

B

FIG. 44.5 Example of Poor Technique During TVS of Cervix. (A) Excessive pressure on the cervix with anterior lip appearing thinner than the posterior lip causing false elongation and increased echogenicity of the cervix. (B) Removal of pressure with equal anterior and posterior lips. Calipers measure appropriate cervical length.

Cervical Ultrasound and Preterm Birth

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FIG. 44.6 Uterine Contractions. (A) TAS longitudinal image shows contraction (*) leading to a falsely elongated cervical canal (calipers), which measures 7.4 cm. (B) After relaxation of the contraction, the cervix (calipers) measures 4.2 cm. P, Placenta. 60

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FIG. 44.7 Pseudodilation Caused by Uterine Contractions. Transabdominal longitudinal scan shows a lower uterine segment contraction (*) leading to a false appearance of dilated cervical canal. The closed cervix (calipers) measures 3.5 cm.

is caused by a lower uterine segment contraction with partial (Fig. 44.7) or complete approximation of the anterior and posterior myometrium with the resultant false appearance of a “funnel” above the closed cervix. he classic tips to recognize this appearance is the artiicially elongated length of the cervix (>5 cm), the normal cervix lying caudal with respect to the pseudodilation, and the transient nature of this appearance.

Normal Cervix Sonographically, the cervix appears as a distinct, sot tissue structure containing midrange echoes. he endocervical canal

FIG. 44.8 Reference Ranges for Cervical Length Across Gestation. First to 99th percentiles are indicated. (With permission from Salomon LJ, Diaz-Garcia C, Bernard JP, Ville Y. Reference range for cervical length throughout pregnancy: non-parametric LMS-based model applied to a large sample. Ultrasound Obstet Gynecol. 2009;33[4]: 459-464.33)

oten appears as an echogenic line surrounded by a hypoechoic zone attributed to the endocervical glands (see Fig. 44.4B). Occasionally, the endocervical canal may appear hypoechoic and minimally dilated along its entire length. Benign nabothian cysts can be seen within the cervical sot tissues. Numerous studies have evaluated cervical length in normal pregnancy. he typical cervix increases its length in the irst trimester because of elaboration of the glandular content of the cervix.27 Salomon et al.33 published a reference curve of cervical length through gestation using TVS based on a large sample (Fig. 44.8). Based on this study, at about 20 weeks’ gestation,

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FIG. 44.9 Cervical Length and Risk of Preterm Delivery Percentile Ranking. Transvaginal ultrasound cervical length percentile rank, at 24 weeks’ gestation, and relative risk of preterm delivery before 35 weeks. (With permission from Iams JD, Goldenberg RL, Meis PJ, et al. The length of the cervix and the risk of spontaneous premature delivery. National Institute of Child Health and Human Development Maternal Fetal Medicine Unit Network. N Engl J Med. 1996;334[9]:567-572.34)

the 10th, 50th, and 90th percentiles of cervical length are 32.3, 41.9, and 50.5 mm, respectively.33 A progressive linear reduction in cervical length occurs over the 10th to 40th week of gestation.

“Short” Cervix With the goal of understanding the relationship between cervical length and SPTB (delivery before 35 weeks’ gestation), in 1996, Iams et al.34 published a prospective, multicenter study in which an unselected general population of women with singleton pregnancies underwent TVS at 24 and 28 weeks’ gestation. Cervical length at both examinations was comparable and normally distributed, with a mean ±SD of 35.2 ± 8.3 mm at 24 weeks and 33.7 ± 8.5 mm at 28 weeks. A correlation between cervical length and the rate of SPTB was determined (Fig. 44.9); if the cervix was less than 26 mm (10th percentile) or less than 13 mm (1st percentile), risk of SPTB was increased by 6.49-fold and 13.99-fold, respectively, compared with the rate of SPTB if the cervix was at the 75th percentile length (40 mm) or greater.34 Based on this landmark study, the deinition of a “short cervix” as less than 25 mm (or