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Pathology
Fifth Edition
VOLUME 1
Chest, Gastrointestinal, and Genitourinary
Radiologic Pathology Correlation
2006
Editors
2007
Ellen M. Chung, LTC, MC, USA
Chief, Pediatric Radiology
Jeffrey R. Galvin, MD
Chief, Chest Radiology
Kelly K. Koeller, MD
Chief, Neuroradiology
Mark D. Murphey, MD
Six Week Course Director
Chief, Musculoskeletal Radiology
All rights reserved. No part of this publication may be reproduced or transmitted in any form
or by any means: electronic, mechanical, photocopy, recording, or any other information
storage and retrieval system without written permission of the publisher.
Great care has been taken to guarantee the accuracy of the information contained in this
volume. However, neither the American Registry of Pathology, Armed Forces Institute of
Pathology, nor the editors and contributors can be held responsible for errors or for any
consequences arising from the use of the information contained herein.
The opinions and assertions contained herein are the private views of the authors and are
not to be construed as official nor as representing the views of the Departments of the Army,
Air Force, Navy, or Defense.
987654321
ISBN 1-933477-00-8
Preface
The Armed Forces Institute of Pathology’s Radiologic Pathologic Correlation
course presented by the Department of Radiologic Pathology enters its 59th year
of educating radiology residents worldwide. For the fifth year, our staff and visiting
lecturers have contributed their lecture material and images to compile Radiologic
Pathology 2006 – 2007, continuing the tradition of presenting richly illustrated
material that teaches the pathologic basis of disease to improve our understanding
of the imaging appearance of disease. We hope the efforts of our authors and
editors have once again accomplished our goal of bringing the outstanding and
unique Radiologic Pathologic Correlation course to your fingertips.
Acknowledgements
iii
Faculty – VOLUME 1
Chest Radiology
Marc S. Levine, MD
Jeffrey R. Galvin, MD Professor of Radiology
Chief, Pulmonary and Mediastinal Radiology
Hospital of the University of Pennsylvania
Department of Radiologic Pathology
Advisory Dean
Armed Forces Institute of Pathology
University of Pennsylvania School of Medicine
Washington, DC
Philadelphia, PA
and
and
Professor of Radiology and Pulmonary Medicine
Former Distinguished Scientist
University of Maryland
Department of Radiologic Pathology
Baltimore, MD
Armed Forces Institute of Pathology
Gerald F. Abbott, MD Washington, DC
Director of Chest Radiology
Rhode Island Hospital Deborah Rubens, MD
and Professor and Associate Chair
Assistant Professor of Radiology Department of Imaging Sciences
Brown University School of Medicine University of Rochester Medical Center
Providence, RI Rochester, NY
and
Aletta A. Frazier, MD Distinguished Scientist
Staff Radiologist and Medical Illustrator Department of Radiologic Pathology
Department of Radiologic Pathology Armed Forces Institute of Pathology
Armed Forces Institute of Pathology Washington, DC
Washington, DC
and Francis J. Scholz, MD
Clinical Associate Professor of Radiology Staff Radiologist
University of Maryland School of Medicine Lahey Clinic Medical Center
Baltimore, MD Burlington, MA
and
Leonard M. Glassman, MD Clinical Professor of Radiology
Washington Radiology Associates, PC Tufts University School of Medicine
Washington, DC Boston, MA
and
Clinical Professor Robert K. Zeman, MD
Department of Radiology Chairman and Professor of Radiology
George Washington University Medical Center George Washington University
Washington, DC Washington, DC
Melissa L. Rosado de Christenson, MD, FACR
Clinical Professor of Radiology
Genitourinary Radiology
The Ohio State University Paula J. Woodward, MD
Columbus, OH Acting Chief, Genitourinary Radiology
and Department of Radiologic Pathology
Adjunct Professor of Radiology Armed Forces Institute of Pathology
Uniformed Services University of the Health Sciences Washington, DC
Bethesda, MD and
Adjunct Professor of Radiology
Rosita M. Shah, MD University of Utah School of Medicine
Clinical Associate Professor of Radiology
Salt Lake City UT
Hospital of the University of Pennsylvania
Philadelphia, PA
Peter L. Choyke, MD
Chief Molecular Imaging Program
Gastrointestinal Radiology National Cancer Institute
Angela D. Levy, COL, MC, USA Bethesda, MD
Chairman and Gastrointestinal Radiology Section Chief and
Department of Radiologic Pathology Professor of Radiology and Nuclear Medicine
Armed Forces Institute of Pathology Uniformed University of the Health Sciences
Washington, DC Bethesda, MD
and William D. Craig, MD
Associate Professor of Radiology and Nuclear Medicine Chief, Genitourinary Radiology
Uniformed Services University of the Health Sciences Department of Radiologic Pathology
Bethesda, MD Armed Forces Institute of Pathology
Bruce P. Brown, MD Washington, DC
Associate Professor of Radiology
University of Iowa
Iowa City, IA
iv
David S. Hartman, MD
Professor of Radiology
Department of Radiology
Pennsylvania State University
M. S. Hershey Medical Center
Hershey, PA
Deborah J. Rubens, MD
Professor and Associate Chair
Department of Imaging Sciences
University of Rochester Medical Center
Rochester, NY
and
Distinguished Scientist
Department of Radiologic Pathology
Armed Forces Institute of Pathology
Washington, DC
Brent J. Wagner, MD
Chairman, Department of Radiology
The Reading Hospital and Medical Center
West Reading Radiology Associates
West Reading, PA
Jade J. Wong-You-Cheong, MD
Associate Professor of Diagnostic Radiology
Director of Ultrasound
University of Maryland School of Medicine
Baltimore, MD
v
Table of Contents – VOLUME 1
Chest Radiology
Jeffrey R. Galvin, MD
An Approach to Diffuse Lung Disease, Sarcoidosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .3
The Idiopathic Interstitial Pneumonias . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .14
Airways Disease: The Movement from Anatomic to Physiologic Assessment . . . . . . . . . . . . . . . . . . . . . . . .26
Inhalational Lung Disease (Asbestosis and Silicosis) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .44
Pulmonary Lymphoid Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .54
Angiitis and Granulomatosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .63
The Pulmonary Complications of Organ Transplantation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .75
The Diagnosis of Pulmonary Embolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .82
Tuberculosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .93
Fungal Disease in the Thorax: Opportunistic and Primary Pathogens . . . . . . . . . . . . . . . . . . . . . . . . . . . . .100
Bronchogenic Carcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .110
Chest Seminar 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .121
Chest Seminar 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .126
Aletta A. Frazier, MD
Pulmonary Hypertension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .131
Pulmonary Metastasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .138
Melissa L. Rosado de Christenson, MD, FACR
Differential Diagnosis of Mediastinal Masses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .148
Chest Seminar: Where is the lesion? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .168
Chest Seminar: Differential Diagnosis of Mediastinal Masses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .173
Rosita M. Shah, MD
Pneumonia: Usual and Unusual Organisms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .178
Gerald F. Abbott, MD
Uncommon Malignant Tumors of the Lung . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .192
Benign Tumors of the Lung and Tumor-like Lesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .199
Pleural Disease I . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .205
Pleural Disease II and Chest Wall . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .213
Leonard M. Glassman, MD (Mammography)
Classic Breast Lesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .220
Basic Breast Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .229
Ductal Carcinoma in Situ (DCIS) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .238
Breast Abnormalities in Young Women . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .246
The Male Breast . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .257
Gastrointestinal Radiology
Angela D. Levy, COL, MC, USA
Benign Hepatic Neoplasms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .267
Malignant Hepatic Neoplasms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .275
Hepatic Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .284
Imaging of Chronic Liver Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .293
Benign Biliary Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .303
Biliary Neoplasms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .313
Pancreatic Neoplasms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .321
Gastric Malignancies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .332
Abdominal Non Hodgkin Lymphoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .344
Small Intestinal Neoplasms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .353
Colorectal Carcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .361
Mesenteric Masses and Cysts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .372
Idiopathic Inflammatory Bowel Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .382
Approach to Inflammatory Diseases of the Colon . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .391
GI Seminar 1: Abdominal Gas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .400
GI Seminar 2: Nonneoplastic Disease of the Stomach . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .405
GI Seminar 3: Pancreatic Duct . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .411
GI Seminar 4: Hepatic Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .417
GI Seminar 5: Complications of Meckel Diverticulum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .422
vi
GI Seminar 6: Beyond Appendicitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .427
GI Seminar 7: Tumors and Tumor-Like Lesions of the Gallbladder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .432
Robert K. Zeman, MD
Cholelithiasis and Cholecystitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .438
Marc S. Levine, MD
Inflammatory Diseases of the Esophagus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .444
Tumors of the Esophagus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .450
Radiology of Peptic Ulcer Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .455
Bruce Brown, MD
Pancreatitis: Imaging Has Made a Difference . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .460
Gastrointestinal Bleeding In The Age of the Endoscope. What Does a Radiologist Have To Contribute? . .468
Francis J. Scholz, MD
Small Bowel Obstruction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .475
Acute Mesenteric Ischemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .487
Malabsorption . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .505
Familial Polyposis and Other Such . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .519
Deborah J. Rubens, MD
The Spleen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .531
Portal Venous Doppler . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .542
Genitourinary Radiology
Paula J. Woodward, MD
Imaging of Uterine Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .551
Approach to Renal Masses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .561
Urinary Tract Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .573
Retroperitoneum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .579
Radiologic Evaluation of the Scrotum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .585
First Trimester Ultrasound . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .594
Fetal CNS Malformations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .602
Fetal Body Anomalies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .607
Peter L. Choyke, MD
Cystic Diseases of the Kidney . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .614
Imaging of Prostate Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .620
William D. Craig, MD
Radiographic Evaluation of Urinary Stone Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .624
Deborah J. Rubens, MD
Testicular Torsion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .630
Brent J. Wagner, MD
Imaging of Ovarian Masses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .637
Adrenal Imaging in Adults . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .645
Imaging of the Urinary Bladder and Urethra . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .649
Jade Wong You Cheong, MD
Non-Neoplastic Disorders Of The Ovary And Adnexae . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .653
Imaging of Solid Organ Transplants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .664
David S. Hartman, MD
The Neglected Nephrogram . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .674
Problem Renal Masses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .681
Paula J. Woodward, MD
GU Seminar 1: MSAFP . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .691
GU Seminar 2: Renal Calcifications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .693
vii
Chest Radiology
An Approach to Diffuse Lung Disease,
Sarcoidosis
Jeffrey R. Galvin, MD
Figure 1-1-1
Radiologic-Pathology Continuum
Figure 1-1-5
Figure 1-1-6
Sarcoidosis: Epidemiology
• Worldwide
➢ both sexes, all races, all ages Panlobular pattern Septal pattern
• Predilection for adults
➢ under 40 years
➢ peak 20-29 years
• U.S. prevalence Figure 1-1-11 Figure 1-1-12
➢ 10 per 100,000 exams
• Highest disease
➢ African-American women
Figure 1-1-14
Bronchovascular distribution of
granulomas in Sarcoidosis
Stage 0 8 –
➢ Normal
Stage 1 51 65
➢ Adenopathy
Stage 2 29 49
➢ Adenopathy &
Parenchyma
Stage 3 12 20
➢ Parenchyma
Sarcoidosis Stage I
Sarcoidosis Stage II
Sarcoidosis Stage IV
Bilateral calcified lymph nodes are common
Sarcoidosis Progression
Peribronchovascular opacities
in sarcoidosis
Peribronchovascular Nodules
Septal Lines
Fibrosis
Conglomerate Mass
Fibrosis and Emphysema
Sarcoidosis: Diagnosis
• Typical clinical and radiologic manifestations
• Non-caseating granulomas
• Transbronchial Bx
• Endobronchial Bx
Histoplasmosis
Silicosis
Berylliosis
Sarcoidosis: Mortality
• Mortality range 5-10%
• Cor Pulmonale related to fibrosis
• Cardiac Arrhythmia
• Pulmonary Hemorrhage
➢ Aspergilloma
Cor Pulmonale
Figure 1-1-19
Dilated Cardiomyopathy
Sarcoidosis: Therapy
• Cardiac, CNS, eye involvement
• Hypercalcemia
• Corticosteroids
➢ Relief of symptoms; resolution of radiologic abnormalities;
improved function
• Cytotoxic agents
➢ Methotrexate, Azathioprine
• Chlorambucil, cyclophosphamide, antimalarials
• Risk of recurrence
Sarcoidosis: Resolution
Sarcoidosis: Prognosis
• Favorable
➢ Acute onset, erythema nodosum,
➢ > 80% spontaneous remission
➢ Löfgren syndrome
➢ Low stage
• Poor
➢ Chronic course, Lupus pernio
➢ Older age at presentation
➢ Hypercalcemia/nephrocalcinosis
➢ Black race, Extrathoracic involvement
Mycetoma in a cystic space
Sarcoidosis Conclusion caused by sarcoidosis
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1987; 148:8-15.
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8. Grenier P. Valeyre D, Cluze I R Brauner MW, Lenoir 5, Chastang C. Chronic diffuse interstitial lung disease:
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9. Gruden JF, Webb WR, Naidich DR, McGuinness G. Multinodular disease: anatomic localization at thin-section
CT—multireader evaluation of a simple algorithm. Radiology 1999; 210(3):711-20.
10. Gurney JW, Schroeder BA. Upper lobe lung disease: physiologic correlates. Radiology 1988; 167:359-366.
11. Heitzman ER. The lung. Second ed. St. Louis: C.V. Mosby, 1984.
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Desquamative Interstitial
Pneumonia [Figure 1-2-7
Desquamative Interstitial
Pneumonia
RB and DIP
Acute Interstitial Pneumonia Smoking related interstitial lung disease with upper lobe
Histology indistinct nodules, reticulation and well defined emphysematous
• Exudative phase spaces combined with lowerlobe ground glass
➢ Hyaline membranes Figure 1-2-9
➢ Edema
➢ Inflammation
• Collapse of alveoli
• Organizing phase
➢ Type II hyperplasia
➢ Loose fibrosis
• Diffuse Alveolar Damage
Katzenstein, Am J Pathol 1986 ; Ichikado, AJR 1997
Cryptogenic Organizing
Pneumonia [Figure 1-2-13 and 1-2-14]
Figure 1-2-14
Hypersensitivity Pneumonitis
RB-ILD
DIP
Figure 1-2-19
Figure 1-2-20
NSIP-IPF
Figure 1-2-22
Organizing pneumonia
NSIP-Hypersensitivity Pneumonitis
Figure 1-2-23
General
1. American Thoracic Society/European Respiratory Society International Multidisciplinary Consensus Classification
of the Idiopathic Interstitial pneumonias. This joint statement of the American Thoracic Society (ATS), and the
European Respiratory Society (ERS) was adopted by the ATS board of directors, June 2001 and by the ERS
Executive Committee, June 2001. Am J Respir Crit Care Med 2002; 165:277-304
2. Wittram C, Mark EJ, McLoud TC. CT-histologic correlation of the ATS/ERS 2002 classification of idiopathic
interstitial pneumonias. Radiographics. 2003 Sep-Oct;23(5):1057-71.
IPF/UIP
1. Hansell DM, Wells AU. CT evaluation of fibrosing alveolitis—applications and insights. J Thorac Imaging 1996;
11(4):231-49.
2. Katzenstein AL, Myers JL. Idiopathic pulmonary fibrosis: clinical relevance of pathologic classification. Am U
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3. Kondoh Y, Taniguchi H, Kawabata Y, Yokoi T, Suzuki K, Takagi K. Acute exacerbation in idiopathic pulmonary
fibrosis. Analysis of clinical and pathologic findings in three cases. Chest 1993; 103(6):1808-12.
4. Liebow AA. Definition and classification of interstitial pneumonias in human pathology. Prog Resp Res 1975; 8:1-
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5. Tobin RW, Pope CE, 2nd, Pellegrini CA, Emond MJ, Sillery J, Raghu G. Increased prevalence of gastroesophageal
reflux in patients with idiopathic pulmonary fibrosis. Am U Respir Crit Care Med 1998; 158(6): 1804-8.
6. Schurawitzki H, Stiglbauer R, Graninger W, Herold C, Polzleitner D, Burghuber OC, Tscholakoff D. Interstitial
lung disease in progressive systemic sclerosis: high-resolution CT versus radiography. Radiology 1990; 176(755-
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7. Coxson HO, Hogg JC, Mayo JR, Behzad H, Whittall KP, Schwait DA, Hartley PC, Galvin JR, Wilson JS,
Hunninghake SW. Quantification of idiopathic pulmonary fibrosis using computed tomography and histology. Am
J Respir Crit Care Med 1997; 155(5):1649-56.
8. Gay SE, Kazerooni EA, Toews GB, Lynch UP, 3rd, Gross BH, Cascade PN, Spizarny DL, Flint A, Schork MA,
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survival. Am U Respir Crit Care Med 1998; 157(4 Pt 1):1063-72.
9. Bjoraker JA, Ryu JH, Edwin MK, Myers JL, Tazelaar Ho, Schroeder DR, Offord KR. Prognostic significance of
histopathologic subsets in idiopathic pulmonary fibrosis. Am U Respir Crit Care Med 1998; 157(1):1 99-203.
DIP
1. Gaensler EA, Goff AM, Prowse CM. Desquamative interstitial pneumonia. N Engl U Med 1966; 274(3)113-28.
2. Ryu JH, Myers JL, Capizzi SA, Douglas WW, Vassallo R, Decker PA.Desquamative interstitial pneumonia and
respiratory bronchiolitis-associated interstitial lung disease. Chest. 2005 Jan;127(1):178-84.
DAD/AIP
1. Bone RC. The ARDS lung. New insights from computed tomography [editorial; comment]. Jama 1993; 269(1
6):21 34-5.
2. Desai SR, Wells AU, Rubens MB, Evans TW, Hansell DM. Acute respiratory distress syndrome: CT abnormalities
at long-term follow-up. Radiology 1999; 210(1):29-35.
3. Greene R. Adult respiratory distress syndrome: acute alveolar damage. Radiology 1987; 163(1):57-66.
4. Ichikado K, Johkoh T, Ikezoe U, Takeuchi N, Kohno N, Arisawa U, Nakamura H, Nagareda T, Itoh H, Ando M.
Acute interstitial pneumonia: high-resolution CT findings correlated with pathology. AUR Am U Roentgenol 1997;
1 68(2):333-8.
5. Johkoh T, Muller NL, Taniguchi H, Kondoh Y, Akira M, Ichikado K, Ando M, Honda 0, Tomiyama N, Nakamura
H. Acute interstitial pneumonia: thin-section CT findings in 36 patients. Radiology 1999; 211(3):859-63.
6. Katzenstein AL, Myers UL, Mazur MT. Acute interstitial pneumonia. A clinicopathologic, ultrastructural, and cell
kinetic study. Am U Surg Pathol 1986; 10(4):256-67.
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8. Primack SL, Hartman TE, Ikezoe U, Akira M, Sakatani M, Muller NL. Acute interstitial pneumonia: radiographic
and CT findings in nine patients [see comments]. Radiology 1993; 188(3):817-20.
NSIP
1. Cottin V, Donsbeck AV, Revel D, Loire R, Cordier JR Nonspecific interstitial pneumonia. Individualization of a
clinicopathologic entity in a series of 12 patients. Am J Respir Crit Care Med 1998; 158(4):1286-93.
2. Katzenstein AL, Fiorelli RF. Nonspecific interstitial pneumonia/fibrosis. Histologic features and clinical
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BOOP/Organizing Pneumonia
1. Akira M, Yamamoto S, Sakatani M. Bronchiolitis obliterans organizing pneumonia manifesting as multiple large
nodules or masses. AJR Am J Roentgenol 1998; 170(2):291-5.
2. Carlson BA, Swensen SJ, O’Connell EJ, Edell ES. High-resolution computed tomography for obliterative
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Assessment of Dyspnea
A Common Clinical Problem
• 55 million adult smokers
• 15 million meet criteria for bronchitis Figure 1-3-1
• 5 million with airway obstruction
• 10 million with asthma
Gordon Snyder
Airways Disease
Direct Signs [Figure 1-3-4]
• Changes
➢ Airway wall
➢ Airway lumen
• Opacities
➢ Tubular
➢ Nodular
➢ Branching
Airways Disease
Indirect Signs
• Mosaic density
➢ Air trapping
• Subsegmental atelectasis
• Ground glass
Airways involvement at the level of “Tree-in-bud” in a patient with a
Airways Disease the secondary lobule respiratory infection
• Emphysema
• Emphysema and Fibrosis
• Alpha-1 deficiency
• Langherhans Cell Histiocytosis
• Bronchiectasis
• Asthma
• Allergic Bronchopulmonary Aspergillosis
• Sarcoidosis
• Diffuse Panbronchiolitis
• Bronchiolitis Obliterans
• Lymphangioleiomyomatosis
Figure 1-3-5
Emphysema
ATS Definition
• Permanent enlargement of airspaces distal to the terminal
bronchiole, accompanied by destruction of the walls without
obvious fibrosis
Emphysema
Emphysema
Classification [Figure 1-3-5]
• Proximal Acinar
➢ Centrilobular
➢ Resp bronchiole
➢ Cigarette smoke
➢ Upper lobes
• Panacinar
➢ Entire acinus
➢ Alpha-1 deficiency
➢ Lower lobes
• Distal Acinar
➢ Paraseptal
➢ Distal acinus
Cigarette smoke related
➢ Subpleura
emphysema is most severe in the
➢ Pneumothorax
upper lobes
Emphysema
Pulmonary Functions
• Important to identify patients at risk
• Reduction in Fev1
➢ Most reproducible
• RV increases followed by TLC
• Volumes and flows Saber trachea
➢ Insensitive to early changes
• Diffusing capacity
➢ Sensitive but non-specific Figure 1-3-7
• Small airways tests
Emphysema
Radiographic Feature
• Hyperinflation
➢ Concave diaphragm
➢ Increased A-P diameter
➢ Retrosternal airspace
• Arterial deficiency pattern
• Bulla
➢ Cystic airspaces > 1cm
• Radiography is insensitive
➢ 41% of moderate disease
➢ 66% of severe disease
Early Emphysema
Bronchiectasis
Postinflammatory
• Primary Ciliary Dyskinesia
➢ Kartagener’s
• Immunodeficiency
• Postinfectious
➢ TB, Measles, pertussis, viral
• Post-toxic bronchitis
➢ gastric acid aspiration
• Immunologic
➢ ABPA
Post Obstructive Bronchiectasis [Figure 1-3-16] Post obstructive bronchiectasis in a patient with
• Neoplasm mucoepidermoid carcinoma
• Foreign body
• Broncholith
• Lymph node enlargement Figure 1-3-17
Bronchiectasis
Clinical Presentation
• Cough
• Purulent sputum
• Hemoptysis (50%)
• Dyspnea
• Rare
➢ clubbing, brain abscess, amyloidosis
Bronchiectasis
Radiographic Features Upper lobe smoking related
• Prominent markings emphysema
• Crowding of Vessels
• “Tram Tracks” Figure 1-3-18
• Loss of volume
• Cystic spaces
Bronchiectasis
CT Features
• Bronchi in the periphery
• “Signet Rings”
• “Tram Tracks”
• Sensitivity
➢ Collimation
RB-ILD
Emphysema [Figure 1-3-17]
Asthma
ATS Definition
• Reversible airway disease
• Increased airway responsiveness
• Persistent airflow obstruction occurs in chronic asthmatic
➢ Why?
• 6% in the American population
➢ Rate has doubled in 20 years
➢ Higher incidence in large cities
Asthma
Extrinsic
• Family history atopy
• Early onset <30 years
• Seasonal symptoms
• Increased IGE
• Positive skin tests
• Often remits
Asthma
Pathology
• Airway smooth muscle
➢ Hypertrophy
• Airway wall
➢ Inflammation
➢ Edema
Airway thickening in asthma
• Airway plugging
➢ Mucus Figure 1-3-25
➢ Inflammatory exudate
Asthma
Radiographic Features [Figure 1-3-24]
• Chest roentgenogram
➢ Often normal
• Airway thickening
➢ Chronic disease
• Rapid attenuation of vessels
➢ hypoxemia
• Pneumomediastinum
➢ pneumothorax
• Hyperinflation
➢ Adaptive
➢ Later air trapping
Silva AJR 183 September 2004
Diffuse Panbronchiolitis
Pathology
• Discrete nodules
• Early infiltration Figure 1-3-30
➢ Interstitium
➢ Respiratory bronchioles
➢ Alveolar ducts
➢ Foamy histiocyte, lymphocyte and plasma cells
• Late secondary ectasia
➢ Proximal terminal bronchioles
Diffuse Panbronchiolitis
Imaging Early
• Radiography
➢ Nodules 5mm
➢ Hyperinflation
• Computed Tomography
➢ Centrilobular nodules
➢ Branching opacities
➢ Mosaic attenuation
Early Diffuse Panbronchiolitis represented by
widespread airways nodules
Diffuse Panbronchiolitis [Figure 1-3-30]
Constrictive Bronchiolitis
Introduction
• Confusing Terminology
➢ Obliterative Bronchiolitis
➢ Bronchiolitis Obliterans
➢ Bronchiolitis Obliterans Organizing Pneumonia
✧ Different disease
✧ Cryptogenic organizing pneumonia
• Small Airways
➢ Fibrosis
➢ Inflammation
• Response to
Severe airway involvement in
➢ Inflammatory disorders
panbronchiolitis
➢ Infectious disorders
Constrictive Bronchiolitis
Classification
• Infection
➢ RSV, adenovirus and mycoplasma
• Toxic Inhalation
➢ Ammonia, acid and NO
• Aspiration: gastric acid
• Collagen Vascular: RA
• Organ Transplantation
• Unknown
Constrictive Bronchiolitis
Histology [Figure 1-3-32]
• Obstruction
➢ Terminal bronchiole Constrictive bronchiolitis
➢ Respiratory bronchioles
• Polyps of fibrosis
• Cellular infiltration
➢ Lymphs
➢ Plasma cells
➢ Histiocytes
Constrictive Bronchiolitis
Imaging [Figures 1-3-33 and 1-3-34]
• Hyperinflation
➢ Localized
➢ Diffuse
• Discrete nodules Figure 1-3-34
➢ Airway associated
• Mosaic pattern
• Airway thickening
• Bronchiectasis
• Air trapping
Figure 1-3-33
Swyer-James Syndrome-Adenovirus
Figure 1-3-37
Lymphangioleiomyomatosis
Clinical Presentation
• Exclusively women
• Reproductive years
• Progressive dyspnea
• Chylous pleural effusions
• Hemoptysis
• Massive hemorrhage
Lymphangioleiomyomatosis
Function
• Obstructive defect
• FEV1 is decreased
• TLC and RV increased
• DLCO reduced
• Hypoxemia
• Hypocapnia
Lymphangioleiomyomatosis
Gross Features [Figures 1-3-37 and 1-3-38]
• Cysts
➢ 0.2-2cm
• Diffuse involvement
• Enlarged thoracic duct
• Enlarged lymph nodes
Lymphangioleiomyomatosis
Thin-walled cysts and a
CT Features [Figure 1-3-39]
pneumothorax in patient
• Thin-walled cysts
with
➢ More sensitive than plain film
lymphangioleiomyomatosis
• Diffuse
• Bilateral involvement
• Adenopathy
Figure 1-3-40
Lymphangioleiomyomatosis [Figure 1-3-40]
Lymphangioleiomyomatosis
Therapy and Prognosis
• Slowly progressive course
➢ Variable
• Progression
➢ Cor pulmonale
➢ Respiratory insufficiency
• 50-80% 5 year survival
➢ Average survival 10 years
• Hormonal therapy
➢ Oophorectomy, progesterone
Asthma
Swyer-James Syndrome
Physiologic Measurement
An Integral Part of Imaging
• Imaging provides physiologic information
➢ not available from pulmonary functions
ABPA
• Air content and blood flow can be quantified
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Pneumonokoniosis
• “It will then be necessary to embrace under a single title all essentially
identical forms of disease
• …the pneumonokoniosis (from Konis, dust) recommends itself” Figure 1-4-1
Zenker 1866 Hematite Mining
Inorganic Dusts
• Silica
• Asbestos
• Coal
• Iron
• Beryllium
Pneumoconiosis
The accumulation of dust in the lungs and the tissue
reaction to its presence
• Dust macules
• Diffuse interstitial fibrosis
• Diffuse alveolar damage
• Alveolar proteinosis
• Giant cell (GIP)
• Granulomatous inflammation
Types and Sizes of Common Aerosols Particles less that 5 microns can be
deposited beyond the conducting
Particle Deposition airways in the alveolar spaces.
Inertial impaction, sedimentation and diffusion [Figure 1-
4-1]
• 10,000-20,000 liters/day
• Deposition related to particle size
• >10 microns deposit in nasopharynx and large airways (100%) Figure 1-4-2
• 1-5 micron particles deposit in lung parenchyma (20%)
Airway Velocity
Inertial impaction, sedimentation and
diffusion
Alveoli in the bases are smaller than those in the The smaller alveoli in the bases enlarge to a
apex. greater degree than those in the apex. Therefore
most airflow is directed towards the bases
Physiologic Gradients-Blood Flow [Figure 1-4-5]
There is increased blood flow and hydrostatic The lymphatics are driven by hydrostatic pressure.
pressure in the dependent vessels Therefore lymphatic flow is best in the dependent
lung.
Silicosis
Mineralogy
• Silicon
➢ Element
• Silica (SiO2)
➢ Mineral
• Silicone
➢ Synthetic polymer
Figure 1-4-9
Silicosis
Pathogenesis
• 5 million particles/cubic foot-lower threshold
• 100 million particles/cubic foot-100% affected
• > 5 micron particle removed in nares and upper airways
• 80% of particles removed in hours to days
• Retained particles consistently .5-.7 microns
Silicosis
Pathogenesis
• Macrophages and polys concentrate
• Macrophages generate oxygen-free radicals
• Macrophages generate fibrogenic proteins
• Immune related tissue damage
➢ Rheumatoid factor, ANA and gamma globulin The silicotic nodule is typical
response to inhaled silica
Silicosis [Figures 1-4-8 to 1-4-11]
Clinical manifestations
• Diagnosis
➢ Typical imaging pattern of adenopathy and nodules
➢ Exposure to high concentration of silica
➢ 10-20 years of exposure
Figure 1-4-13
• Simple silicosis
➢ Asymptomatic
• Symptoms with PMF
• Intense exposure
➢ Silicoproteinosis
• TB and cancer
Simple Silicosis
Pathology [Figure 1-4-12]
• Progress to mature nodules: 3 zones
➢ Central dense fibrosis
➢ Mid-zone concentric collagen
➢ Peripheral dust laden cells
Simple Silicosis
Imaging manifestations [Figure 1-4-13]
• Adenopathy common
• Calcification 10-20%
• Calcification 5-10%
➢ Eggshell pattern
Simple Silicosis
Imaging manifestations
• Well-circumscribed nodules
➢ 1-10 mm
• Upper lobe and posterior
➢ Lymphatic gradient
➢ CT more sensitive
• Pleural lesions
➢ Candle-wax or pseudoplaques
Eggshell calcification
Silicosis
Computed tomographic technique
• Thick sections of value in nodular diseases
➢ Small nodules easier to differentiate from vessels
• Thin sections 1-2 mm collimation at 10 mm intervals or 3-5 selected Crazy paving pattern associated
images with prior thick section CT with alveolar proteinosis
• High spatial frequency algorithm
• Supine Figure 1-4-16
• No contrast
Nonoccupational Exposure
Asbestos
Serpentine: chrysotile Figure 1-4-19 Figure 1-4-20
• 95% of commercial use
• Curly and pliable
• Textile manufacture
• Fragments easily
• Chemically unstable
➢ Dissolves easily
• Less pathogenic
Asbestos
Amphiboles: amosite,
crocidolite, anthophilite,
tremolite and actinolite
• 5% of commercial use
• Straight, broad fiber
• Do not fragment easily
Pleural effusions are the most Rounded atelectasis is usually
• Long fibers (>20 microns)
common early complication of preceded by a pleural effusion
➢ Not cleared
asbestos exposure
• More likely coated
• Higher carcinogenic potential
Figure 1-4-21
Asbestos Related Chest Disease
[Figures 1-4-19 to 1-4-21]
• Pleural effusions
• Pleural plaques
• Round atelectsis
• Pleural thickening
➢ Diffuse
• Mesothelioma
• Asbestosis
• Lung cancer
Asbestosis is a lower
lobe subpleural process
Pleural Plaques
• Postero-lateral parietal pleura
• Central diaphragm
• Absent
➢ Apices and costophrenic angles
• Almost always bilateral The visceral pleural stripe is best seen between the ribs
• Sharply demarcated
• Millimeters to 10 cm
• May calcify extensively
• Highly suggestive of asbestos exposure
Roberts, AJCP 1971
Figure 1-4-23
Pleural Plaques
Imaging
• Radiography insensitive
➢ (8-40% of autopsy cases)
• Companion shadows
➢ Fat and muscle
• HRCT
➢ Best sensitivity and specificity
Pleural Effusion
Definition
• History of exposure to asbestos
• Confirmation of effusion
➢ Imaging of thoracentesis
• Absence of other disease related to effusion
• Absence of malignant tumor for 3 years
Epler, JAMA 1982 Visceral pleural plaques
Pleural Effusion
Differential diagnosis
• Lung cancer
• Tuberculosis
• Benign asbestos effusion
• Mesothelioma
Round Atelectasis
• Described 1928 Loeschke
• Usually asymptomatic
• Folded lung vs inflammatory reaction
• Associated conditions Round atelectasis is associated with
➢ Asbestos exposure, CHF, infarct, TB and histoplasmosis pleural effusion
• Preceded by effusion
Round Atelectasis
Histology [Figure 1-4-25]
• Irregular fibrous thickening of the visceral pleura
• Extensive pleural folding beneath the fibrosis
• Layers of invaginated pleura bound by fibrous adhesions
• Surrounding lung collapsed or fibrotic
Figure 1-4-26
Menzies, AJSP 1987
Round Atelectasis
Imaging criteria [Figure 1-4-26]
• Well-circumscribed
• Round or oval opacity
• “Comet tail” sign
• Pleural thickening
• Volume loss
Asbestosis
Pathologic definition
• Interstitial fibrosis
➢ Associated with asbestos bodies
• Biopsy
➢ Not the standard of practice
Asbestosis
• Dose-response relationship
• Probable exposure threshold
• Latency period inversely proportional to exposure level
• Latency is several decades
• Cigarette smoke may act synergistically
Round atelectasis
Asbestosis
Histology
• Early
➢ Fibrosis of respiratory bronchioles
• Progression
➢ Terminal bronchioles, alveolar ducts and alveolar septa
• Minimum 2 asbestos bodies in area of fibrosis
Craighead, Arch Pathol Lab Med, 1982
Asbestosis
Chest radiography
• Lower lobe
➢ Irregular opacities
➢ Nonspecific
➢ Associated pleural disease
• Large inter-observer variation
➢ Low perfusion
• Normal in 26% of path proven cases
Short Lines
Honeycombing
Asbestosis vs UIP
• Asbestos exposure in the last 30 years is low
• Clinical asbestosis requires substantial exposure
• Asbestos exposed individuals can have other interstitial lung diseases
• Band like opacities merging with the pleura are rare in UIP
• Upper zone fibrosis and ground glass are rare in asbestosis
Gaensler, ARRD, 1991 – Al-Jarad, Thorax, 1992
Asbestosis
High-resolution CT
• Short lines and parenchymal bands are statistically most significant
• Strong association with diffuse pleural disease
• Multifocal
• HRCT finds asbestosis in exposed individuals with normal radiographs and
PFT’s
• Obstructive PFT’s correlate with emphysema
Aberle, AJR, 1988 – Aberle, Radiology, 1988 – Staples, ARRD, 1989
Asbestosis
Dependent density
• Posterior blood flow
➢ 5X’s greater
• Posterior alveoli
➢ Smaller or collapsed
➢ Less steep ventilatory gradient
➢ Closing volumes
(10-40% of VC)
Asbestosis
Computed tomographic technique
• 1.5-2 mm collimation
• 10 mm interval
• High spatial frequency algorithm
• Prone
• Thick section supine: CA screen?
Tuberculosis
Silicosis
Asbestosis
Lymphomatoid Granulomatosis
[Figure 1-5-15]
• Pathologic features
➢ Majority of cases are B-cell lymphomas
➢ Reactive small T-cells
➢ Malignant B-cells
✧ Majority of infiltrate
➢ Epstein-Barr Virus
➢ Angiocentric infiltration
➢ Necrosis
✧ Peribronchovascular
✧ Peripheral
Lymphomatoid Granulomatosis
• Clinical
➢ 7-85 years (mean 48 yrs)
➢ Male:Female (2:1) Lymphomatoid Granulomatosis is an
➢ Malaise and weight loss angiocentric B-cell lymphoma which
➢ Lung involvement 100% often demonstrates areas of necrosis.
➢ Cough and dyspnea
➢ Skin 39-53%
✧ Nodules, ulcers and rash Figure 1-5-16
➢ CNS 37-53%
➢ Renal 32-40%
➢ High mortality rate 53-90%
➢ Most proceed to lymphoma
Lymphomatoid Granulomatosis
• Imaging
➢ Nodules 80%
✧ Multiple
✧ Bilateral (80%)
➢ Mid and lower lobes
➢ Cavitation 20%
➢ Large masses Chest CT on the left demonstrates a
✧ Correspond to infarcts bronchovascular distribution of
➢ Diffuse reticulonodular opacities nodules that are shown to be areas of
➢ Hilar adenopathy 25% infarction on gross examination.
Prolonged Chemotherapy
Figure 1-5-18
Pulmonary Lymphoid Disorders
Derivations of BALT
• Hyperplasias of BALT
• Non-Hodgkin lymphomas
• Immune impairment
➢ Posttransplantation Lymphoproliferative Disease
PTLD
➢ AIDS
➢ Other
Figure 1-5-21
Figure 1-5-23
Lymphomatoid Granulomatosis
References
General
1. Koss MN. Pulmonary lymphoid disorders. Semin Diagn Pathol. 1995 May;12(2):158-71.
2. Travis WD, Galvin JR.Non-neoplastic pulmonary lymphoid lesions. Thorax. 2001 Dec;56(12):964-71.
Pathogenesis of Vasculitis
Upper Airway
• Chronic nasal obstruction
➢ Chronic discharge
• Destruction of cartilaginous nasal septum
• “Saddle nose deformity”
• Laryngeal involvement
➢ Subglottic stricture
• Eustachian tube obstruction
• Otitis media
• Cochlear nerve vasculitis
Pulmonary
• Most commonly affected (94%)
• Multiple bilateral nodules or masses
Airway narrowing is a common
• Cavitation common (30-50%)
complication
• Occasionally solitary mass or nodule
➢ Dx difficult
➢ All patients progress
• Less common
➢ Diffuse alveolar hemorrhage
• Pleural lesion and effusions are rare
Changing Presentation
Microscopic
polyangiitis
Wegener’s Granulomatosis: Laboratory
• ANCA
➢ Serum Antineutrophil Cytoplasmic Autoantibody
• c-ANCA cytoplasmic pattern
➢ Proteinase 3
➢ 99% specificity and 96% sensitivity in active disease
➢ Positivity drops to 30% in remission
• p-ANCA perinuclear pattern
➢ Reacts with myeloperoxidase
➢ positive in collagen vascular diseases
Bronchocentric Granulomatosis
Clinical and Demographics – Non-Asthmatics
• Average age 50 years
• Males=Females
• Fungal infections
➢ Histo, blastomyces, aspergillus
• Mycobacterial infections
• Rheumatoid arthritis
• Wegener’s granulomatosis
• Idiopathic
Fungal Infection ?
References
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Introduction
• Organ transplant first performed the 1960’s
• Solid organ for vital organ failure
• Hematopoietic stem cell (HSC)
➢ Standard therapy
✧ Malignant, hematologic, autoimmune and genetic diseases
• Not proven in breast cancer
Immunologic Impact
• Profound neutropenia
• Prolonged depression
➢ Cellular function
➢ Humoral function
• Graft-vs-host
➢ Direct effect
➢ Steroids
Pulmonary Hemorrhage
• 21% of BMT patients
• 12th day posttransplantation
• Neutrophil recovery
• Sudden onset:
➢ Dyspnea, cough, fever and hypoxemia
• Rare hemoptysis Typical infarct with a halo of blood in an aspergillus
• Mortality 50-80% infection
• Radiographic abnormalities before symptoms
• Bilateral ground glass opacities
➢ May be localized
Figure 1-7-7
Cytomegalovirus Pneumonia
• 10-40% of BMT patients
• 6-12 weeks posttransplantation
• Mortality rate of 85%
• Reactivation of latent virus in 70%
➢ Remainder infected by “CMV positive”
blood products
• Anti-viral therapy improves prognosis
GVHD and IPS In the early phase (exudative) there is diffuse consolidation
and ground glass often with peripheral clearing
GVHD and Infection
Figure 1-7-12
GVHD and IPS
Radiation Pneumonitis
• Related to dose of TBI
• Presents within 90 days
• Cough, fever, and dyspnea
• Threshold lowered by chemotherapy
Mediastinal Emphysema
• Correlates
➢ Idiopathic interstitial pneumonia
• Increased likelihood with more radiation
• Not a serious complication by itself
• May be a harbinger of pneumothorax
Bronchiolitis Obliterans
• 2-13% of BMT’s Bronchiolitis obliterans
• Low immunoglobulin level demonstrating mosaic
• Chronic GVHD attenuation
➢ Sicca syndrome
Figure 1-7-14
• 100 days posttransplantation
• Gradual deterioration of PFT’S
• Airflow obstruction
➢ Fixed
• Reduction in diffusing capacity
• Imaging
➢ Mosaic attenuation
➢ Expiratory accentuation
➢ Centrilobular nodules
➢ Patchy consolidation
Diffuse Opacities
• Pulmonary edema Bronchiolitis obliterans demonstrating indistinct
• Hemorrhage nodules and branching opacities
• Diffuse alveolar damage
• Viral pneumonia Figure 1-7-15
• Pneumocystis pneumonia
Fluid Overload
Organizing Pneumonia
BMTP
BMTP Aspergillus
BMTP: Edema
References
General
1. Franquet T, Muller NL, Lee KS, Gimenez A, Flint JD.High-resolution CT and pathologic findings of noninfectious
pulmonary complications after hematopoietic stem cell transplantation. AJR Am J Roentgenol. 2005 Feb;184(2):629-
37
2. Kotloff RM, Ahya VN, Crawford SW.Pulmonary complications of solid organ and hematopoietic stem cell
transplantation. Am J Respir Crit Care Med. 2004 Jul 1;170(1):22-48. Epub 2004 Apr 7
Pulmonary Embolus
• Frequent
• Potentially fatal
• Largely undiagnosed
Baglin, J Clin Path, 1997
Predisposing Causes
• 1° thrombophlebitis 39%
• Bed rest 32%
• Recent surgery 31%
• Venous insufficiency 25%
• Recent fracture 15%
• Myocardial infarction 12%
• Malignancy 8%
• CHF 5%
• No Predisposition 6%
Chest CT Findings
• Atelectasis 100%
• Consolidation 57%
• Hampton’s hump 50%
• Ground glass 57%
• Pleural Effusions 87%
• Mosaic attenuation
Truong, ARRS, 1998
V/Q Physiology
Ventilation/Perfusion Scanning
Clinical Science Probability (%)
80-100 20-79 0-19 All Probabilities
• High 96% 88% 56% 87% (103/118)
• Intermediate 66% 28% 16% 30% (104/345)
• Low 40% 16% 4% 14% (40/296)
• Normal 0% 6% 2% 4% (5/128)
• Total 68% 30% 9% 28% (252/887)
PIOPED
CT Angiography
Pulmonary CT Angiography
Negative Predictive Value of a Normal CT
• No prospective, consecutive studies
• “The safety of withholding anticoagulants…is uncertain”
Pulmonary CT Angiography
Negative Predictive Value of a Normal CT
n Follow-up NPV
Mayo 69 3m 97%
Feretti 109 3m 97%
Garg 78 6m 99%
Loomis 81 6m 100%
Goodmann 198 3m 99%
Remy-Jardin 71 3m 97%
Tillie-Leblond 185 12m 98%
Kavanagh 85 9m 99%
Conclusion
• The clinical diagnosis of PE is unreliable
• The chest radiograph is usually abnormal
• V/Q readings restricted to “reliable categories”
• Small clots are a problem for all modalities
• Outcome studies are key
• CT angiography is the modality of choice
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23. Revel MP, Petrover D, Hernigou A, Lefort C, Meyer G, Frija G. Diagnosing pulmonary embolism with four-
detector row helical CT: prospective evaluation of 216 outpatients and inpatients. Radiology. 2005 Jan;234(1):265-
73.
Tuberculosis
• Leading cause of death from infectious disease
• 8-10 million new cases/year
• 2-3 million deaths/year
• 1/3 of world population infected
• > 90% of new cases in developing countries
• 80% 15-59 years of age
• Highest incidence
➢ Southeast Asia: 247/100,000
➢ Sub-Saharan Africa: 191/100,000
✧ HIV co-infection: 60% of children, 70% of adults
Tuberculosis: History
• Ancient disease
• 1882: Robert Koch
➢ Isolation of M. tuberculosis
• 1944: streptomycin
• 1952: INH
Mycobacteria
• Tuberculosis complex
➢ M. tuberculosis, M. bovis, M. africnum, M. microti
• M. tuberculosis and M. bovis
➢ > 95% of pulmonary mycobacterioses
• Slow growth
• Person-to-person transmission
Tuberculosis: Pathogenesis
• Inhaled bacteria [Figure 1-9-2]
➢ Mid to lower lung zones
➢ Ghon focus
Tuberculosis: Pathogenesis
• Inhaled bacteria
➢ Mid to lower lung zones
➢ Ghon focus
• Regional lymph node spread [Figures 1-9-3]
➢ Ranke complex
• Lymphatic/hematogenous dissemination
• Cell-mediated immunity In primary tuberculosis the ineffective
• Delayed hypersensitivity macrophages carry bacteria to
➢ Caseous necrosis regional lymph nodes where they
➢ 2-10 weeks proliferate and disseminate
• Healing
Lymphadenopathy is hallmark
of primary TB and is more
common in children
Figure 1-9-8
The lymph nodes which surround
airways may cause narrowing that
results in atelectasis
Figure 1-9-9
Postprimary TB implies
reactivation of dormant bacilli. It is
characterized by tissue destruction
Figure 1-9-12
Thoracoplasty
Oleothorax
Postprimary Tuberculosis-Nodules
Postprimary Tuberculosis-Airways
Tuberculosis: Complications
• End-stage disease
• Hemoptysis Images demonstrate broncho-esophageal fistula
➢ Bronchial arteries in chronic cavities which was a complication of plumbage
➢ Mycetoma
➢ Rassmussen (pulmonary artery) aneurysm
• Chest wall involvement
• Pericardial involvement
• Empyema
➢ BPF, empyema necessitatis
Hemoptysis-Bronchial Artery
Hemoptysis-Mycetoma
End-Stage Lung
Tuberculosis-Chest Wall
Tuberculosis-Pericardial
Tuberculosis: HIV/AIDS
• CD4>200
➢ Well formed granulomas
➢ Upper lobe cavities, consolidation and nodules
• CD4<200
➢ Poorly formed granulomas
➢ Adenopathy, consolidation and miliary disease
• CD4<60
➢ No hypersensitivity reaction
➢ Organisms spread from GI tract
➢ Miliary Disease
Tuberculosis: Diagnosis
• Conventional methods
➢ Acid-fast smear: 1 day
➢ Culture: 1-2 weeks
➢ Identification: 2-3 weeks
➢ Drug susceptibility testing: 3-4 weeks
• Radiometric methods
• Polymerase chain reaction (PCR)
• HPLC
References
General
1. Leung AN.Pulmonary tuberculosis: the essentials. Radiology. 1999 Feb;210(2):307-22
Opportunistic Invaders
• Immunocompromised host
➢ Mucosal disruption
➢ Reduced cellular and/or humoral immunity Figure 1-10-1
• Ubiquitous
• Lack dimorphism
• Multiple organisms may occur
Primary Pathogens
• May infect healthy individuals
• Dimorphism
➢ Saprophytes in the soil
➢ Spores via germination
• Most disease mild or subclinical
• Fulminant or chronic disease may occur
• Specific geographic regions
➢ Endemic
Coccidioidomycosis
Histoplasmosis: Pathology
• Distinction from tuberculosis
➢ Histoplasmosis relatively benign
➢ Immunity to histoplasmosis short lived Figure 1-10-3
✧ 20% lose immunity each year From three to 5
✧ Continuous reinfection days following
– Primary and postprimary not appropriate inhalation the
spores germinate
Histoplasmosis: Clinical and release
• Asymptomatic yeast forms. The
➢ 95-99% of infection in endemic areas yeast within the
➢ Parenchymal opacities in 10-25% alveoli are rapidly
➢ Small inoculum or prior infection (cellular phagacytosed by
macrophages
immunity) and moderate inoculum
• Symptomatic
➢ Acute
✧ Moderate vs large inoculum
➢ Chronic
➢ Disseminated
• Late complications
➢ Histoplasmoma
➢ Broncholithiasis
➢ Mediastinal granuloma
➢ Mediastinal fibrosis
Figure 1-10-4
Histoplasmosis: Acute Clinical Lymphocyte-
• Signs and symptoms
mediated
➢ “Flulike”: fever, chills, cough
cellular
➢ Retrosternal pain
immunity
✧ Mediastinal lymph node involvement
develops at 10-
➢ Erythema nodosum in women
14 days
➢ Arthralgia
controlling the
• Shorter incubation with prior exposure
infection
through a
Histoplasmosis: Acute Radiology necrotizing
• Poorly defined areas of consolidation
granulomatous
✧ Single or multiple
response
• Hilar lymph node enlargement
• Numerous discrete nodular shadows in heavy
exposure
✧ 3-4 mm
✧ Symptoms precede radiographic change
✧ Nodules change to punctate calcifications
Histoplasmosis: Histoplasmoma
• Solitary nodule (.5-3 cm)
➢ Sharply defined
➢ Smaller satellite lesions
➢ Central or diffuse calcification
✧ Diagnostic of benign lesion if less that 3 cm
➢ May increase in size
✧ Similar reaction to fibrosing mediastinitis
• Hilar calcification common on ipsilateral side
• Fungal nodules account for 30% of all solitary
nodules
• 87% are less than 2.5 cm in diameter
Figure 1-10-8
Histoplasmosis: Mediastinal granuloma
• Pathology
➢ Direct infection of hilar and mediastinal lymph
nodes
• Clinical
➢ Often asypmtomatic with discovery of a
mediastinal mass on chest radiograph
➢ SVC or esophageal obstruction less common
• Radiology
➢ Middle mediastinal mass
✧ Subcarinal or paratracheal
➢ Enhancing capsule with low attenuation center
➢ Mass may be low signal on T2 weighted MR
because of fibrous tissue or calcification
Figure 1-10-9
Histoplasmosis: Fibrosing
Mediastinitis
• Pathology
➢ Proliferation of acellular collagen and
fibrous tissue within the mediastinum
➢ Most cases in the United States are an
immunological response to H. capsulatum
✧ Focal form: paratracheal and
subcarinal
✧ Calcification
➢ Idiopathic form
✧ Diffuse, infiltrating
✧ Noncalcified
✧ Multiple mediastinal compartments
• Clinical
➢ Signs and symptoms of obstruction to
mediastinal structures Mediastinal granuloma is the result of direct infection of
✧ Superior vena cava, pulmonary veins mediastinal lymph nodes. Acutely the lymph nodes
demonstrate low attenuation with an enhancing capsule
or arteries, central airway or
esophagus
Blastomycosis
Blastomycosis: Pathology
• Initial response is neutrophilic
• Chronic inflammatory response
• Both responses may coexist
• Progression
➢ Coalescence of patchy consolidation
➢ Airway perforation
➢ Cavitation
• Ulcerative bronchitis is common Figure 1-10-13
Blastomycosis: Radiologic Manifestations
• Consolidation most common
➢ Upper lobe 2:1
➢ Rounded, ill-defined
➢ Masslike opacities
✧ Central or paramediastinal
✧ Carinoma mimic
✧ Solitary nodules
➢ Air bronchograms (88% CT)
➢ Cavitation
• Nodules
➢ Intermediate size
➢ Remote from consolidation
➢ Satellite lesions
• Miliary disease Blastomycosis often with an upper lobe areas of mass-
➢ Hematogenous dissemination like consolidation
Similar to Postprimary TB
Blastomycosis: Treatment
• Pulmonary disease may be self-limited even if
extensive
• Extrapulmonary disease requires treatment
• Amphotericin B IV or oral Keotconazole
Miliary disease may complicate infection with
Blastomycosis
Coccidioidomycosis: Epidemiology
and Ecology Figure 1-10-15
• Ecological niche
• Dimorphic fungus
• Clinical
➢ Acute Disease
✧ 100,000 new cases each year, essentially all
in the southwest
✧ No racial, sex or age predilection in acute
disease
✧ Most inhabitants of the endemic area
infected in the first year of exposure
✧ Incubation period 10-16 days
✧ 60% are asymptomatic
✧ Symptoms when present include
– Fever, pleuritic chest pain, cough
– Valley Fever: allergic form with erythema
nodosum or multiforme
✧ Severity of disease related to immune status Coccidioidomycosis is associated exclusively with the
and race desert southwest
– Filipinos, African Americans and
Hispanics more likely to suffer dissemination
➢ Chronic Disease (5%)
✧ Symptoms persist without dissemination
✧ May be mildly immunocompromised
➢ Dissemination
✧ Rare occurrence
– Immunocompromise
– Non-Caucasian (Filipino, African American and Hispanic)
– Early dissemination more common and carries a poor prognosis
– Mortality rate or 50% even with early treatment
Coccidioidomycosis: Pathology
• Lung the usual portal of entry
• Neutrophilic response early
➢ Especially in response to ruptured spherules
➢ Spherules ingested by macrophages
• Granulomatous and giant cell reaction follows
• Necrosis may occur
Histoplasmosis
Blastomycosis
As the infection heals the inflammatory area rounds up and is The nodule may enlarge by adding fibrous tissue to the
surrounded by a fibrous capsule. Over a prolonged period periphery
calcification may develop in the nodule and regional lymph
nodes
Figure 1-10-22
Figure 1-10-23
Figure 1-10-24
Figure 1-10-25
Clinical Presentation
• Central tumors
➢ Cough
➢ Wheezing
➢ Hemoptysis
➢ Pneumonia
• Extrapulmonary invasion
➢ Pain
➢ Pancoast Syndrome
➢ SVC Syndrome
• Metastases
• Paraneoplastic Syndromes
• Asymptomatic 10%
Paraneoplastic Syndromes
• Cachexia, malaise and fever
• Ectopic hormone production
➢ ACTH
➢ ADH
➢ Hypercalcemia
➢ Clubbing and HPO
➢ Thrombotic endocarditis
➢ Non-bacterial
• Migratory thrombophlebitis
Figure 1-11-3
Figure 1-11-4
Pancoast Tumor:
Superior Sulcus Tumor
• Characteristic pain
➢ 8th cervical
➢ 2nd thoracic trunk
• Horner’s Syndrome
• Destruction of bone
• Hand muscle atrophy
Pancoast, JAMA, 1992
Small Cell Lung Cancer
• Rapid growth
• Considered metastatic at presentation
• Poorest survival
• Strongest association with cigarette
smoking
Adenocarcinoma: Etiology
• Cigarette smoke causatively linked to lung
cancer
➢ 1950
➢ Squamous cell 18X’s Adeno
➢ Squamous cell: central
Adenocarcinoma: Etiology
[Figure 1-11-10]
• Cigarette smoke causatively linked to lung
cancer
• Adenocarcinoma most common
➢ Peripheral
• Filtered low-yield cigarettes
➢ Smaller particles
➢ Reduced nicotine Large cell cancers are commonly necrotic but rarely cavitate
➢ Greater depth of puffs
➢ Increased number of puffs
➢ N-nitrosamines Figure 1-11-10
• Other factors - 10%
➢ Passive smoke
➢ Particulates
➢ Cooking practices
Necrosis
Figure 1-11-12
Figure 1-11-13
AAH
Bronchioloalveolar Carcinoma
BAC Recurrence
BAC often presents as as area of
BAC vs Adenocarcinoma consolidation
The precursor lesion to BAC is AAH BAC demonstrates lepidic growth and presents as an
area of ground glass and/or consolidation
General
1. Travis W, Colby T, Shimasato Y, Brambilla E. Histological Typing of Lung and Pleural Tumors., International
Classification of Tumors. Third ed. Berlin: Springer Verlag, 1999.
2. Colby T, Koss M, Travis W. Tumors of the Lower Respiratory Tract, Atlas of Tumor Pathology. Third ed. Washington,
DC: Armed Forces Institute of Pathology, 1999.
3. Travis WD, Brambilla E, et al: Pathology and Genetics of Tumours of the Lung, Pleura, Thymus and Heart (WHO
Classification of Tumours), IARC Press, 2004 (Oxford).
4. Patel AM, Peters SG. Clinical manifestations of lung cancer Mayo Clin Proc 1993; 68(3):273-7.
5. Davila DG, Williams DE. The etiology of lung cancer. Mayo Clin Proc 1993; 68(2): 170-82.
6. Travis WD, Lubin J, Ries L, Devesa S. United States lung carcinoma incidence trends: declining for most histologic
types among males, increasing among females. Cancer 1996; 77(12):2464-70.
7. Travis WD, Travis LB, Devesa SS. Lung cancer [published erratum appears in Cancer 1995 Jun 15;75(12):2979].
Cancer 1995; 75(1 Suppl):191-2O2.
8. Pisani RJ. Bronchogenic carcinoma: immunologic aspects. Mayo Clin Proc 1993; 68(4):386-92.
9. Whitesell PL, Drage CW. Occupational lung cancer Mayo Clin Proc 1993; 68(2):1 83-8.
10. Patel AM, Davila DG, Peters SG. Paraneoplastic syndromes associated with lung cancer [see comments]. Mayo Clin
Proc 1993; 68(3):278-87.
11. Morabia A, Wynder EL. Cigarette smoking and lung cancer cell types. Cancer 1991; 68(9):2074-8.
12. Ko YC, Lee CH, Chen MJ, Huang CC, Chang WY, Lin HJ, Wang HZ, Chang PY. Risk factors for primary lung cancer
among non-smoking women in Taiwan. Int J Epidemiol 1997; 26(1):24-31.
13. Kitamura H, Kameda Y, Ito T, Hayashi H. Atypical adenomatous hyperplasia of the lung. Implications for the
pathogenesis of peripheral lung adenocarcinoma [see comments]. Am J CIin Pathol 1999; 111(5):610-22.
14. Karsell PR, McDougall JC. Diagnostic tests for lung cancer. Mayo Clin Proc 1993; 68(3):288-96.
15. Dalager NA, Pickle LW, Mason TJ, Correa P, Fontham E, Stemhagen A, Buffler PA, Ziegler RG, Fraumeni JF, Jr. The
relation of passive smoking to lung cancer Cancer Res 1986; 46(9):4808-11.
16. Charloux A, Hedelin G, Dietemann A, Ifoundza T, Roeslin N, Pauli G, Quoix E. Prognostic value of histology in
patients with non-small cell lung cancer. Lung Cancer 1997; 17(1):123-34.
17. Charloux A, Ouoix E, Wolkove N, Small D, Pauli G, Kreisman H. The increasing incidence of lung adenocarcinoma:
reality or artefact? A review of the epidemiology of lung adenocarcinoma. Int J Epidemiol 1997; 26(1 ):14-23.
18. Muller NL, Miller RR. Neuroendocrine carcinomas of the lung. Semin Roentgenol 1990; 25(1 ):96-1 04.
19. Travis WD, Rush W, Flieder DB, Falk E=R, Fleming MV, Gal AA, Koss MN. Survival analysis of 200 pulmonary
neuroendocrine tumors with clarification of criteria for atypical carcinoid and its separation from typical carcinoid.
Am J Surg Pathol 1998; 22(8):934-44.
20. Hardy J, Smith I, Cherryman G, Vincent M, Judson I, Perren T, Williams M. The value of computed tomographic
(CT) scan surveillance in the detection and management of brain metastases in patients with small cell lung cancer
Br J Cancer 1990; 62(4):684-6.
21. Sone S, Takashima S, Li F, Yang Z, Honda T, Maruyama Y, Hasegawa M, Yamanda T, Kubo K, Hanamura K, Asakura
K. Mass screening for lung cancer with mobile spiral computed tomography scanner [see comments]. Lancet 1998;
351 (9111):1242-5.
Key Points
• Radiologic findings distinguish precapillary (arterial) from postcapillary
(venous) pulmonary hypertension
• Idiopathic and secondary conditions are included in the differential diagnosis
• Vascular histopathology and secondary cardiac changes are often reflected in
the radiology of pulmonary hypertension
Figure 1-14-1
Figure 1-14-2
Postcapillary (venous) circulation drains the capillary beds of the alveoli. Veins and
venules course back to the left atrium within interlobular septa
Figure 1-14-5
Eisenmenger Physiology
• Congenital L-to-R shunt
➢ VSD, ASD, PDA
➢ Endocardial Cushion Defect
• Shunt reversal (R-to-L) follows sustained elevation in PVR
• PAH irreversible & requires lung transplantation
Pulmonary Thromboendarterectomy
• 15-30% CTEPH patients are candidates
• Thrombi from main to segmental or subsegmental level
• Intima & superficial media removed w/ thrombi
• Operative mortality 8-23%
• Improved long term survival - 75% at six years
Chronic thromboembolic disease:
Other thromboembolic materials mural-based soft tissue masses and
calcium in the lumen of right main PA
Intravenous Talcosis
• Chronic IV injection of crushed tablets (Methadone, amphetamines)
• Thrombogenic pharmaceutical binding agent: magnesium silicate Figure 1-14-12
• Granulomas coalesce into birefringent particles
PCH/PVOD
• Capillary proliferation & dilatation
• Venous medial hypertrophy & intimal proliferation
• Recanalized thrombus in veins & venules
PCH/PVOD
• Young adults (M:F is 2:1)
• Pediatric in 1/3 of cases
• Fatal within 3-5 years
• Associations
➢ Chemotherapy
➢ Prior viremia
➢ HIV
➢ ? Toxic exposure PVOD, a rare cause of postcapillary
• Current Debate pulmonary hypertension: prominent
➢ Separate entities? interlobular septa and subpleural edema
➢ Contiguous spectrum of injury?
➢ Cause-effect scenario?
PVOD/PCH
• Difficult to discern from primary PAH clinically
• Vasodilators contraindicated: severe pulmonary edema
• CT clues
➢ Septal lines
➢ GG nodules (+/-)
➢ Normal left atrium
References
1. Bergin CJ, Rios G, King MA, Belezzuoli E, Luna J, Auger WR. Accuracy of high-resolution CT in identifying
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8:758-761.
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origin: high-resolution CT findings. Radiographics 1994; 14:739-746.
12. Randall PA, Heitzman ER, Bull MJ, et al. Pulmonary arterial hypertension: a contemporary review. Radiographics
1989; 9:905-927.
Key Points
• The pathogenesis of pulmonary metastases is complex
• The spectrum of radiological manifestations reflects pathways of spread
• Many extrathoracic malignancies produce characteristic radiologic patterns of
pulmonary metastases
Nodular Metastases
• Rounded, coalescent or multilobulated
• Multiple
• Peripheral, basilar
Hematogenous metastases arise from tumor cells
• Variable sizes
which penetrate vessels and lymphatics at the
• Mixed areas of viability, necrosis, hemorrhage
primary site, and are transported to the right
heart via the systemic venous circulation
Parenchymal Nodules:
Multidetector Chest CT
• High sensitivity
➢ 95% for nodules >1cm
➢ 91% for nodules .5-1cm
• Low specificity (60% in 40-65 y.o. adults) Figure 1-15-2
➢ intrapulmonary lymph nodes
➢ granulomatous diseases
✧ sarcoidosis
✧ silicosis
➢ amyloidosis
➢ infection
Figure 1-15-5
Pulmonary Metastases:
Unusual Manifestations
• Cavitary, calcified or solitary pulmonary nodules
• Lymphangitic carcinomatosis
• Tumor thromboembolism
• Endobronchial metastases
• Pleural-based metastases
Figure 1-15-7
Cannonball metastases in a young
adult male with a soft tissue sarcoma
(scout; axial lung and mediastinal CT
images)
Figure 1-15-8
Solitary Metastasis
• Unusual: 1-28% of all metastatic lesions
• 3-10% of all SPNs are solitary metastases
• Variable margins
➢ well-defined Calcified metastases in middle-aged
➢ multilobulated female with ovarian cancer
➢ spiculated
Solitary Metastasis
Lymphangitic Carcinomatosis:
Imaging Features - Chest radiograph
• Normal (50%)
• Kerley B lines Figure 1-15-11
• Reticulonodular opacities
• Subpleural edema
• Pleural effusion (30-50%)
• Hilar,mediastinal lymphadenopathy (20-40%)
• Bilateral or unilateral findings
Lymphangitic Carcinomatosis
Imaging Features: Chest CT [Figure 1-15-11]
• Smooth or nodular thickening of
➢ Bronchovascular bundles
➢ Interlobular septa (Kerley’s lines; polygonal
arcades)
➢ Lobar fissures (subpleural edema)
• Ground glass opacities
Lymphangitic carcinomatosis in a middle aged
• Focal or unilateral distribution (50%)
female with breast cancer
➢ lung or breast CA
• Pleural effusion
• Lymphadenopathy (up to 50%)
Tumor Embolism
• Lodges in distal arterioles (100-200 micron diameter)
• 26% cancer pts (at autopsy)
• <1% clinically significant
• Complications
➢ Cor pulmonale (PAH)
➢ Lung infarction
➢ Lung hemorrhage
• Parenchymal or lymphatic mets if extravasation
Figure 1-15-15
Parenchymal Nodules
Indications for Metastasectomy
• To cure, but only if
➢ Complete resection possible
➢ No extrathoracic metastases (EXCEPT colon CA with liver mets)
➢ No therapeutic alternative (chemotherapy-insensitive tumors)
➢ Multiple nodules NOT necessarily a contraindication
• To prolong 5-year survival
➢ Colorectal cancer: up to 20-50%
➢ Osteogenic & soft tissue sarcomas: up to 40%
➢ Melanoma, renal cell, head & neck, female GU: up to 30%
➢ Thyroid, parathyroid: up to 61%
Yoneda et al. Curr Opin Pulm Med 2000;6:356-363.
“A Sarcoid-like Reaction”
• Rare but well-documented
• Follows resection or treatment
➢ Lymphoma (Hodgkin & Non-Hodgkin)
➢ AML
➢ Lung CA
➢ Testicular CA
➢ Gastric CA
➢ Renal CA
• Radiologic manifestations
➢ Mediastinal, hilar lymphadenopathy
➢ Pulmonary nodules or consolidations
➢ Systemic sarcoidosis absent
➢ Positive on FDG-PET: mimics recurrence
• Biopsy required for confirmation
• ? Local immunologic response to tumor cells
References
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Thorac Imag 1987; 2(4):38-43.
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2004; 200(10);701-5.
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2000; 217:257-261.
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Learning Objectives:
• To define the mediastinum and describe the mediastinal compartments
• To provide a classification for a practical approach to the imaging diagnosis of
mediastinal masses
• To list clinical and cross-sectional imaging features that allow a focused differential
diagnosis
• To describe lesions with pathognomonic imaging features
• To differentiate neoplastic from non-neoplastic conditions with emphasis on
management
Figure 1-16-2
Figure 1-16-3
Mediastinal Masses
• Neoplasia
➢ Malignant (secondary / diffuse)
➢ Benign and malignant (primary / focal)
• Congenital cysts
• Glandular enlargement
• Vascular lesions
• Herniations / Esophageal abnormalities Figure 1-16-4
• Miscellaneous conditions
Lymphoma
• Non-Hodgkin lymphoma - 75% of all cases
• 50-70% of mediastinal lymphoma is Hodgkin disease
➢ 15-21% is non-Hodgkin lymphoma
• Hodgkin – 66% intrathoracic at presentation
➢ Non-Hodgkin – 37% intrathoracic at presentation
• Treatment: Radiotherapy, chemotherapy
Hodgkin Disease: Microscopic Features
Lymphoma: Clinical Features
• Hodgkin Disease Figure 1-16-6
➢ Males = Females (NSHD, 2 X more common in females)
➢ Bimodal distribution: 2nd to 3rd and > 5th decades
➢ Lymphadenopathy: cervical, supraclavicular
➢ 20-30%; fever, night sweats, wt. loss
• Non-Hodgkin lymphoma
➢ Systemic disease with constitutional symptoms: lymphadenopathy,
local invasion
➢ Lymphoblastic - male children / adolescents
➢ Diffuse large-B cell - young adult females
Secondary Neoplasia
• Diffuse, bilateral mediastinal enlargement
• Lymphadenopathy
• Local invasion
• Metastases
• Other imaging features of malignancy
Non-Neoplastic Lymphadenopathy
• Infection
➢ Fungal: Mediastinal fibrosis; Calcification
➢ Other granulomatous infections
• Sarcoidosis
➢ Bilateral symmetric hilar lymphadenopathy
➢ Typical lung parenchymal involvement
• Castleman disease
➢ Enhancement / calcification (10%)
Mediastinal Fibrosis
• Granulomatous lymphadenopathy
• Young patients with signs and symptoms of obstruction Figure 1-16-10
➢ Trachea, bronchi, esophagus, vessels
• Mediastinal mass, circumscribed or locally invasive,
calcification
• Systemic antifungal agents, excision, dilatation,
bypass graft
• 30% mortality
Thymoma
• Epithelial neoplasm, most common primary thymic neoplasm
• Slow growth, “benign” behavior
• M=F; 70% in the 5th and 6th decades
• Most patients asymptomatic
• 25-30% with symptoms of compression/invasion
• Associated parathymic syndromes:
➢ Myasthenia gravis
➢ Pure red cell aplasia
➢ Hypogammaglobulinemia
Figure 1-16-16
Figure 1-16-17
Thymic Carcinoid
• Neuroendocrine neoplasm; atypical carcinoid (necrosis / mitoses / invasion) Figure 1-16-20
• Males > Females; 3:1; wide age range (average, 43 yrs)
• 50% functionally active
➢ ACTH – Cushing syndrome (33-40%)
• MEN type 1 – (Wermer syndrome) (19-25%)
➢ Hyperparathyroidism (90%), islet cell tumor of pancreas
(80%) pituitary adenoma (65%)
Thymic Carcinoma
• Male > Female; wide age range (mean: 5th decade)
• Several cell types identical to primary lung cancer; R/O
metastases
• WHO Type C thymoma
Thoracic Meningocele
• Intrathoracic extrusion of meninges and their fluid content
• Well-defined spherical paravertebral mass
• Enlarged neuroforamen, pressure erosion, sclerosis Figure 1-16-31
• Homogeneous, fluid attenuation / signal
Ganglioneuroblastoma/Neuroblastoma
• Infants and young children
• Asymptomatic; chest wall pain, paraplegia, Horner syndrome, diarrhea,
hemothorax
• Elevation of urine catecholamines
➢ Elevation of urine/serum VMA (screening)
• Neuroblastoma – Elongate paravertebral mass
➢ 50% < 2 years
➢ 90% < 5 years
➢ May be congenital
Paraganglioma
• Middle mediastinum: Aortopulmonary paraganglia
➢ Paravertebral: Aortico sympathetic paraganglia
➢ Heart
• Adults (average age 30-40 yrs)
➢ Males > Females; 2:1
➢ Asymptomatic; excess catecholamines Neuroblastoma, imaging features:
• Well-defined spherical mass Unilateral calcified paravertebral mass in
➢ Homogeneous/heterogeneous a neonate with intraspinal extension
• Marked contrast enhancement
➢ 90% uptake of I131 or I123 MIBG
Primary Neoplasia
• Benign
➢ Focal, unilateral mass
➢ No lymphadenopathy
Figure1-16-33
➢ No local invasion
• Malignant (invasive)
➢ Focal, unilateral mass
➢ Lymphadenopathy
➢ Local invasion
Figure 1-16-36
Figure 1-16-37
Bronchogenic cyst, imaging features: spherical subcarinal mass that may not exhibit
water attenuation
Congenital Cysts
• Focal, spherical
• Unilocular
• Thin-walled
• No mural nodules
• No lymphadenopathy
• Along foregut-derived structures
Thymic Hyperplasia
• Lymphoid hyperplasia (lymphofollicular / autoimmune thymitis) -
secondary follicles with germinal centers; may not produce
thymus enlargement
• Myasthenia gravis, hyperthyroidism, lupus, scleroderma, RA, Thymic cyst, gross features: multilocular
cirrhosis cyst
• True hyperplasia - global increase in the size and weight of the Figure 1-16-39
thymus
• Rebound hyperplasia - following chemotherapy (2 weeks to 14
months), steroids or severe insult
• Ant. mediastinal widening
• Homogeneous soft tissue
• Maximal thickness
➢ Under 20 years – 1.8 cm
➢ Over 20 years – 1.3 cm
• Follicular thymic hyperplasia – normal or mildly enlarged thymus
Figure 1-16-42
Figure 1-16-43
Parathyroid Adenoma
• Ectopic parathyroid glands: superior pole of thymus (39%),
mediastinum (2%), intrathyroid (0.2-3.5%)
• Primary hyperparathyroidism post surgical parathyroidectomy
• MEN I
• Imaging
➢ Tc99m / Tl201 subtraction imaging
➢ T123 / Tl201
➢ Tc99m - Sestamibi (mitochondria)
➢ Single radionuclide/Dual radionuclide
• CT/MRI correlation of mediastinal uptake
Glandular Enlargement
• Anatomically related to normal gland
• Continuity with normal gland
• Function similar to that of normal gland
Lymphangioma, microscopic features:
Interconnecting endothelial lined
Lymphangioma vascular channels
• Benign mesenchymal mediastinal tumor
• Proliferation of lymphatic vessels without communication with lymphatic tree
• Developmental vs. neoplasm vs. hamartoma
• Asymptomatic / symptoms of compression
• Mediastinal extension of cystic hygroma (10%), soft palpable mass; 90%
diagnosed in infancy
• Mediastinal mass in asymptomatic child / adult
Lymphangioma, gross
features: Multilocular
cystic appearance due to
enlargement of vascular
Lymphangioma, imaging features: Multilocular cystic mediastinal mass with channels
extension into the axilla
Figure 1-16-46
Herniations
• Intrathoracic extension of abdominal contents
➢ Bowel
➢ Omental fat
• Esophageal hiatus
• Morgagni hernias
Miscellaneous – Achalasia
• Absent peristalsis and incomplete relaxation of esophageal sphincter
• Primary – deficiency of ganglion cells in myenteric plexus
• Secondary – (pseudo achalasia) Chagas disease and primary or secondary
malignancy at the GE junction
• Esophageal dilatation with air-fluid levels
➢ Esophageal displacement to the right, mass effect on mediastinum,
pulmonary consolidation (aspiration)
Miscellaneous - EMH
• Extramedullary hematopoiesis
• Compensatory formation of blood elements outside osseous medulla
• Hemolytic anemia
• Unilateral or bilateral paravertebral mass; may exhibit internal fat attenuation
• Adjacent medullary expansion
References
General
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radiographic classifications of the mediastinum. J Comput Assist Tomogr 2001; 25: 489-492.
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Thymoma
1. Rosado-de-Christenson ML, Galobardes J, Moran CA. Thymoma: Radiologic-Pathologic Correlation.
RadioGraphics 1992; 12: 151-168.
2. Thomas CR, Wright CD, Loehrer PJ, Sr. Thymoma: state of the art. J Clin Oncol 1999; 17: 2280-2289.
3. Tomiyama N, Müller NL, Ellis SJ, et al. Invasive and noninvasive thymoma: distinctive CT features. J Comput
Assist Tomogr 2001; 25: 388-393.
Thymic Malignancy
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AJR 2001: 176: 433-439.
2. Rosado-de-Christenson ML, Abbott GF, Kirejczyk WM, Galvin JR, Travis WD. Thoracic carcinoids: Radiologic-
pathologic correlation. RadioGraphics 1999; 19: 707-736.
Thymolipoma
1. Rosado-de-Christenson ML, Pugatch RD, Moran CA, Galobardes J. Thymolipoma: analysis of 27 cases. Radiology
1994; 193: 121-126.
Thymic Hyperplasia
1. Budavari AI, Whitaker MD, Helmers RA. Thymic hyperplasia presenting as anterior mediastinal mass in 2 patients
with Graves disease. Mayo Clin Proc 2002; 77: 495-499.
2. Hara M, McAdams HP, Vredenburgh JJ, Herndon JE, Patz EF Jr. Thymic hyperplasia after high-dose chemotherapy
and autologous stem cell transplantation: incidence and significance in patients with breast cancer. AJR 1999; 173:
1341-1344.
Lymphoma
1. Harris NL, Jaffe ES, Stein H, et al. A revised European-American classification of lymphoid neoplasms: a proposal
from the international lymphoma study group. Blood 1994; 84: 1361-1392.
2. Fraser RS, Müller NL, Colman N, Paré PD. Lymphoproliferative disorders and leukemia. In: Fraser RS, Müller NL,
Colman N, Paré PD, eds. Fraser and Paré’s Diagnosis of Diseases of the Chest. Fourth edition. Philadelphia:
Saunders, 1999; 1269-1330.
Non-Neoplastic Lymphadenopathy
1. Atasoy C, Fitoz S, Erguvan B, Akyar S. Tuberculous fibrosing mediastinitis: CT and MRI findings. J Thorac Imag
2001; 16: 191-193.
2. McAdams HP, Rosado de Christenson ML, Fishback NF, Templeton PA. Castleman disease of the thorax: radiologic
features with clinical and histopathologic correlation. Radiology 1998; 209: 221-228.
3. Rossi SE, McAdams HP, Rosado-de-Christenson ML, Franks TJ, Galvin JR. Fibrosing mediastinitis.
RadioGraphics 2001; 21:737-757.
Neurogenic Neoplasms
1. Ichikawa T, Ohtomo K, Araki T, et al. Ganglioneuroma: computed tomography and magnetic resonance features.
Br J Radiol 1996; 69: 114-121.
2. Marchevsky AM. Mediastinal tumors of peripheral nervous system origin. Semin Diagn Pathol 1999; 16: 65-78.
3. Moon WK, Im J-G, Han MC. Malignant schwannomas of the thorax: CT findings. J Comput Assist Tomogr 1993;
17: 274-276.
4. Rossi SE, Erasmus JJ, McAdams HP, Donnelly LF. Thoracic manifestations of neurofibromatosis-I. AJR 1999;
173: 1631-1638.
Endocrine Lesions
1. Buckley JA, Stark P. Intrathoracic mediastinal thyroid goiter: imaging manifestations. AJR 1999; 173: 471-475.
2. Fraser RS, Müller NL, Colman N, Paré PD. Masses situated predominantly in the anterior mediastinal
compartment. In: Fraser RS, Müller NL, Colman N, Paré PD, eds.
3. Fraser and Paré’s Diagnosis of Diseases of the Chest. Fourth edition. Philadelphia: Saunders, 1999; 2875-2937.
4. Hopkins CR, Reading CC. Thyroid and parathyroid imaging. Semin US CT MRI 1995; 16: 279-295.
Vascular Lesions
1. Charruau L, Parrens M, Jougon J, et al. Mediastinal lymphangioma in adults: CT and MR imaging features. Eur
Radiol 2000; 10: 1310-1314.
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Thorac Imaging 1996; 11: 83-85.
3. McAdams HP, Rosado-de-Christenson ML, Moran CA. Mediastinal hemangioma: radiographic and CT features
in 14 patients. Radiology 1994; 193: 399-402.
4. Shaffer K, Rosado-de-Christenson ML, Patz EF Jr, Young S, Farver CF. Thoracic lymphangioma in adults: CT
and MR imaging features. AJR 1994; 162:283-29-89.
5. Henseler KP, Pozniak MA, Lee FT Jr, Winter TC III. Three-dimensional CT angiography of spontaneous
portosystemic shunts. RadioGraphics 2001; 21: 691-704.
6. Ibukuro K, Tsukiyama T, Mori K, Inoue Y. Preaortic esophageal veins: CT appearance. AJR 1998; 170: 1535-
1538.
7. Ibukuro K, Tsukiyama T, Mori K, Inoue Y. Precaval draining vein from paraesophageal varices: Radiologic-
anatomic correlation. AJR 1999; 172: 651-654.
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demonstration on MR imaging. Abdom Imaging 2000; 25: 462-470.
9. Lee SJ, Lee KS, Kim SA, Kim TS, Hwang JH, Lim JH. Computed radiography of the chest in patients with
paraesophageal varices: Diagnostic accuracy and characteristic findings. AJR 1998; 170: 1527-1531.
Miscellaneous Lesions
1. Fraser RS, Müller NL, Colman N, Paré PD. The diaphragm. In: Fraser RS, Müller NL, Colman N, Paré PD, eds.
Fraser and Paré’s Diagnosis of Diseases of the Chest. Fourth edition. Philadelphia: Saunders, 1999; 2987-3010.
2. Mueller CF, Klecker RJ, King MA. Case 3. Achalasia. AJR 2000; 175: 867; 870-871
3. Woodfield CA, Levine MS, Rubesin SE, Langlotz CP, Laufer I. Diagnosis of primary versus secondary achalasia.
Reassessment of clinical and radiographic criteria. AJR 2000; 175: 727-731.
4. Dunnick NR. Image interpretation session: 1999. Extramedullary hematopoiesis in a patient with beta
thalassemia. RadioGraphics 2000; 20: 266-268.
5. Gilkeson RC, Basile V, Sands MJ, Hsu JT. Chest case of the day. Extramedullary hematopoiesis (EMH). AJR
1997; 169: 267, 270-273.
6. Moellers M-C, Bader JB, Alexander C, Samnick S, Kirsch C-M. Localization of extramedullary hematopoiesis
with Tc-99m-labeled monoclonal antibodies (BW 250/183). Clin Nuc Med 2002; 27: 354-357.
Learning Objectives
• To review the radiologic features of thoracic radiologic abnormalities based on
location
• To enumerate the radiologic characteristics that allow lesion localization and
the formulation of a focused radiologic differential diagnosis
Splenosis
• Auto-transplantation of splenic tissue typically following splenic rupture
• Most common manifestation: Multiple peritoneal nodules
• Thoracic splenosis:
➢ Multiple pleural-based nodules
➢ May be missed on radiography
➢ 99mTC-tagged heated RBC scintigraphy
➢ Liver-spleen scan
Learning Objectives
• To review concepts of differential diagnosis of mediastinal masses
• To emphasize importance of demographics, location and morphology in the
formulation of a focused differential diagnosis
S. pneumoniae: Demographics
• S. pneumoniae most frequent isolate in CAP
➢ 8-76% incidence
• Recognized risk factors
➢ alcoholism, splenic dysfunction, viral pneumonia, congenital and acquired
immune deficiencies
S. pneumoniae: Demographics
• 25% incidence of bacteremia
• 25-40% mortality, unchanged >30y
➢ Age >65
➢ CHF,DM
➢ Alcoholism
➢ Thrombocytopenia
➢ Renal dysfunction
➢ Number of lobes
Chest 1993; 103:1152-56
S. pneumoniae: Pathology
• Aspiration to peripheral air spaces
• Alveolus represents site of initial inflammatory lesion
• Spread occurs by contignous involvement of adjacent alveoli
• 3 pathologic stages
S. pneumoniae: Pathology
• ACUTE RESPONSE
➢ Increased capillary permeability
➢ Protein rich edema
➢ Contiguous alveolar filling via Pores of Kohn and Canals of Lambert
• RED HEPATIZATION
➢ PMN infiltration and intra-alveolar hemorrhage
• GRAY HEPATIZATION
➢ Macrophage infiltration and uptake of blood products
S. pneumoniae: Radiology
• Spread at alveolar level results in nonsegmental distributions characteristic of Figure 1-19-1
early lobar pneumonia
• Round pneumonia
➢ Manifestation of nonsegmental distribution
➢ Most common in pediatric infection with S.pneumoniae
S. pneumoniae: Radiology
• LOBAR pattern
➢ Prominent air bronchograms
➢ Preserved volume
S. pneumoniae: Radiology
• 48% of consecutive hospitalized pts demonstrated focal lobar
patterns
• 33%, multifocal lobar patterns
• 16% lobular pattern
• Dominant pattern did not vary with immune status or disease
severity Lobar pattern consolidation due to S.
AJR 2000;175:1533 pneumoniae
S. pneumoniae: Radiology
• Small pleural effusions up to 60%
• Infrequent cavitation
➢ Associated with serotype 3
• Most frequent organism in pulmonary gangrene
➢ Vascular thrombosis from severe necrosis
➢ Intracavitary mass (sloughed lung)
M. pneumoniae: Demographics
• 15-35% of CAP
➢ 50% of CAP during summer months
• Peak age 5-25 yo
• Self limited
➢ Few fatal cases associated with ARDS
➢ Increased severity in sickle cell anemia
• Most frequent etiology in Atypical Pneumonia Syndrome
➢ Atypical radiographic features
➢ Prominent extrapulmonary complaints
M. pneumoniae: Pathology
• Eaton agent-1944
➢ Gram -- filamentous rod
➢ Absent cell wall
• Acute cellular bronchiolitis
➢ Superficial inflammation involving luminal surface of bronchi, bronchioles
➢ Associated interstitial infiltrates
M. pneumoniae: Radiology
• CT Findings [Figure 1-19-3]
➢ 86% centrilobular nodules
➢ 82% bronchovascular thickening
➢ 59% consolidation with lobular distribution
Reittner, AJR 2000; 174:37
Bronchopneumonia pattern due to
Respiratory Viruses M. pneumoniae
• Influenzae A,B,C
• Para-influenzae
• Respiratory syncytial virus
• Adenovirus Figure 1-19-3
• Herpes viruses
• SARS
Influenzae A: Demographics
• 10-20% CAP
• 10,000-40,000 deaths/ influenzae epidemic
• Peak incidence
➢ Pediatric population
• Highest mortality-adult and aged
➢ Superinfection
➢ S.aureus
➢ S.pneumoniae
Influenzae A: Pathology
• St 1 infection of epithelial cells, proliferation and necrosis
• St 2 bronchial and alveolar wall edema,hemorrhage HRCT of M. pneumoniae
• Ulceration, bacterial infection
Influenzae A: Radiology
• INTERSTITIAL pattern
➢ Reticular Figure 1-19-4
➢ Nodular
➢ Peribronchial thickening
➢ Subpleural edema
➢ Hilar haze
Influenzae A: Radiology
[Figure 1-19-4]
• Bilateral, parahilar, lower
lobe
• Air trapping
• Prominent GGO
(left) CXR
(right) HRCT Influenzae pneumonia mimicking edema
Respiratory Herpesviruses
• HSV-1, HSV-2, VZV, EBV, CMV
➢ Primary infection, latency, reactivation
➢ Up to 40% mortality
• Risk factors Swyer James Syndrome due to
➢ Immune-suppression, lung transplantation, airway pediatric viral pneumonia
management, pregnancy
Varicella Pneumonia
• Complication of adult chickenpox Figure 1-19-6
➢ 5-50% incidence
• Prominent acinar opacities
➢ 5-10mm nodules, coalescence
➢ Patchy GGO
Kim AJR 1999;172:113
• May heal with miliary calcifications
L. pneumophila: Demographics
• 15% of CAP
➢ Epidemic and sporadic forms
➢ Legionnaire’s disease= pneumonic form
➢ Peak summer
• Aerobic Gram -- bacillus
• Proliferates in warm, humid environments
Figure 1-19-7
L. pneumophila: Pathology
• Bronchocentric inflammation
L. pneumophila: Demographics
• Acute onset
• Prominent extrapulmonary symptoms
➢ Neurologic manifestations, diarrhea, renal insufficiency
• 10% mechanical ventilation
• 15% mortality in cases requiring hospitalization
K. pneumoniae: Demographics
• Nosocomial or community acquired
• 5-10% lobar pneumonias
• 25% bacteremic, 50% mortality
• Males, >60yo
• Risk factors: alcoholism, COPD, DM
K. pneumoniae: Pathology
• Gram -- bacillus
➢ Abundant PMN infiltration of alveoli, edema
➢ Lobar expansion - Friedlander’s pneumonia
➢ Massive necrosis HRCT in Legionella pneumonia
➢ Common association with gangrene demonstrating bronchocentric
nodules and pleural effusion
K. pneumoniae: Radiology
• Lobar pattern
➢ Bulging fissures
• Abscess 30-50%
• Necrotizing pneumonia at CT
➢ Low density areas with small cavities
Moon JCAT 1995;19:176
S. aureus: Radiology
• Aerogenous infection [Figures 1-19-8 and 1-19-9]
➢ Multifocal Broncho-pneumonia
• Hematogenous infection [Figure 1-19-10]
➢ Multifocal, discrete nodular or wedge shaped abnormality with
normal intervening lung
• Cavitation / abscess (25-75%)
• Pneumatoceles (60% ped infection)
• Pleural effusions / empyema (50%)
Figure 1-19-9
Nosocomial Pneumonia
• Rising incidence parallels usage of antibiotics
• Gram negative infections
➢ 40-50% increase 1950-60
➢ 55-65% nosocomial infections
➢ 50% nosocomial pneumonia
➢ 75% ICU pneumonia
Diagnosis
• Quantitative cultures
➢ Tracheal aspirate 10 5-6 cfu/ml
➢ BAL 10 4 cfu/ml
➢ Protected specimen brush 10 3 cfu/ml
➢ False negative and false positive rates 20-30%
Baughman Chest 2000
Pathophysiology
• Direct inhalation
• Hematogenous spread
• Aspiration
➢ 45% incidence in sleep
➢ Altered gag reflex, consciousness, GI motility
➢ NG / ET
Pathophysiology
• Abnormal gram negative airway colonization
➢ 25% 24hr
➢ 40% 7d
• Gastric alkalinization
• Serious illness
• Antibiotic TX
Johanson Ann Intern Med 1972
Pathophysiology
• Repetitive aspiration leads to
• Bronchiolitis
• Lobular (broncho) pneumonia
➢ Peribronchiolar neutrophilic infiltrate (104 cfu/g)
Microbiology
• Normal flora
• Gram – bacilli
• S. aureus
• Anaerobes
• Legionella
• Respiratory viruses
Microbiology
• Early <5d
➢ H. influenzae
➢ S. pneumoniae
➢ S. aureus
• Late >5d
➢ S. aureus
➢ P. aeruginosa
➢ Enterobacteriaceae
➢ Acinetobacter spp.
➢ Stenotrophomonas maltophilia
P. aeruginosa: Pathology
• Micro-abscesses
• Necrotic vasculits
➢ Sm-med pulmonary arteries
• Hemorrhage
P. aeruginosa: Radiology
• Bronchopneumonia pattern
➢ Discrete nodules may be indicative of vasculitis
• Frequent cavitation
• Pleural effusions/empyema
A. Israelii; Demographics
• Normal oral flora Figure 1-19-12
• Sites of infection:
➢ Cervicofacial 55%
➢ Abdomen 20%
➢ Pulmonary 25%
• Risk factors: poor oral hygiene, aspiration
Smego RA. Clin Infec Dis 1998;26:1255
A. Israelii: Pathology
• Multifocal abscesses
• Interconnecting sinus tracts
• Sulphur granule
➢ Spoke-wheel arrangement of neutrophils surrounding Pneumonia with chest wall
filamentous organism involvement due to A. israelli
N. Asteroides: Pathology
• Peribronchial abscesses, granulomatous inflammation
• Extensive necrosis
➢ May mimic M.TB or fungal infection
N. Asteroides: Radiology
• Extrapulmonary disease 50% with 40-90% mortality
➢ CNS 25%
➢ Skin and subcutaneous abscesses
N. Asteroides: Radiology
• Consolidation
➢ Mass-like
➢ Cavitary
• Pleural and chest wall involvement 30-50%
• Adenopathy 40%
Parasitic Infection
• Pulmonary involvement due to hypersensitivity or direct invasion
➢ Echinococcosis
➢ Paragonimiasis
➢ Ascariasis Figure 1-19-13
➢ Strongyloidiasis
Parasitic Infection
• Radiographic findings may overlap with other
infections
➢ Fleeting, patchy infiltrates
➢ Reticulonodular opacities
➢ Bronchopneumonia
➢ Atelectasis
Echinococcus granulosus
• Cestode (tapeworm), endemic to S.America,
Australia, Middle East, Africa and Mediterranean
• Definitive host - dog,wolf
Intermediate host - sheep, cow, deer, moose
Echinococcus granulosus
• Duodenum - portal venous system liver
➢ 45-75% isolated liver involvement
➢ 15-35% pulmonary involvement
Intact (right lung) and ruptured (left lung)
echinococcal cysts
Echinococcus granulosus [Figure 1-19-13]
• Pulmonary cysts acquired in childhood
• Diagnosis 30-40yo
• Intact cyst - asymptomatic
• Eosinophilia 25-40%
Paragonimiasis westermani
• Trematode (lung fluke)
➢ endemic to Asia
➢ Contaminated freshwater crab
• Jejunum – peritoneal cavity – diaphragm – pleura – lung
• Chronic granulomatous reaction
Ascariasis lumbricoides
• Roundworm infection
• Most common parasitic infection
➢ Endemic worldwide
➢ 25-95% prevalence
➢ Highest incidence in children
• Large iingestion associated with pneumonitis
• Small bowel – systemic circulation – alveoli - trachea – small bowel
Strongyloides stercoralis
• Round worm
• Skin – systemic circulation – alveoli – trachea – small bowel
B. Anthracis: Anthrax
• Gram+ spore forming rod
➢ Dormant spores are virulent
• Infection typical in livestock
• Exotoxin production associated with hemorrhagic mediastinitis, edema and
pleuritis
Earls Radiology:222:305, 2001
Complications of Pneumonia
• Pneumatocele
➢ Ball-valve mechanism
➢ Rapid evolution
➢ No lung destruction
• Most common with S.aureus
Figure 1-19-15
➢ 60% of peds infection
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pneumoniae pneumonia: radiographic and high-resolution CT features in 28 patients. AJR Am J Roentgenol. 2000
Jan;174(1):37-41.
7. Shah RM, Gupta S, Angeid-Backman E, O'Donnell J. Pneumococcal pneumonia in patients requiring
hospitalization: effects of bacteremia and HIV seropositivity on radiographic appearance. AJR Am J Roentgenol.
2000 Dec;175(6):1533-6.
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bacteremia in three community teaching hospitals from 1980 to 1989.Chest. 1993 Apr;103(4):1152-6.
9. Collins J, Muller NL, Kazerooni EA, Paciocco G. CT findings of pneumonia after lung transplantation. AJR Am J
Roentgenol. 2000 Sep;175(3):811-8.
10. Donnelly LF, Klosterman LA. Pneumonia in children: decreased parenchymal contrast enhancement--CT sign of
intense illness and impending cavitary necrosis. Radiology. 1997 Dec;205(3):817-20.
11. Earls JP, Cerva D Jr, Berman E, Rosenthal J, Fatteh N, Wolfe PP, Clayton R, Murphy C, Pauze D, Mayer T,
Bersoff-Matcha S, Urban B. Inhalational anthrax after bioterrorism exposure: spectrum of imaging findings in two
surviving patients. Radiology. 2002 Feb;222(2):305-12.
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effusions in medical ICU patients: how useful is routine thoracentesis? Chest. 2002 Jan;121(1):178-84.
13. Heussel CP, Kauczor HU, Heussel G, Fischer B, Mildenberger P, Thelen M. Early detection of pneumonia in
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14. Johanson WG Jr, Pierce AK, Sanford JP, Thomas GD. Nosocomial respiratory infections with gram-negative
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15. Smego RA Jr, Foglia G. Actinomycosis. Clin Infect Dis. 1998 Jun;26(6):1255-61; quiz 1262-3. Review.
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Carcinoids
• Gastrointestinal tract 90%
• Lung
• Thymus
• Biliary tract
• Ovarian teratomas
Bronchial Carcinoid
• Typical carcinoid
➢ Low-grade malignancy
• Atypical carcinoid
➢ Moderate-grade malignancy
Typical Carcinoid
• 0.6-2.4% of all pulmonary neoplasms
• Low grade malignancy
• Good prognosis
➢ 95% five-year survival
• Not associated with smoking
Neuroendocrine Tumors:
World Health Organization criteria (1999) [Figures1-20-1]
• Typical carcinoid: <2 mitoses per 10 HPF
• Atypical carcinoid: 2-10 mitoses per 10 HPF
• Large cell neuroendocrine ca: 11 or more mitoses per 10 HPF (median 70)
• Small cell ca: 11 or more mitoses per 10 HPF (median 80)
Atypical Carcinoid
• Morphology between Typical Carcinoid and Small Cell Ca
• Tend to be larger, more invasive, peripheral
• Age: Decade older than Typical
• Symptoms: similar to Typical
• Imaging: similar to Typical
Figure 1-20-4
Figure 1-20-6
Bronchial carcinoid. Partially endobronchial (‘iceberg”)
tumor in left upper lobe
Figure 1-20-7
Carcinosarcoma
• Rare - 0.3% of all lung neoplasms
• Middle aged and elderly males
• Poor prognosis
• Aggressive: local invasion, widespread metastases, and rapid
death
Carcinosarcoma: Gross
• Peripheral
➢ Large mass
➢ Average diameter 6 cms.
➢ Frequent necrosis and hemorrhage
• Central
➢ Endobronchial growth
➢ May extend to adjacent parenchyma
➢ Tumor-distended bronchi may resemble mucus plugs
Pulmonary Blastoma
• Primary lung tumor
• Mix of epithelial and mesenchymal components
• Both components blastomatous and immature
• Morphologic mimic of embryonal lung
• ? a variant of carcinosarcoma
“Hamartoma”
• Albrecht, 1904
• Tumor-like malformation
• Tissues normal to location
• In excess or disarray (disorganized)
• “Adult”, “Classic”, “Local” hamartoma
Hamartoma
• Acquired lesion
• Disorganized growth of tissues normally found in lung
• Benign neoplastic proliferation
• Probably derived from bronchial wall mesenchymal cell
(“benign mesenchymoma”)
Hamartoma
• Most common benign tumor of lung
• 77% of benign lung tumors
• 8% of SPNs
• 3% of all lung tumors
Hamartoma: Demographics
• Age range: 30-70 years
• Peak incidence: 6th decade
• Female: Male = 3:2 (1:1 for endobronchial hamartoma)
• Asymptomatic in 90%
< 8% obstructive symptoms
Hamartoma: Clinical
• Most are peripheral and asymptomatic
• If symptomatic: hemoptysis
• If bronchial obstruction: pneumonitis
• Fever, cough, expectoration, chest pain
Hamartoma: Microscopic
• Cartilage nests (lobules) in 95%
• Surrounded by fibrous tissue
• Mature fat cells
• Cleft-like invaginations of entrapped respiratory epithelium
Hamartoma: Distribution
• Peripheral > Central
• 80 – 90 % Peripheral
• No lobar predilection
Hamartoma: Radiographic
• Sharply defined, lobulated subpleural Hamartoma. Unenhanced chest CT demonstrates a
• Most < 3 cm peripheral solitary nodule with focal fat attenuation
• Calcification on CXR (10-15% )
• Rarely see fat on CXR Figure 1-21-2
• May enlarge on serial CXRs
• Up to 3 to 5 mm per year
Hamartoma: Calcification
• 10 – 15% speckled or “Popcorn”
• “Popcorn” less frequent than once thought
• Diagnostic when present
➢ Nodular growths within lesion
➢ Protrude in different directions
“Carney’s Triad”
• Gastric smooth muscle tumors
• Extra-adrenal paraganglioma
• Pulmonary chondroma
• Association unclear
• Young females < 20 years
• May have only 2/3 of the triad Hamartoma. Unenhanced chest CT demonstrates
Carney JA. Cancer 1979 speckled calcification in a central endobronchial tumor
with associated loss of volume in the left lung
Hamartoma: Endobronchial
• Morphologically identical to parenchymal
• Often polypoid. Sessile or thin pedicle
• Manifest by airway obstruction
• Micro: more fat, lack clefts, cartilage scant or absent
Papillomas
• Branching or coarsely lobulated tumor
• Arise from and project above an epithelial surface
• Rare pulmonary tumors
• Solitary (rare) or Multiple (papillomatosis)
• Proximal or peripheral
Solitary Papillomas
• Rare
• Usually in adults
• Papillary exophytic growth
• Trachea, main or lobar bronchi
• Males >40 years of age
• Post-obstructive pneumonia, bronchiectasis
Papillomas: Microscopic
• Non-keratinizing squamous cells
• Fibrovascular core
• Form papillomatous projections
Papillomatosis: Gross
• Cauliflower-like excresences
• Protrude into bronchial lumens
• May extend into parcenchyma as nodules or cavities
Tracheobronchial Papillomatosis
• Many remain limited to trachea
• 1% Develop lung disease
• Patients with lung disease may develop
• Squamous cell carcinoma
Papillomatosis: Imaging
• Multiple nodules
• Cavities, 2-3 mm thick walls
• Air-fluid levels
Inflammatory Pseudotumor
• Uncommon. Reactive or neoplastic process?
• May begin as organizing pneumonia
• May have aggressive features:
➢ Vascular invasion
➢ Vertebral destruction
➢ Recurrence
Inflammatory Pseudotumor
• Solitary nodule or mass in 70%
• Well-defined
• May manifest as consolidation
• May mimic neoplasm
• Endobronchial lesions occur in 10% Figure 1-21-6
Infectious Granulomas
• Mycobacterial 64%
• Fungal 30%
• Parasitic 6%
Granuloma: Infectious
• Tuberculoma or Histoplasmoma
• Satellite lesions common
• Usually small, smooth
• Often calcified when healed
Pleural Imaging
• Radiography / CT
➢ Inconspicuous
➢ Visceral + Parietal = 0.2 mm
• Thin-collimation
➢ 1-2 mm thick line
➢ Intercostal regions
➢ Normal fluid
➢ Endothoracic fascia Pneumothorax in a supine patient manifesting as a
➢ Innermost intercostal m. “deep sulcus” and hyperlucency overlying the left
hemidiaphragm
Pleural Anatomy [Figure 1-22-2]
Caudal limit of pleura lower than lung
Costal and diaphragmatic pleura contact to form costophrenic recess
Pleural Anatomy
• Junction Lines
• Apposition of layers of pleura
➢ Anterior
➢ Posterior
Major Fissure: CT
Propeller-like morphology [Figure 1-22-3]
• Upper thorax
➢ Anterior concave
➢ Lateral-facing
• Inferior thorax
➢ Anterior convex Chest CT (lung window) demonstrates right upper
➢ Medial-facing lobe loss-of-volume manifested by displacement of
the right major fissure. An endobronchial carcinoid
Standard Fissures: Radiography obstructs the origin of the right upper lobe
• Minor fissure bronchus
➢ “Lights up” in CHF
➢ Interstitial edema
(Subpleural interstitium)
Figure 1-22-4
Minor Fissure: CT
• Lucent area
• Devoid of vasculature
• 44% triangular
• 8% round / ovoid
• Ground glass attenuation
Pulmonary Ligament
• Formed by Parietal & Visceral pleura
• Courses inferiorly & posteriorly
• Contains bronchial veins, lymphatics, nodes
Figure 1-22-7
Chest CT demonstrates an
inferior accessory fissure
(arrow).
Pleural Effusion
Cardiac Decompensation [Figure 1-22-9]
• Most common cause
• Increased hydrostatic pressure
• Bilateral >80%
• Unilateral = right-sided
• Pseudotumor
Figure 1-22-9 Chest CT demonstrates inferior accessory fissure
Lateral chest (arrowhead) and right and left pulmonary
radiograph ligaments (arrows)
demonstrates
lenticular opacity of
fluid accumulation in
the minor fissure
(pseudotumor)
Figure 1-22-10
Round Atelectasis: CT
• Rounded subpleural mass
• Broadly abuts contiguous pleural thickening
• Air-bronchogram hilar aspect
• Bronchovascular “comet tail”
• Loss of volume in same lobe
Pleural Fibrosis
• 2nd most common pleural abnormality
• Result of many primary diseases of the pleura
• Complication of inflammatory disease
• Most localized to single area
• Less often diffuse
➢ May have functional abnormalities
Pneumothorax
• Air within the pleural space
• Spontaneous
➢ Primary
➢ Secondary
• Traumatic
MI=IV
Pleural Neoplasms
• Primary
• Localized fibrous tumor
• Malignant mesothelioma
• Secondary
• Pleural metastases
➢ Bronchogenic carcinoma
➢ Other carcinomas
➢ Lymphoma
➢ Invasive thymoma
Malignant Mesothelioma
• Most common primary pleural neoplasm
• 2,000 to 3,000 cases / year in USA
• 10% of exposed individuals
• Shipyards / asbestos plants
• Sixth to eighth decades
• Male : Female 3-6 : 1
• Amphiboles most tumorigenic
• Latency: 30-40 years
Malignant Mesothelioma: MR
• Staging
• Comparable / superior to CT
• Tumor enhancement
• Increased signal intensity
Pleural Metastases
Most common pleural neoplasm
• Common
➢ Adenocarcinoma
✧ Lung, breast, ovary, stomach
• Less common: Figure 1-23-7
➢ Lymphoma, Thymoma
• Imaging
➢ Pleural effusion
➢ Pleural masses
➢ Or both
Pleural Metastases
• Hematogenous / Lymphatic
• Direct extension
➢ Lung ca, breast ca
• Drop metastases
➢ Invasive thymoma
• May be bilateral
Pleural Thickening
Figure 1-23-10
Leonard M. Glassman, MD
Figure 1-24-1
Most Lesions are Non-specific [Figure 1-24-1]
• Differentials can be given
• High likelihood diagnoses can be made
• Is this a cyst or a solid mass?
Normal Variants
• Pectoralis major
• Lymph nodes
Figure 1-24-2
CC view showing a
rounded density medially,
the medial end of the
Non specific lobulated mass which could be a
pectoralis major muscle
cyst, benign solid mass or a carcinoma
Figure 1-24-3
Left: Lymph node with hilar notch Six examples of benign lymph nodes.
Right: Core biopsy specimen of normal lymph The top three are with traditional real time scanning
node and the bottom three with compound scanning
Fatty Lesions
• Hamartoma Accessory nipple in a patient at
• Lipoma the inframammary crease
• Fat necrosis
• Galactocele Figure 1-24-9
Figure 1-24-10
Palpable axillary
accessory breast Visible bilateral axillary accessory
tissue breast tissue
Fat Necrosis
• 50% have history of trauma
➢ Including surgery & XRT
• Oil cyst
• Partially calcified lesion
• Can be spiculated
• Can progress from fatty to spiculated
Fibrocystic Changes [Figures 1-24-22 and 1-24-23] Figure 1-24-22 Figure 1-24-23
• Exaggerated physiologic phenomenon
➢ Cysts
➢ Apocrine metaplasia and hyperplasia
➢ Stromal alterations
➢ Mild epithelial hyperplasia
➢ Mild adenosis
Figure 1-24-26
Microcystic nodule of
apocrine metaplasia
Pneumocystogram of a
benign cyst
Figure 1-24-35
Figure 1-24-39
Figure 1-24-40
Surface calcification in a
fibroadenoma
Calcified Fibroadenoma
[Figures 1-24-40 and 1-24-41]
Skin Calcifications
• Faint peripheral clusters with lucent centers
• Tangent view Left: Dense calcification (popcorn like) in a
fibroadenoma
Dermal Localization [Figure 1-24-42] Right: Sclerotic fibroadenoma with calcification
Figure 1-24-41
Figure 1-24-42
Secretory Calcifications
• Large rods
➢ Luminal calcifications
➢ Oriented toward nipple
➢ Relatively smooth surface Left: Calcification in artery
➢ May branch Right: Calcification in duct
Loa Loa [Figure 1-24-44 Figure 1-24-44 Figure 1-24-45
• Also called eye worm
• Found in rain forest and swamps of West
Africa, especially Cameroon
• Transmitted by day biting Chrysops flies
• Loa loa filarial nematode
• Larvae develop over 1 year
• Mature worms up to 3-6 cm x 0.5 cm
Osteosarcoma
• Primary in the breast
• 27 to 89 years old
• Median 64.5 years
• Highly aggressive tumors
Calcified loa loa worm
Primary Osteosarcoma [Figure 1-24-45]
Mass with dense osteoid
National Flower of the Radiologist is the Hedge matrix
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Normal Anatomy
• Glandular cone
➢ Breast disease occurs here
• Retromammary fascia
• Retromammary fat (left) Normal ductal distribution from nipple to
• Muscle lobules;
• Ribs (right) : Normal duct with single cell epithelial
layer and clear lumen
Segmental Anatomy
• 15 - 20 lobes or segments
Figure 1-25-3
Normal Ducts [Figures 1-25-1 and 1-25-2]
Congenital Anomalies
• Athelia
➢ Rarest anomaly of the breast
➢ Absence of the nipple
• Amastia
➢ Agenesis of breast & nipple
➢ Associated with hypoplasia of the ipsilateral pectoral muscles in 90%
➢ Can be iatrogenic Figure 1-25-4
Congenital Anomalies
• Polythelia
• Polymastia
Mastitis
• 3% of primary diagnoses at biopsy
• Many different types Very dense parenchyma in a
➢ Infection normal pregnant patient
➢ Systemic
➢ Antigen-antibody reaction Figure 1-25-5
➢ Idiopathic
Chronic Mastitis
• Chronic infection
➢ TB Focal parenchymal
➢ Fungus density from acute
• Immunologic bacterial mastitis
➢ Diabetes
➢ Amyloid
➢ Wegener granulomatosis Figure 1-25-6
➢ Sarcoid
➢ Churg – Strauss
• Idiopathic
➢ Necrobiotic xanthogranulomatosis
➢ Granulomatous mastitis
Carcinoma Arising in a
Fibroadenoma
• Rare
• Most often lobular neoplasia (LCIS) or (left) Fibroadenoma showing pushing
DCIS but not invasion of surrounding tissue. Fibroadenoma showing
• Invasive carcinoma very rare (right) Invasive carcinoma without the sharp borders and
➢ Usually grows in from outside sharp border because of invasion, not enhanced thru transmission
pushing. of sound
Fibroadenoma Phyllodes
Figure 1-25-11
Figure 1-25-14
Carcinosarcoma [Figure 1-25-13]
Figure 1-25-16
Lobular Neoplasia
• High incidence of bilaterality and multifocality
➢ Consider it a bilateral disease
• High risk marker for the development of invasive carcinoma
➢ Up to 15% in either breast equally within 20 years
➢ Lobular or ductal features
• If found on core biopsy 19% upgraded to carcinoma on excision
➢ Usually LN2 or LN3
• Pleomorphic and florid LCIS (subset of LN3) diagnosis carries highest risk
(left) Irregular calcifications in invasive ductal (left) Irregular calcification and spiculation in this
carcinoma invasive ductal carcinoma
(right) Specimen showing irregular (right) Specimen of this case showing irregular
calcifications in irregular ductal lumens in this calcifications in irregular lumens and necrotic
invasive ductal carcinoma tissue spaces
Figure 1-25-25
Paget’s Disease [Figures 1-25-26 and 1-25-27]
• Red nipple and areola
• Scaling eczematoid reaction
• 50% have a palpable mass
• Must have Paget’s cells in skin
• Usually has underlying carcinoma
Figure 1-25-26
Figure 1-25-27
Figure 1-25-30
Circumscribed
macrolobulated mass
was a papillary
carcinoma
Figure 1-25-31
Figure 1-25-33
Figure 1-25-34
Angiosarcoma
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The Problems
• How big is the problem?
• How do we classify the disease?
• How do we diagnose it?
• What is adequate treatment?
Is It Malignant?
• 30 to 60% of underdiagnosed DCIS becomes invasive cancer within 25 years
• Usually in the same breast and near the biopsy site
Epidemiology
• Same risks as for invasive cancer
➢ Increasing age
➢ Early menarche
➢ Family history
➢ Previous breast biopsy
➢ Nulliparity or late age at first birth
Classifications of DCIS
• DIN
• European Commission Working Group
• Lagios
• Modified Lagios
• Nottingham
• UKNBCSP
• Van Nuys
Diagnosis of DCIS
• Mass
• Mammographic calcifications
➢ Can’t distinguish from invasive carcinoma
➢ Associated mass usually invasive disease
Mass
• Rare today
• Usually small
Small indistinct mass
DCIS Mass Close-up [Figure 1-26-2] represents DCIS
Calcification
• Size (left) Large obscured mass was entirely DCIS.
• Number (right) Small vertically oriented solid mass
• Distribution represents DCIS
• Shape
• Change over time Figure 1-26-5
Size of Particles
• < 1 mm
➢ Evaluate malignant potential by smallest particles in the
abnormality
Number
• Cluster is 5 particles or more in 1 cubic cm.
Figure 1-26-4
Figure 1-26-9
Segmental distribution of
granular calcifications was
DCIS
Irregular Rods
• Made up of many tiny pieces on magnification
• Not solid large rods
➢ Secretory disease
• Often branch
Casting
• Granular calcifications filling the lumen of an irregular duct Figure 1-26-11
• Often branch
Figure 1-26-13
Biopsy
• Imaging guided biopsy with specimen radiography
➢ Usually stereotactic
• Wire guided excision with specimen radiography
Treatment
• Simple mastectomy without axillary dissection
➢ 25% of patients choose this option
➢ Large lesions in small breasts
➢ Multiple lesions
➢ No radiation
❖ Unavailability
❖ Prior radiation
❖ Collagen vascular disease
➢ Patient preference
• Reconstruction
Radiation Therapy
• 1.8 to 2.0 Gy fractions Monday through Friday
• 45 to 50 Gy total dose
• Boost 10 to 20 Gy to surgical bed
• No axillary radiation
Chemotherapy
• No cytotoxic drugs
• Tamoxifen 20 mg daily for 5 years
➢ Newer drugs possible with fewer side effects
➢ Decreases invasive recurrences
➢ No change in survival
❖ Survival is over 90% without chemotherapy
Treatment of Recurrence
• DCIS
➢ Mastectomy if radiation given previously
➢ Mastectomy or wide excision with radiation
• Invasive carcinoma
➢ Treat like any invasive cancer
➢ Can not give radiation twice
Follow-up
• Lifetime
• Annual mammography
➢ First exam 6 months after completion of treatment
➢ Every 6 months for the first two years?
➢ Use of magnification views common
❖ Most common in first exam after treatment
Summary
• DCIS is carcinoma without the ability to spread YET
• It is detected on mammography as calcification
• Adequate detection and treatment decreases the incidence of invasive cancer
and therefore death
1. Consensus Conference on the classification of ductal carcinoma in situ. The Consensus Conference Committee.
Cancer 1997; 80:1798-1802.
2. Cornfield DB, Palazzo JP, Schwartz GF, et al. The prognostic significance of multiple morphologic features and
biologic markers in ductal carcinoma in situ of the breast: a study of a large cohort of patients treated with surgery
alone. Cancer 2004; 100:2317-2327.
3. Hashimoto BE, Kramer DJ, Picozzi VJ. High detection rate of breast ductal carcinoma in situ calcifications on
mammographically directed high-resolution sonography. J Ultrasound Med 2001; 20:501-508.
4. Hermann G, Keller RJ, Drossman S, et al. Mammographic pattern of microcalcifications in the preoperative diagnosis
of comedo ductal carcinoma in situ: histopathologic correlation. Can Assoc Radiol J 1999; 50:235-240.
5. Hermann G, Keller RJ, Halton K, Schwartz I, Rabinowitz JG, Tartter P. Nonpalpable ductal carcinoma in situ versus
infiltrating carcinoma of the breast--can they be differentiated by mammography? Can Assoc Radiol J 1991; 42:219-
222.
6. Holland R, Hendriks JH. Microcalcifications associated with ductal carcinoma in situ: mammographic-pathologic
correlation. Semin Diagn Pathol 1994; 11:181-192.
7. Ikeda DM, Birdwell RL, Daniel BL. Potential role of magnetic resonance imaging and other modalities in ductal
carcinoma in situ detection. Magn Reson Imaging Clin N Am 2001; 9:345-356, vii.
8. Moon WK, Myung JS, Lee YJ, Park IA, Noh DY, Im JG. US of ductal carcinoma in situ. Radiographics 2002; 22:269-
280; discussion 280-281.
9. Morris EA, Liberman L, Ballon DJ, et al. MRI of occult breast carcinoma in a high-risk population. AJR Am J
Roentgenol 2003; 181:619-626.
10. Page DL, Lagios MD. Pathology and clinical evolution of ductal carcinoma in situ (DCIS) of the breast. Cancer Lett
1994; 86:1-4.
11. Schwartz GF, Solin LJ, Olivotto IA, Ernster VL, Pressman PI. Consensus Conference on the Treatment of In Situ
Ductal Carcinoma of the Breast, April 22-25, 1999. Cancer 2000; 88:946-954.
12. Sewell CW. Pathology of high-risk breast lesions and ductal carcinoma in situ. Radiol Clin North Am 2004; 42:821-
830.
13. Silverstein MJ, Lagios MD, Groshen S, et al. The influence of margin width on local control of ductal carcinoma in
situ of the breast. N Engl J Med 1999; 340:1455-1461.
14. Stomper PC, Connolly JL, Meyer JE, Harris JR. Clinically occult ductal carcinoma in situ detected with mammography:
analysis of 100 cases with radiologic-pathologic correlation. Radiology 1989; 172:235-241.
15. Waldman FM, DeVries S, Chew KL, Moore DH, 2nd, Kerlikowske K, Ljung BM. Chromosomal alterations in ductal
carcinomas in situ and their in situ recurrences. J Natl Cancer Inst 2000; 92:313-320.
16. Yen TW, Hunt KK, Mirza NQ, et al. Physician recommendations regarding tamoxifen and patient utilization of
tamoxifen after surgery for ductal carcinoma in situ. Cancer 2004; 100:942-949.
32 Fibroadenoma
• Age 0-35
➢ 3 Age 5-9
➢ 8 Age 10-14
➢ 3 Age 15-19
Fibroadenoma
• Multiple in 16 – 25% of patients clinically
• Found in 25% of breasts examined microscopically
• Can undergo myxoid change or hyalinization
➢ Gelatinous nodule
➢ Calcification
Fibroadenoma
• Originate in lobules (TDLU)
• Stages of development
➢ Proliferation of epithelial and stromal elements in (left) Two intermediate density circumscribed
multiple lobules fibroadenomas.
➢ Confluence of the hyperplastic lobules (right) Sharply bordered horizontally oriented oval
➢ Formation of fibroadenomatous nodules solid mass representing a fibroadenoma
➢ Nodules coalesce to form FA
Figure 1-27-3
Phyllodes Tumor
• Low grade
➢ Pushing margins
➢ Mild atypia (left) CT scan showing left breast mass with areas
➢ May recur locally of liquefaction necrosis.
➢ Rare metastases (right) Gross specimen of low grade Phyllodes
• High grade with areas of necrosis
➢ Invasive margin
➢ Moderate to severe atypia Figure 1-27-5
➢ Common local recurrence
➢ Hematogenous metastases
Phyllodes Tumor
• Treatment
➢ Wide local excision
Figure 1-27-8
Figure 1-27-9
Hamartoma
• Fibroadenolipoma
• Palpable mass or mammographic finding
➢ Can be large and not palpable
• Encapsulated normal breast elements
Figure 1-27-11
Diabetic Mastopathy
• Focal fibrosis in the breast
• Diabetes mellitus type 1 since childhood
➢ Poorly controlled
➢ Complications from vasculitis elsewhere
• Occurs in young to middle age
Figure 1-27-14
Figure 1-27-17
Figure 1-27-18
Malignant
• No malignant lesion under age 15 in our series
• Invasive ductal carcinoma
➢ DCIS Figure 1-27-19
• Sarcoma
➢ Angiosarcoma most common
• High grade phyllodes
• Lymphoma
• Metastasis
Ductal Carcinoma
• Age 15-35
➢ 2 age 15-19
➢ 2 Age 20-24
➢ 4 Age 25-29
➢ 18 Age 30-35
• 2 Secretory carcinoma
Figure 1-27-22
Figure 1-27-24
Sarcoma
• Malignant mesenchymal tumors
• 1% of malignant tumors in all ages
➢ Higher % in young women
• After radiation therapy 2-15 years
• Many histological subtypes
Angiosarcoma
• 14 – 82 years
➢ Mean of 35
• Lobulated mass
• Highly aggressive lesion
➢ Axillary metastasis rare
➢ Hematogenous metastasis
usual
(left) Large mass replacing the entire breast in angiosarcoma
Angiosarcoma (34) [Figure 1-27- (right) Angiosarcoma
25]
Lymphoma
• Primary or secondary (left) Lobulated mass representing a high grade
• Focal mass or diffuse process phyllodes tumor
(right) Lobulated edge of high grade phyllodes
Lymphoma (27) [Figure 1-27-27] tumor well seen on ultrasound
Metastatic Disease
• Neurofibrosarcoma
• Medulloblastoma Figure 1-27-27
• In adults (male and female)
➢ Melanoma
➢ Lung
➢ Prostate
➢ Lymphoma
Figure 1-27-29
Conclusions
• Ultrasound is the primary modality in this age group
• Mammography is reserved for screening, likely malignant lesions and the older
patients in this group
• MRI indications are evolving
• Cysts are rare especially in the younger age groups
• Most solid lesions are benign
➢ Fibroadenoma most common
• Juvenile hypertrophy and juvenile papillomatosis are unique to this age group
and have specific appearances on imaging
• Malignant lesions occur and look like malignant lesions in older women
➢ Invasive ductal carcinoma most common
References
1. Bock K, et.al. Pathologic Breast Conditions in Childhood and Adolescence. Evaluation by Sonographic Diagnosis.
J Ultrasound Med 2005; 24:1347-1354.
2. Chateil JF, Arboucalot F, Perel Y, Brun M, Boisserie-Lacroix M, Diard F. Breast metastases in adolescent girls: US
findings. Pediatr Radiol 1998; 28:832-835.
3. Ciftci AO, Tanyel FC, Buyukpamukcu N, Hicsonmez A. Female breast masses during childhood: a 25-year review. Eur
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4. Elsheikh A, Keramopoulos A, Lazaris D, Ambela C, Louvrou N, Michalas S. Breast tumors during adolescence. Eur
J Gynaecol Oncol 2000; 21:408-410.
5. El-Tamer MB, Song M, Wait RB. Breast masses in African American teenage girls. J Pediatr Surg 1999; 34:1401-
1404.
6. Green I, Dorfman RF, Rosai J. Breast involvement by extranodal Rosai-Dorfman disease: report of seven cases. Am
J Surg Pathol 1997; 21:664-668.
7. Greydanus DE, Parks DS, Farrell EG. Breast disorders in children and adolescents. Pediatr Clin North Am 1989;
36:601-638.
8. Harris VJ, Jackson VP. Indications for breast imaging in women under age 35 years. Radiology 1989; 172:445-448.
9. Karl SR, Ballantine TV, Zaino R. Juvenile secretory carcinoma of the breast. J Pediatr Surg 1985; 20:368-371.
10. Kronemer KA, Rhee K, Siegel MJ, Sievert L, Hildebolt CF. Gray scale sonography of breast masses in adolescent
girls. J Ultrasound Med 2001; 20:491-496; quiz 498.
11. Murphy JJ, Morzaria S, Gow KW, Magee JF. Breast cancer in a 6-year-old child. J Pediatr Surg 2000; 35:765-767.
12. Pettinato G, Manivel JC, Kelly DR, Wold LE, Dehner LP. Lesions of the breast in children exclusive of typical
fibroadenoma and gynecomastia. A clinicopathologic study of 113 cases. Pathol Annu 1989; 24 Pt 2:296-328.
Leonard M. Glassman, MD
Figure 1-28-1
Development
• Birth to puberty same as female
Imaging
• Less than 1% of breast imaging
➢ Mammography
➢ Ultrasound
➢ MRI
➢ CT
Figure 1-28-5
Benign Disease
• Gynecomastia
• Pseudogynecomastia
• Papilloma
• Adenoma
• Myofibroblastoma
➢ More common in men than women
• Granular cell tumor
• Fibrocystic change
Benign Disease
• No lactating adenomas
➢ No pregnancy
• Rare lobular tumors
➢ No lobules without progesterone
➢ Rare invasive lobular carcinomas reported
Benign Disease
• Rare biphasic tumors
➢ Fibroadenoma, phyllodes, carcinosarcoma
➢ Lesions begin in TDLU (lobules)
✧ Lobular development rare in men
Gynecomastia
• Potentially reversible enlargement of the male breast
• Presents as soft mobile tender subareolar mass
• Simultaneous proliferation ducts and stroma without encapsulation
➢ Florid (early) phase
✧ Begins as increased number of ducts and epithelial proliferation with
edema and cellular fibroblastic stroma
✧ Reversible phase
➢ Fibrotic (late) stage
✧ Progresses to dilated ducts, moderate epithelial proliferation and
fibrosis
Gynecomastia
• 2cm or more of subareolar tissue in non obese male
• Common “normal” finding
➢ 55% of men at autopsy
➢ Peak incidence 60 – 69 years
➢ Significant if new or symptomatic
• Palpable unilateral or bilateral subareolar mass
➢ Often conical shape
• 65% of breast lesions in elderly males
➢ 25% Carcinoma
➢ 10% Other lesions
Gynecomastia
• Response to hyperestrogenism or estrogen like response
• Absolute increase in estrogen HCG or estrogen precursors
➢ Secretion by tumors
✧ Leydig cell tumor
✧ Germ cell tumors
✧ Hepatoma
✧ Adrenal cortical tumors
✧ Pituitary tumors
Gynecomastia
• Absolute increase in estrogen HCG or estrogen precursors
➢ Estrogen therapy
✧ Prostate carcinoma
✧ Topical estradiol to scalp
Gynecomastia
• Relative increase in estrogen
➢ Testicular failure or atrophy
✧ Idiopathic
✧ Cytotoxic chemotherapy
➢ Puberty and senescence
✧ Transient in puberty (1 – 2 years)
➢ Klinefelter’s syndrome (XXY)
➢ Testicular feminization syndrome
Gynecomastia
• Hyperthyroidism
➢ Reverses when the patient is euthyroid
Symptomatic male with prominent
• Refeeding after malnutrition or starvation
subareolar tissue
• Onset of hemodialysis
Gynecomastia
• Mammographic patterns
➢ Nodular glandular (florid phase)
➢ Dendritic (fibrotic phase) Irregular dense Symptomatic male
➢ Diffuse glandular (very high estrogen levels) tissue behind the with diffusely dense
nipple pattern
Nodular Pattern [Figure 1-28-6]
• Fan shaped density radiating from the nipple
➢ May be more prominent in UOQ
➢ Blends into surrounding fat
Non specific
lobulated mass
proven to be a
cystic
lymphangioma
Pleomorphic Hyalinizing
Angioectatic Tumor of Soft Parts [Figure 1-28-16]
Figure 1-28-22
Metastasis
• Prostate most common in males
• Hematogenous spread from primary
• Usually in patients with widespread disease
➢ Occasionally solitary
• Usually round or oval circumscribed lobulated non-calcified mass
Lymphoma
• Primary or secondary
• Usually a unilateral mass
➢ Can be diffuse thickening rarely
➢ No calcification or retraction
Gynecomastia Carcinoma
• Age 60’s Age 60’s
• Soft Soft or hard
• Mobile Mobile or fixed Typical rounded
• Tender usually Tender or painless masses in
• Subareolar Subareolar metastatic disease
➢ Central Eccentric usually
• Unilateral or bilateral Unilateral usually
• Nodular, fibrotic or diffuse Mass, large or small Figure 1-28-24
Gynecomastia Carcinoma
• Nodular Large mass
➢ Fan shaped Lobulated border
• Fibrotic Small mass
➢ Subareolar density with Spiculations
extensions into fat
Conclusion
• Disease presents as mass pain or nipple discharge
• Gynecomastia and invasive ductal cancer are the most common lesions in the
male breast
➢ There are other rarer benign and malignant lesions Large water density
• Gynecomastia and carcinoma can look similar mass in a male
➢ Biopsy is sometimes necessary to separate gynecomastia from carcinoma breast with a
• All lesions eccentric to the nipple need biopsy unless they are preexisting lipoma
characteristically benign
➢ Contain fat Figure 1-28-25
➢ Lymph node
Figure 1-28-26
1. Appelbaum AH, Evans GF, Levy KR, Amirkhan RH, Schumpert TD. Mammographic appearances of male breast disease.
Radiographics 1999; 19:559-568.
2. Braunstein GD, Glassman HA. Gynecomastia. Curr Ther Endocrinol Metab 1997; 6:401-404.
3. Chantra PK, So GJ, Wollman JS, Bassett LW. Mammography of the male breast. AJR Am J Roentgenol 1995; 164:853-858.
4. Dershaw DD, Borgen PI, Deutch BM, Liberman L. Mammographic findings in men with breast cancer. AJR Am J Roentgenol
1993; 160:267-270.
5. Evans GF, Anthony T, Turnage RH, et al. The diagnostic accuracy of mammography in the evaluation of male breast disease.
Am J Surg 2001; 181:96-100.
6. Fentiman IS, Fourquet A, Hortobagyi GN. Male breast cancer. Lancet 2006; 367:595-604.
7. Giordano SH. A review of the diagnosis and management of male breast cancer. Oncologist 2005; 10:471-479.
8. Giordano SH, Cohen DS, Buzdar AU, Perkins G, Hortobagyi GN. Breast carcinoma in men: a population-based study. Cancer
2004; 101:51-57.
9. Gunhan-Bilgen I, Bozkaya H, Ustun EE, Memis A. Male breast disease: clinical, mammographic, and ultrasonographic
features. Eur J Radiol 2002; 43:246-255.
10. Haraldsson K, Loman N, Zhang QX, Johannsson O, Olsson H, Borg A. BRCA2 germ-line mutations are frequent in male breast
cancer patients without a family history of the disease. Cancer Res 1998; 58:1367-1371.
11. Hill TD, Khamis HJ, Tyczynski JE, Berkel HJ. Comparison of male and female breast cancer incidence trends, tumor
characteristics, and survival. Ann Epidemiol 2005; 15:773-780.
12. Hodgson NC, Button JH, Franceschi D, Moffat FL, Livingstone AS. Male breast cancer: is the incidence increasing? Ann Surg
Oncol 2004; 11:751-755.
13. Iredale R, Brain K, Williams B, France E, Gray J. The experiences of men with breast cancer in the United Kingdom. Eur J
Cancer 2006; 42:334-341.
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15. Michels LG, Gold RH, Arndt RD. Radiography of gynecomastia and other disorders of the male breast. Radiology 1977;
122:117-122.
16. Pappo I, Wasserman I, Halevy A. Ductal carcinoma in situ of the breast in men: a review. Clin Breast Cancer 2005; 6:310-314.
17. Shi AA, Georgian-Smith D, Cornell LD, et al. Radiological reasoning: male breast mass with calcifications. AJR Am J
Roentgenol 2005; 185:S205-210.
Hemangioma
• Most common benign hepatic tumor
➢ Likely a hamartoma rather than true neoplasm
• 1% to 7% of the population
➢ Most common in adult women
➢ Least common in pediatric population
• More common in women, 5:1
➢ Estrogen influences
➢ May enlarge during pregnancy
• Symptoms
➢ 85% asymptomatic
➢ Pain
➢ Palpable mass
➢ Rupture
Hemangioma
• Kasabach-Merritt syndrome
➢ Hemolytic anemia and consumptive coagulopathy
• Erythropoietin secretion
➢ Erythrocytosis
• Associations
➢ Focal nodular hyperplasia
➢ Tuberous sclerosis
Hemangioma - Pathology
• Peripheral feeding vessels
• Blood filled spaces
• Endothelial lining
• Fibrosis from
➢ Slow flowing blood
➢ Thrombosis
➢ Hyalinization
➢ Scar formation
Hemangioma - CT and MR
• Peripheral globular enhancement
in arterial phase
• Slow centripetal filling during
portal venous/equilibrium
• Rapid enhancement pattern
➢ Capillary hemangiomas
➢ "Flash fill" phenomenon Classic appearance of hemangioma on CT.
• MR There is discontinuous, nodular, peripheral enhancement and gradual
➢ Homogenous hyperintense contrast filling in the lesion
T2
➢ Progressive hyperintensity Figure 2-1-3
as TE increases
➢ "Light bulb" phenomenon
Hemangioma - MR
Hemangioma - Pedunculated
Hemangioma - Multiplicity
[Figure 2-1-4]
FNH - MR
• T1 isointense
➢ Low signal scar
• T2 iso or slightly hyperintense
➢ High signal scar
• Gd-DTPA FNH on CT showing late enhancement of the central scar and
➢ Rapid homogeneous peripheral vessels
enhancement
➢ May have flash enhancement
➢ Delayed enhancement of the scar
➢ Rim-like enhancement late
• T2 with ferumoxide
➢ Lesion decreases signal
➢ Except scar
FNH - Ferumoxide-enhanced MR
Paley MR, et al. AJR 2000; 175:1: 159-63
Hepatocellular Adenoma
• Third most common benign liver tumor
• Composed of benign hepatocytes
• Almost always occur in women
➢ Mean age, 30 years
➢ History of oral contraceptive use
➢ Declining incidence
• Surgical resection
➢ Risk of hemorrhage
➢ Small risk of malignant transformation to HCC
• Hepatocyte proliferation
➢ Exogenous estrogens
➢ Ovarian tumors
➢ Anabolic steroids
➢ Antiestrogens
➢ Glycogenosis, type Ia and III
➢ Hurler syndrome
Hepatocellular Adenoma
Hemosiderin Rings
Hepatocellular Adenoma
Focal Fat and Capsule
[Figure 2-1-10]
Hepatocellular Adenoma Hepatocellular adenoma with focal fat and a capsule on CT with the
Diffuse Low Attenuation corresponding gross specimen
[Figure 2-1-11]
Hepatocellular Adenoma -
Imaging Difficulties
• Nonhemorrhagic
• Fibrosis/scar formation
• Multiple
➢ Glycogenosis
➢ Hepatocellular adenomatosis Diffuse low attenuation in hepatocellular adenoma due to intracellular
glycogen
Hepatocellular Adenoma -
Multifocality
• Multiple estrogen-associated adenomas
• Hepatocellular adenomatosis
Hepatocellular adenomatosis
Biliary Cystadenoma
• Benign tumor, but
➢ May recur after excision
➢ May develop into cystadenocarcinoma
• Middle-aged women
➢ 42 - 55 years
➢ Ovarian stroma histologically
• Cystic neoplasms
➢ Unilocular or multilocular
➢ Septations
➢ Mural nodules
➢ Calcification
Lipomatous Tumors
• Angiomyolipoma
➢ Benign
➢ Composed of adipose, smooth muscle, and blood vessels
➢ Most cases sporadic
➢ Tuberous sclerosis in 6%
• Myelolipoma
➢ Rare
➢ Benign
➢ Composed of myeloid, adipose, and blood vessels
Myelolipoma
Summary - Hemangioma
• Sonography
➢ Homogenous
➢ Hyperechoic
• CT/MR
➢ Peripheral nodular enhancement
• Tagged-RBC
Summary - FNH
• CT/MR
➢ Rapid enhancement
➢ Homogenous tumor
➢ Hypodense/intense scar
➢ Delayed scar enhancement
➢ Delayed peripheral enhancement
• Sulfur colloid
Summary - HCA
• For imaging diagnosis Echogenic angiomyolipomas on
➢ Female patient sonography
➢ Oral contraceptive use
➢ Evidence of hemorrhage
• Suggest HCA Figure 2-1-15
➢ Diffuse low attenuation
➢ Diffuse fat on MR
➢ Appropriate patient
• BIOPSY !
Summary - Biliary
Cystadenoma
• Cystic neoplasm
➢ Septations
➢ Nodules
Multiple hepatic angiomyolipomas in a patient with tuberous sclerosis
➢ Calcification
who has angiomyolipomas in the right kidney and a history of left
• Most common in middle-aged
nephrectomy for a hemorrhagic angiomyolipoma
women
Hemangioma
1. Freeny PC, Marks WM. Patterns of contrast enhancement of benign and malignant hepatic neoplasms during bolus
dynamic and delayed CT. Radiology 1986; 160:613-618.
2. Birnbaum BA, Noz ME, Chapnick J, et al. Hepatic hemangiomas: diagnosis with fusion of MR, CT, and Tc-99m-
labeled red blood cell SPECT images. Radiology 1991; 181:469-474.
3. Quinn SF, Benjamin GG. Hepatic cavernous hemangiomas: simple diagnostic sign with dynamic bolus CT.
Radiology 1992; 182:545-548.
4. Yamashita Y, Ogata I, Urata J, Takahashi M. Cavernous hemangioma of the liver: pathologic correlation with
dynamic CT findings. Radiology 1997; 203:121-125.
5. Kim T, Federle MP, Baron RL, Peterson MS, Kawamori Y. Discrimination of small hepatic hemangiomas from
hypervascular malignant tumors smaller than 3 cm with three-phase helical CT. Radiology 2001; 219:699-706.
Hepatocellular Adenoma
1. al-Otaibi L, Whitman GJ, Chew FS. Hepatocellular adenoma. AJR Am J Roentgenol 1995; 165:1426.
2. Casillas VJ, Amendola MA, Gascue A, Pinnar N, Levi JU, Perez JM. Imaging of nontraumatic hemorrhagic
hepatic lesions. Radiographics 2000; 20:367-378.
3. Grazioli L, Federle MP, Ichikawa T, Balzano E, Nalesnik M, Madariaga J. Liver adenomatosis: clinical,
histopathologic, and imaging findings in 15 patients. Radiology 2000; 216:395-402.
4. Ichikawa T, Federle MP, Grazioli L, Nalesnik M. Hepatocellular adenoma: multiphasic CT and histopathologic
findings in 25 patients. Radiology 2000; 214:861-868.
Biliary Cystadenoma
1. Palacios E, Shannon M, Solomon C, Guzman M. Biliary cystadenoma: ultrasound, CT, and MRI. Gastrointest
Radiol 1990; 15:313-316.
2. Buetow PC, Buck JL, Pantongrag-Brown L, et al. Biliary cystadenoma and cystadenocarcinoma: clinical-imaging-
pathologic correlations with emphasis on the importance of ovarian stroma. Radiology 1995; 196:805-810.
3. Levy AD, Murakata LA, Abbott RM, Rohrmann CA, Jr. From the archives of the AFIP. Benign tumors and
tumorlike lesions of the gallbladder and extrahepatic bile ducts: radiologic-pathologic correlation. Armed Forces
Institute of Pathology. Radiographics 2002; 22:387-413.
Hepatocellular Carcinoma
• Neoplasm composed of malignant hepatocytes
• Fifth most common cancer worldwide
Hepatocellular Carcinoma
Gross Pathology
• Key features relevant to imaging
➢ Capsule
➢ Necrosis/hemorrhage/fibrosis
➢ Vascular invasion
➢ Macroscopic fat
➢ No calcification when HCC occurs in chronic liver disease
Hepatocellular Carcinoma -
Sonographic Features
• Variable and nonspecific
➢ Small lesions, hypoechoic
and uniform
➢ Large lesions, focal and
heterogeneous
➢ Diffuse, multinodular pattern
• Suggestive features Mosaic appearance of HCC on sonography, CT, and gross pathology
➢ High velocity arterial flow
➢ Peripheral hypoechoic rim
Figure 2-2-3
Hepatocellular Carcinoma Hypoechoic [Figure 2-2-1]
Hepatocellular
Carcinoma
Small HCC in Cirrhosis
[Figure 2-2-4]
Hepatocellular
Carcinoma HCC with capsule and macroscopic fat
Capsule and
Macroscopic Fat [Figure 2-2-5] Figure 2-2-6
Hepatocellular Carcinoma
Mosaic Pattern with Capsular Enhancement [Figure 2-2-6]
Hepatocellular Carcinoma
Mosaic Pattern
Hepatocellular Carcinoma
Fibrosis
Hepatocellular Carcinoma
Multifocal with Portal Vein Invasion
Hepatocellular Carcinoma
Solitary and Portal Vein Invasion
Fibrolamellar carcinoma
Intrahepatic Cholangiocarcinoma -
Pathologic Features [Figure 2-2-11]
• Morphology
➢ Solitary
➢ Multifocal Intrahepatic cholangiocarcinoma showing
➢ Diffuse capsular contraction and
• Satellite nodules biliary dilatation peripheral to the mass
• Marked fibrosis
• No capsule
• Rare
➢ Hemorrhage and necrosis Figure 2-2-13
➢ Calcification
Intrahepatic
Cholangiocarcinoma
CT and MR Features
• Irregular borders
➢ Infiltrative
• Enhancement pattern
➢ Due to
fibrosis/hypovascularity
➢ Delayed peripheral to central Intrahepatic cholangiocarcinoma on MR showing central to peripheral
• Biliary dilatation peripheral to the enhancement on gadolinium enhanced T1-weighted images.
tumor The gross photograph shows
• Capsular contraction characteristic fibrosis within the tumor
• Vascular invasion
Intrahepatic Cholangiocarcinoma
[Figures 2-2-12 and 2-2-13]
Angiosarcoma
• Malignant neoplasm of
endothelial cells
• Rare
➢ But, most common hepatic Angiosarcoma on CT and MR showing central hemorrhage that is
sarcoma fluid attenuation on CT and high signal on T1-and T2-weighted MR
• Etiologic associations
➢ Vinyl chloride
➢ Arsenical compounds
➢ Radiation therapy
➢ Anabolic steroids
Angiosarcoma
• More common in men, 3:1
• Clinical presentation Figure 2-2-15
➢ Variable
➢ Hemoperitoneum
➢ Metastasis in 60%, spleen, lung
Epithelioid Hemangioendothelioma
[Figure 2- 2-15]
• Rare malignancy of endothelial origin
➢ Contains dense fibrous stroma
• Imaging
➢ Multifocal, lesions coalesce over time
➢ Peripheral enhancement Epithelioid hemangioendothelioma
➢ Central fibrous stroma showing multifocality and capsular
➢ Retracted liver capsule contraction
➢ May calcify
Summary Angiosarcoma
• Rare
• Key features
➢ Evidence of hemorrhage
➢ Splenic metastasis at presentation
References
Hepatocellular Carcinoma
1. Winter TC, 3rd, Takayasu K, Muramatsu Y, et al. Early advanced hepatocellular carcinoma: evaluation of CT and
MR appearance with pathologic correlation. Radiology 1994; 192:379-387.
2. Takayasu K, Furukawa H, Wakao F, et al. CT diagnosis of early hepatocellular carcinoma: sensitivity, findings, and
CT-pathologic correlation. AJR Am J Roentgenol 1995; 164:885-890.
3. Baron RL, Oliver JH, 3rd, Dodd GD, 3rd, Nalesnik M, Holbert BL, Carr B. Hepatocellular carcinoma: evaluation
with biphasic, contrast-enhanced, helical CT. Radiology 1996; 199:505-511.
4. Kelekis NL, Semelka RC, Worawattanakul S, et al. Hepatocellular carcinoma in North America: a
multiinstitutional study of appearance on T1-weighted, T2-weighted, and serial gadolinium-enhanced gradient-
echo images. AJR Am J Roentgenol 1998; 170:1005-1013.
5. Loyer EM, Chin H, DuBrow RA, David CL, Eftekhari F, Charnsangavej C. Hepatocellular carcinoma and
intrahepatic peripheral cholangiocarcinoma: enhancement patterns with quadruple phase helical CT--a comparative
study. Radiology 1999; 212:866-875.
6. Winston CB, Schwartz LH, Fong Y, Blumgart LH, Panicek DM. Hepatocellular carcinoma: MR imaging findings
in cirrhotic livers and noncirrhotic livers. Radiology 1999; 210:75-79.
7. Ward J, Guthrie JA, Scott DJ, et al. Hepatocellular carcinoma in the cirrhotic liver: double-contrast MR imaging
for diagnosis. Radiology 2000; 216:154-162.
8. Murakami T, Kim T, Takamura M, et al. Hypervascular hepatocellular carcinoma: detection with double arterial
phase multi-detector row helical CT. Radiology 2001; 218:763-767.
9. Brancatelli G, Federle MP, Grazioli L, Carr BI. Hepatocellular carcinoma in noncirrhotic liver: CT, clinical, and
pathologic findings in 39 U.S. residents. Radiology 2002; 222:89-94.
10. Iannaccone R, Laghi A, Catalano C, et al. Hepatocellular carcinoma: role of unenhanced and delayed phase multi-
detector row helical CT in patients with cirrhosis. Radiology 2005; 234:460-467.
Fibrolamellar Carcinoma
1. Ichikawa T, Federle MP, Grazioli L, Madariaga J, Nalesnik M, Marsh W. Fibrolamellar hepatocellular carcinoma:
imaging and pathologic findings in 31 recent cases. Radiology 1999; 213:352-361.
2. McLarney JK, Rucker PT, Bender GN, Goodman ZD, Kashitani N, Ros PR. Fibrolamellar carcinoma of the liver:
radiologic-pathologic correlation. RadioGraphics 1999; 19:453-471.
3. Soyer P, Roche A, Levesque M, Legmann P. CT of fibrolamellar hepatocellular carcinoma. J Comput Assist
Tomogr 1991; 15:533-538.
4. Titelbaum DS, Hatabu H, Schiebler ML, Kressel HY, Burke DR, Saul SH. Fibrolamellar hepatocellular carcinoma:
MR appearance. J Comput Assist Tomogr 1988; 12:588-591.
5. Titelbaum DS, Burke DR, Meranze SG, Saul SH. Fibrolamellar hepatocellular carcinoma: pitfalls in nonoperative
diagnosis. Radiology 1988; 167:25-30.
6. Blachar A, Federle MP, Ferris JV, et al. Radiologists' performance in the diagnosis of liver tumors with central
scars by using specific CT criteria. Radiology 2002; 223:532-539.
Intrahepatic Cholangiocarcinoma
1. Choi BI, Park JH, Kim YI, et al. Peripheral cholangiocarcinoma and clonorchiasis: CT findings. Radiology 1988;
169:149-153.
2. Tani K, Kubota Y, Yamaguchi T, et al. MR imaging of peripheral cholangiocarcinoma. J Comput Assist Tomogr
1991; 15:975-978.
3. Kim TK, Choi BI, Han JK, Jang HJ, Cho SG, Han MC. Peripheral cholangiocarcinoma of the liver: two-phase
spiral CT findings. Radiology 1997; 204:539-543.
4. Loyer EM, Chin H, DuBrow RA, David CL, Eftekhari F, Charnsangavej C. Hepatocellular carcinoma and
intrahepatic peripheral cholangiocarcinoma: enhancement patterns with quadruple phase helical CT--a comparative
study. Radiology 1999; 212:866-875.
5. Zhang Y, Uchida M, Abe T, Nishimura H, Hayabuchi N, Nakashima Y. Intrahepatic peripheral
cholangiocarcinoma: comparison of dynamic CT and dynamic MRI. J Comput Assist Tomogr 1999; 23:670-677.
Angiosarcoma
1. Peterson MS, Baron RL, Rankin SC. Hepatic angiosarcoma: findings on multiphasic contrast-enhanced helical CT
do not mimic hepatic hemangioma. AJR Am J Roentgenol 2000; 175:165-170.
2. Koyama T, Fletcher JG, Johnson CD, Kuo MS, Notohara K, Burgart LJ. Primary hepatic angiosarcoma: findings at
CT and MR imaging. Radiology 2002; 222:667-673.
3. Levy AD. Malignant liver tumors. Clin Liver Dis 2002; 6:147-164.
4. Thompson WM, Levy AD, Aguilera NS, Gorospe L, Abbott RM. Angiosarcoma of the Spleen: Imaging
Characteristics in 12 Patients. Radiology 2005. In Press
Epithelioid Hemangioendothelioma
1. Ishak KG, Sesterhenn IA, Goodman ZD, Rabin L, Stromeyer FW. Epithelioid hemangioendothelioma of the liver:
a clinicopathologic and follow-up study of 32 cases. Hum Pathol 1984; 15:839-852.
2. Miller WJ, Dodd GD, Federle MP, Baron RL. Epithelioid hemangioendothelioma of the liver: imaging findings
with pathologic correlation [see comments]. AJR Am J Roentgenol 1992; 159:53-57.
3. Makhlouf HR, Ishak KG, Goodman ZD. Epithelioid hemangioendothelioma of the liver: a clinicopathologic study
of 137 cases. Cancer 1999; 85:562-582.
4. Mermuys K, Vanhoenacker PK, Roskams T, D'Haenens P, Van Hoe L. Epithelioid hemangioendothelioma of the
liver: radiologic-pathologic correlation. Abdom Imaging 2004; 29:221-223.
Hepatic Infections
• Pyogenic Abscess
• Amebic Abscess
• Echinococcal Infections
• Schistosomiasis
• Clonorchiasis
• Infections in the Immunocompromised host
➢ Candidasis
➢ Pneumocystis
Amebic Abscess: CT
• Enhancing wall (3-15 mm)
➢ Round
➢ Smooth or irregular
➢ Peripheral zone of edema Amebic abscess
• Low attenuation/complex fluid
➢ Septations
➢ Fluid/debris level
• Extrahepatic extension
Echinococcus: E. granulosus
E. granulosus
E. granulosus:
Water Lily Sign [Figures 2-3-7 and 2-3-8]
E. granulosus:
Complications and Treatment
• Cyst rupture
➢ Anaphylaxis Laminated membranes and water lily sign of E. granulosus
➢ Biliary tract, peritoneal cavity
➢ Pleural, pericardial cavity
• Treatment Figure 2-3-8
➢ Surgical excision
➢ Laparoscopic excision
➢ Percutaneous drainage
+ sclerosing scolicidal agents
E. multilocularis:
Pathologic Features
• Alveolar hydatid disease
• Propagation by external budding
• Invade surrounding tissue
➢ Infiltrative mass
➢ No limiting host tissue
➢ Resembles neoplasm
E. multilocularis:
Imaging Features
• Ultrasound
➢ Echogenic
➢ Single or multiple
➢ Ill-defined walls Water lily sign of E. granulosus
➢ Partially calcified
• CT
➢ Geographic Figure 2-3-9
➢ Infiltrating lesions
➢ Amorphous calcification
E. multilocularis
Schistosomasis: S. japonicum
Schistosomasis: S. mansoni
Schistosomasis: Imaging
Features
• S. japonicum
➢ Hepatic calcification
➢ “Turtle back” configuration
• S. mansoni
➢ Low attenuation, rounded foci
➢ Low attenuation, linear branching
Symmers' fibrosis
bands
Biliary Parasites
• Parasites that invade bile ducts
➢ Trematodes
❖ Clonorchis sinensis
❖ Fasciola gigantica, Fasciola
hepatica
Schistosomiasis japonicum on CT
❖ Opisthorchis viverrini
❖ Opisthorchis felineus
➢ Nematodes
❖ Ascariasis lumbricoides
➢ Cestodes
❖ Taenia saginata
Figure 2-3-14
Cholangiogram shows a
filling defect, peripheral
intrahepatic strictures,
and dilatation due to
infestation of Clonorchis
sinensis
Fasciola Hepatica
Disseminated Candidiasis
• Synonym: hepatosplenic candidiasis
• Pathogenesis
➢ Prolonged neutropenia
➢ Mucosal damage to the GI tract
➢ Local invasion of candida with entry into the hepatosplenic circulation
• Clinical manifestations
➢ Neutropenic with fever
➢ Return of neutrophil count
• Organ Involvement
➢ Spleen 94%, liver 75%, kidney 69%
Figure 2-3-15
I
II
III
IV
Figure 2-3-16
Hepatosplenic Candidiasis:
CT Features [Figure 2-3-16]
• Concentric rings
• Hypodense nodules
• Punctate calcification
Hepatosplenic Candidiasis:
MR Features
• Low T1, high T2
• Fat-suppressed T2 improves detection Hepatic candidiasis on MDCT
• Gd-FLASH most sensitive
• Splenic gamna-gandy bodies false positive T1
Pneumocystis jiroveci
• Previously classified as Pneumocystis carinii
• Now considered a fungus
• Opportunistic infection
➢ AIDS
➢ Organ transplant recipients
Summary: Echinococcus
• E. granulosus
➢ Daughter cysts
➢ Water-lily sign Sonogram and CT of disseminated pneumocystis
➢ Rim-like calcification
• E. multilocularis
➢ Infiltrating mass
➢ Calcification
Schistosomiasis
1. Araki T, Hayakawa K, Okada J, Hayashi S, Uchiyama G, Yamada K. Hepatic schistosomiasis japonica identified
by CT. Radiology 1985; 157:757-760.
2. Fataar S, Bassiony H, Satyanath S, et al. CT of hepatic schistosomiasis mansoni. AJR Am J Roentgenol 1985;
145:63-66.
3. Monzawa S, Uchiyama G, Ohtomo K, Araki T. Schistosomiasis japonica of the liver: contrast-enhanced CT
findings in 113 patients. AJR Am J Roentgenol 1993; 161:323-327.
4. Lee RC, Chiang JH, Chou YH, et al. Intestinal schistosomiasis japonica: CT-pathologic correlation. Radiology
1994; 193:539-542.
5. Willemsen UF, Pfluger T, Zoller WG, Kueffer G, Hahn K. MRI of hepatic schistosomiasis mansoni. J Comput
Assist Tomogr 1995; 19:811-813.
6. Cheung H, Lai YM, Loke TK, et al. The imaging diagnosis of hepatic schistosomiasis japonicum sequelae. Clin
Radiol 1996; 51:51-55.
7. Mortele KJ, Ros PR. Imaging of diffuse liver disease. Semin Liver Dis 2001; 21:195-212.
Hepatosplenic Candidiasis
1. Ho B, Cooperberg PL, Li DK, Mack L, Naiman SC, Grossman L. Ultrasonography and computed tomography of
hepatic candidiasis in immunosuppressed patients. J Ultrasound Med 1982; 1:157-159.
2. Shirkhoda A. CT findings in hepatosplenic and renal candidiasis. J Comput Assist Tomogr 1987; 11:795-798.
3. Pastakia B, Shawker TH, Thaler M, O'Leary T, Pizzo PA. Hepatosplenic candidiasis: wheels within wheels.
Radiology 1988; 166:417-421.
4. Thaler M, Pastakia B, Shawker TH, O'Leary T, Pizzo PA. Hepatic candidiasis in cancer patients: the evolving
picture of the syndrome. Ann Intern Med 1988; 108:88-100.
5. Gorg C, Weide R, Schwerk WB, Koppler H, Havemann K. Ultrasound evaluation of hepatic and splenic
microabscesses in the immunocompromised patient: sonographic patterns, differential diagnosis, and follow-up. J
Clin Ultrasound 1994; 22:525-529.
6. Rudolph J, Rodenwaldt J, Ruhnke M, Hamm B, Kopka L. Unusual enhancement pattern of liver lesions in
hepatosplenic candidiasis. Acta Radiol 2004; 45:499-503.
Cirrhosis: Definition
• Endpoint of chronic liver disease
Cirrhosis: Pathology
• Hepatocyte injury and loss
• Fibrosis
• Nodule formation
• Architectural reorganization
• Nodules
➢ Micronodular (<3mm)
➢ Macronodular (>3mm)
➢ Mixed
• Liver volume
➢ Early, hepatomegaly from inflammation
➢ Late, small liver from fibrosis
Cirrhosis: Imaging
• Cannot assess severity
• Role of imaging
➢ Assess disease complications
➢ Evaluation of portal hypertension
➢ HCC surveillance
Cirrhosis: Sonography
• Fibrosis
➢ Increased parenchymal echogenicity
➢ Decreased penetration of the ultrasound beam
➢ Poor visualization of hepatic vasculature
➢ Loss of triphasic hepatic vein doppler
➢ Increased pulsatility of portal vein doppler
• Nodules
• Volume redistribution
• Portal hypertension
Figure 2-4-3
Cirrhosis with high attenuation regenerating nodules (siderotic Cirrhosis with regenerating nodules
nodules) on noncontrast CT on CT
Cirrhosis: Hemangioma
Steatosis
• Nomenclature
➢ Fatty infiltration, fatty change, nonalcoholic fatty liver disease (NAFLD)
• Very common
• Pathogenesis
➢ Abnormal fatty acid metabolism
➢ Insulin/glucagon imbalance
➢ Shift to lipogenesis
Focal Steatosis
vs. Focal Sparing
Budd-Chiari Syndrome
• Hepatic venous outflow obstruction
• Primary
➢ Membranous (web) obstruction of hepatic veins 1.5 T MR fat and water proton signal
• Secondary intensity
➢ Hypercoaguable states, infections, neoplasms, trauma
Budd-Chiari Syndrome:
Pathophysiology
• Sinusoidal dilatation
• Increase sinusoidal pressure
• Centrolobular hepatocyte necrosis
• Centrolobular fibrosis
➢ Lobular collapse
➢ Nodular regeneration Focal fat on in-phase images and out-of-phase images
Budd-Chiari Syndrome:
Enhancement Patterns
• Noncontrast
➢ Heterogeneous hypodensity
❖ Hepatic parenchymal congestion
➢ Hyperdense thrombi
• Contrast enhancement
➢ Patchy enhancement
➢ Normal central hepatic, left lobe, and caudate lobe Normal hepatic vein (upper image)
enhancement and Budd Chiari (lower image)
➢ Late peripheral enhancement
Figure 2-4-14
Budd-Chiari Syndrome
[Figure 2-4-14]
Figure 2-4-16
Hemochromatosis
• Hereditary hemochromatosis
➢ Increased intestinal absorption of iron
➢ Iron predominantly within hepatocytes
➢ Highest incidence of cirrhosis and HCC (14%)
• Secondary hemochromatosis
➢ Multiple transfusions
➢ Iron predominantly in the reticuloendothelial system
Hereditary Hemochromatosis
(HHC): Pathology
Hemosiderosis
Hemochromatosis: Increased CT
Attenuation (75-135 HU)
Figure 2-4-18
Hereditary Hemochromatosis
Increased Hepatic CT
Attenuation
• Differential Diagnosis
➢ Iron deposition
➢ Glycogen storage disease
➢ Amiodarone
➢ Wilson’s disease Hereditary Hemochromatosis
➢ Chronic arsenic poisoning
Hemochromatosis: MR
• T2*-gradient echo imaging is most sensitive
➢ Quantitate with liver:muscle ratio
• Decrease signal on T2-weighted images
➢ Hereditary = iron in liver and pancreas
➢ Secondary = iron in liver and spleen
Summary: Cirrhosis
• Endpoint of chronic liver disease
• Nodules
➢ Regenerative
➢ Dysplastic
➢ HCC
• HCC false positives
References
Cirrhosis
1. Baron RL, Peterson MS. From the RSNA refresher courses: screening the cirrhotic liver for hepatocellular carcinoma
with CT and MR imaging: opportunities and pitfalls. Radiographics 2001; 21 Spec No:S117-132.
2. Brancatelli G, Baron RL, Peterson MS, Marsh W. Helical CT screening for hepatocellular carcinoma in patients with
cirrhosis: frequency and causes of false-positive interpretation. AJR Am J Roentgenol 2003; 180(4):1007-1014.
3. Dodd GD, 3rd, Baron RL, Oliver JH, 3rd, Federle MP. Spectrum of imaging findings of the liver in end-stage cirrhosis:
Part II, focal abnormalities. AJR Am J Roentgenol 1999; 173(5):1185-1192.
4. Dodd GD, 3rd, Baron RL, Oliver JH, 3rd, Federle MP. Spectrum of imaging findings of the liver in end-stage cirrhosis:
part I, gross morphology and diffuse abnormalities. AJR Am J Roentgenol 1999; 173(4):1031-1036.
5. Hussain HK, Syed I, Nghiem HV, et al. T2-weighted MR imaging in the assessment of cirrhotic liver. Radiology
2004; 230(3):637-644.
6. Ohtomo K, Baron RL, Dodd GD, 3rd, et al. Confluent hepatic fibrosis in advanced cirrhosis: appearance at CT.
Radiology 1993; 188(1):31-35.
7. Ohtomo K, Itai Y, Ohtomo Y, Shiga J, Iio M. Regenerating nodules of liver cirrhosis: MR imaging with pathologic
correlation. AJR Am J Roentgenol 1990; 154(3):505-507.
8. Shimizu A, Ito K, Koike S, Fujita T, Shimizu K, Matsunaga N. Cirrhosis or chronic hepatitis: evaluation of small
(<or=2-cm) early-enhancing hepatic lesions with serial contrast-enhanced dynamic MR imaging. Radiology 2003;
226(2):550-555.
Budd-Chiari Syndrome
1. Noone TC, Semelka RC, Siegelman ES, et al. Budd-Chiari syndrome: spectrum of appearances of acute, subacute,
and chronic disease with magnetic resonance imaging. J Magn Reson Imaging 2000; 11:44-50.
4. Brancatelli G, Federle MP, Grazioli L, Golfieri R, Lencioni R. Large regenerative nodules in Budd-Chiari syndrome
and other vascular disorders of the liver: CT and MR imaging findings with clinicopathologic correlation. AJR Am
J Roentgenol 2002; 178:877-883.
5. Maetani Y, Itoh K, Egawa H, et al. Benign hepatic nodules in Budd-Chiari syndrome: radiologic-pathologic correlation
with emphasis on the central scar. AJR Am J Roentgenol 2002; 178:869-875.
Objectives
• Congenital Disorders
➢ Caroli disease
➢ Choledochal cyst
➢ Polycystic Liver Disease
• Inflammatory Disorders
➢ Primary sclerosing cholangitis
➢ AIDS-related cholangiopathy
➢ Recurrent Pyogenic Cholangitis
➢ Acute Pyogenic Cholangitis
Differential Diagnosis
• Obstructive biliary dilatation
• Caroli disease
• Choledochal cyst
• Polycystic liver disease
• Cholangitis
➢ RPC, Pyogenic Figure 2-5-1
41-year-old male with history of renal
stones and diagnosis of medullary
sponge kidney presents with abdominal
pain, sepsis, elevated LFTs [Figure 2-5-1]
Congenital Disorders
• Caroli disease
• Choledochal cyst
• Polycystic liver disease
Saccular and fusiform biliary dilatation in
Caroli Disease Caroli disease
• Autosomal recessive
• Secondary to ductal plate malformation (DPM)
• Associated with renal disorders
➢ ARPCKD, ADPCKD
➢ Medullary sponge kidney
➢ Medullary cystic disease
Ductal Plate
• Embryologic precursor of intrahepatic bile ducts
Anomalous pancreaticobiliary
junction showing union of the
common bile duct and pancreatic
duct proximal to the duodenal wall
and sphincter complex
Todani Type I
Tubulovillous Adenoma
Differential Diagnosis
• Obstructive biliary dilatation
• Caroli disease
• Choledochal cyst
• Polycystic liver disease Polycystic liver disease occurring in
• Cholangitis ADPCKD
➢ RPC, Pyogenic
Summary: Congenital
Disorders
• Exclude obstructive
dilatation
• Congenital disorders
➢ Caroli disease
❖ Intrahepatic
➢ Choledochal cyst
❖ Extrahepatic
➢ Polycystic liver disease
❖ Noncommunicating Primary sclerosing cholangitis
cysts
Inflammatory Disorders
• Primary sclerosing cholangitis
• AIDS-related cholangiopathy
• Recurrent pyogenic cholangitis
• Acute pyogenic cholangitis
MRCP
PSC: Cholangiocarcinoma
• Stricture (90%)
➢ Long strictures (>1cm) ERCP of primary sclerosing cholangitis showing beading and
➢ Completely obstructing strictures pruning of the intrahepatic bile ducts. The extrahepatic bile
➢ Associated mass duct shows mural irregularity with focal stricture formation
• Multicentric (10%)
• Polypoid mass
AIDS Cholangiopathy
• Cholangiographic features
➢ Beading
➢ Pruning
➢ Mural irregularity
➢ Filling defects (granulation tissue)
➢ Papillary stenosis (papillitis)
➢ No EHD stenosis or diverticula
Illustration of AIDS cholangiopathy showing
disease distribution
AIDS Cholangiopathy
• Sonographic features
➢ Gallbladder wall thickening
❖ Acalculous cholecystitis
➢ Bile duct wall thickening
➢ Hyperechoic nodule in distal
CBD (papillitis)
AIDS Cholangiopathy
Acalculous cholecystitis
[Figure 2-5-17]
Recurrent Pyogenic
Cholangitis (RPC) [Figure 2-5-18]
• Clinical syndrome
➢ Pigmented stones
➢ Recurrent infection
• Unknown etiology
➢ Biliary parasites
➢ Malnutrition AIDS cholangiopathy with papillary stenosis
➢ Portal bacteremia
• Complications Figure 2-5-17
➢ Biliary cirrhosis
➢ Cholangiocarcinoma
Figure 2-5-20
Summary
• PSC
➢ Fibrosis
• AIDS cholangiopathy
➢ Papillary stenosis Illustration showing typical manifestations of acute
➢ Acalculous cholecystitis pyogenic cholangitis
• RPC
➢ Stones
➢ Focal dilatation
• Pyogenic cholangitis
➢ Obstruction
References
Caroli Disease
1. Choi BI, Yeon KM, Kim SH, et al: Caroli disease: central dot sign in CT. Radiology 174:161, 1990
2. Desmet VJ: Ludwig symposium on biliary disorders--part I. Pathogenesis of ductal plate abnormalities. Mayo
Clinic Proceedings 73:80, 1998
3. Krause D, Cercueil JP, Dranssart M, et al: MRI for evaluating congenital bile duct abnormalities. J Comput Assist
Tomogr 26:541, 2002
4. Levy AD, Rohrmann CA, Jr., Murakata LA, et al: Caroli's disease: radiologic spectrum with pathologic correlation.
AJR 179:1053, 2002
5. Marchal GJ, Desmet VJ, Proesmans WC, et al: Caroli disease: high-frequency US and pathologic findings.
Radiology 158:507, 1986
Choledochal Cyst
1. Babbitt DP, Starshak RJ, Clemett AR: Choledochal cyst: a concept of etiology. AJR 119:57, 1973
2. Govil S, Justus A, Korah I, et al: Choledochal cysts: evaluation with MR cholangiography. Abdom Imaging
23:616, 1998
3. Levy AD, Rohrmann CA, Jr.: Biliary cystic disease. Curr Probl Diagn Radiol 32:233, 2003
4. Liu CL, Fan ST, Lo CM, et al: Choledochal cysts in adults. Arch Surg 137:465, 2002
5. O'Neill JA, Jr.: Choledochal cyst. Curr Probl Surg 29:361, 1992
6. Savader SJ, Benenati JF, Venbrux AC, et al: Choledochal cysts: classification and cholangiographic appearance.
AJR 156:327, 1991
7. Savader SJ, Venbrux AC, Benenati JF, et al: Choledochal cysts: role of noninvasive imaging, percutaneous
transhepatic cholangiography, and percutaneous biliary drainage in diagnosis and treatment. J Vasc Interv Radiol
2:379, 1991
8. Todani T, Watanabe Y, Fujii T, et al: Anomalous arrangement of the pancreatobiliary ductal system in patients with
a choledochal cyst. Am J Surg 147:672, 1984
9. Todani T, Watanabe Y, Narusue M, et al: Congenital bile duct cysts: Classification, operative procedures, and
review of thirty-seven cases including cancer arising from choledochal cyst. Am J Surg 134:263, 1977
10. Wearn FG, Wiot JF: Choledochocele: not a form of choledochal cyst. J Can Assoc Radiol 33:110, 1982
AIDS Cholangiopathy
1. Chen XM, LaRusso NF: Cryptosporidiosis and the pathogenesis of AIDS-cholangiopathy. Semin Liver Dis 22:277,
2002
2. Collins CD, Forbes A, Harcourt-Webster JN, et al: Radiological and pathological features of AIDS-related
polypoid cholangitis. Clin Radiol 48:307, 1993
3. Da Silva F, Boudghene F, Lecomte I, et al: Sonography in AIDS-related cholangitis: prevalence and cause of an
echogenic nodule in the distal end of the common bile duct. AJR Am J Roentgenol 160:1205, 1993
4. Defalque D, Menu Y, Girard PM, et al: Sonographic diagnosis of cholangitis in AIDS patients. Gastrointest Radiol
14:143, 1989
5. Dolmatch BL, Laing FC, Ferderle MP, et al: AIDS-related cholangitis: radiographic findings in nine patients.
Radiology 163:313, 1987
Objectives
• Biliary adenocarcinoma
➢ Intrahepatic cholangiocarcinoma
➢ Intraductal cholangiocarcinoma
➢ Hilar (Klatskin) cholangiocarcinoma
➢ Extrahepatic duct adenocarcinoma
• Differential diagnosis
➢ Benign strictures
➢ Other neoplasms
Biliary Adenocarcinoma
• Incidence in U.S.
➢ ~2000 to 2500 cases per year
• Incidence worldwide
➢ Up to 10 times greater in Asian countries
• More common in men
➢ 2:1
Biliary Adenocarcinoma
• High risk groups
➢ Autoimmune diseases
❖ PSC, ulcerative colitis, primary biliary cirrhosis
➢ Congenital anatomic anomalies
❖ Caroli, choledochal cyst, anomalous pancreaticobiliary junction
❖ Abnormal tumor suppressor genes, FAP, NF1
➢ Infection
❖ Biliary parasites, recurrent pyogenic cholangitis
Biliary Adenocarcinoma
• Clinical presentation
➢ Jaundice
➢ Pain
➢ Fever if secondary cholangitis
Biliary Adenocarcinoma
• Moderately to well differentiated
• Desmoplastic stroma
• Infiltrative margins
➢ NO CAPSULE
Biliary Adenocarcinoma
• Dismal 5-year survival
• < 20% resectable at diagnosis
• Curative resection
➢ Tumor free margins
➢ “No touch” technique
Biliary Adenocarcinoma
• Intrahepatic Cholangiocarcinoma
Biliary Adenocarcinoma
• Intraductal Cholangiocarcinoma
Biliary Adenocarcinoma
• Hilar Cholangiocarcinoma
Intrahepatic Cholangiocarcinoma:
Pathologic Features
• Solitary, large mass
• No capsule
• Dense fibrous stroma
• No necrosis or hemorrhage
• Multifocal mass
• Satellite lesions
• Intrahepatic metastasis
Intrahepatic Cholangiocarcinoma
• Differential diagnosis
➢ Metastasis
➢ HCC
➢ Gallbladder adenocarcinoma
➢ Rare, sarcoma
• Identifying key features of ICC
➢ Evidence of fibrous stroma
➢ Contrast enhancement pattern
➢ Capsular contraction
Hilar Cholangiocarcinoma
Role of Preoperative Imaging
• Determination of resectablility
• Surgical planning
➢ Bismuth-Corlette classification1
➢ Define extent of duct involvement
1Bismuth H, Corlette MB. Surg Gynecol Obstet 1975, 140: 170-178.
Classic sonographic appearance
Hilar Cholangiocarcinoma: Unresectability of hilar cholangiocarcinoma
• Bilateral tumor extension showing biliary dilatation and an
➢ Into secondary ducts ill-defined hilar mass
➢ Into hepatic parenchyma
➢ Hepatic artery or portal vein
• Occlusion main portal vein Figure 2-6-4
• N2 nodes
• Distant mets
• Medically unfit patients
Bismuth-Corlette: Type I
[Figures 2-6-6 and 2-6-7]
• Tumor below confluence
Bismuth-Corlette: Type II Hilar cholangiocarcinoma. Ill-defined mass adjacent to bile duct stent
[Figure 2-6-8] and extending into hepatoduodenal ligament
• Tumor at confluence
Bismuth-Corlette: Type IV
[Figures 2-6-10 and 2-6-11]
• Tumor in bilateral ducts
Hilar cholangiocarcinoma on MRCP and percutaneous transhepatic
cholangiography
Figure 2-6-10
Figure 2-6-9
Figure 2-6-11
EHBD Adenocarcinoma
Figure 2-6-14
Figure 2-6-15
Differential Diagnosis
• Post-inflammatory benign strictures
➢ Pancreatitis
➢ Post radiation or chemotherapy
• Inflammatory strictures
➢ Primary sclerosing cholangitis
➢ AIDS cholangiopathy
➢ Recurrent pyogenic cholangitis
➢ Biliary parasites
• Other neoplasms
➢ Gallbladder adenocarcinoma
➢ Pancreatic adenocarcinoma
➢ Metastasis
➢ Granular cell tumor
➢ Biliary papillomatosis
Figure 2-6-18
Summary
• Biliary Adenocarcinomas
➢ Uncommon
• Peripheral intrahepatic cholangiocarcinoma
➢ Mass forming tumors
➢ Delayed, patchy enhancement
➢ Look for imaging evidence of fibrosis
• Intraductal cholangiocarcinoma
➢ Rare
➢ Intraductal masses
➢ Biliary obstruction
• Hilar cholangiocarcinoma
➢ Most common subtype
➢ Look for discontinuous biliary dilatation
➢ Determination of resectablility
• Extrahepatic duct adenocarcinoma
➢ Must differentiate from a benign stricture
Klatskin / PSC
References
Intrahepatic Cholangiocarcinoma
1. Choi BI, Lee JM, Han JK: Imaging of intrahepatic and hilar cholangiocarcinoma. Abdom Imaging 29:548, 2004
2. Ishak KG, Goodman ZD, Stocker JT: Tumors of the Liver and Intrahepatic Bile Ducts. Washington, D.C.: Armed
Forces Institute of Pathology under the auspices of Universities Associated for Research and Education in
Pathology For sale by the Armed Forces Institute of Pathology, 2001
3. Kim TK, Choi BI, Han JK, et al: Peripheral cholangiocarcinoma of the liver: two-phase spiral CT findings.
Radiology 204:539, 1997
4. Lim JH: Cholangiocarcinoma: morphologic classification according to growth pattern and imaging findings. AJR
Am J Roentgenol 181:819, 2003
5. Tani K, Kubota Y, Yamaguchi T, et al: MR imaging of peripheral cholangiocarcinoma. J Comput Assist Tomogr
15:975, 1991
6. Vilgrain V, Van Beers BE, Flejou JF, et al: Intrahepatic cholangiocarcinoma: MRI and pathologic correlation in 14
patients. J Comput Assist Tomogr 21:59, 1997
7. Worawattanakul S, Semelka RC, Noone TC, et al: Cholangiocarcinoma: spectrum of appearances on MR images
using current techniques. Magn Reson Imaging 16:993, 1998
8. Yalcin S: Diagnosis and management of cholangiocarcinomas: a comprehensive review. Hepatogastroenterology
51:43, 2004
9. Zhang Y, Uchida M, Abe T, et al: Intrahepatic peripheral cholangiocarcinoma: comparison of dynamic CT and
dynamic MRI. J Comput Assist Tomogr 23:670, 1999
Objectives
• Adenocarcinoma
➢ Ductal adenocarcinoma
➢ Mucinous noncystic adenocarcinoma
• Intraductal papillary mucinous neoplasm
• Cystic neoplasms
➢ Intraductal papillary mucinous neoplasm
➢ Solid and pseudopapillary epithelial neoplasm
➢ Mucinous cystic neoplasm
➢ Microcystic adenoma
• Endocrine neoplasms
• Metastasis
Pancreatic Adenocarcinoma:
Pathology [Figure 2-7-1]
• Microscopy
➢ Moderately to well differentiated
Pathology of ductal adenocarcinoma of the pancreas
➢ Desmoplastic stromal reaction
• Gross Pathology
➢ Fibrotic
➢ Infiltration and invasion of adjacent structures
➢ Hemorrhage and necrosis uncommon
Nonresectability
• Invasion of adjacent organs, Ductal adenocarcinoma of the pancreas showing a rounded contour
except duodenum to the uncinate process
• Tumor diameter > 5 cm
• Encasement or occlusion of vessels Figure 2-7-4
➢ SMA, SMV, portal vein
➢ Celiac trunk and major
branches
➢ +/- isolated focal involvement
of PV or SMV
➢ Accuracy of CT 88%-90%
➢ 3D CT angiography
• Distant nodal metastasis
• Liver metastasis
Ductal adenocarcinoma of the pancreas showing atrophy of the distal
Resectable? No, stomach
pancreas
and vascular invasion
Resectable? YES
Nonresectable adenocarcinoma of the pancreas
Mucinous Noncystic
Adenocarcinoma
(Infiltrating Colloid Carcinoma)[Figure 2-7-6]
• Rare variant of adenocarcinoma Figure 2-7-6
• Marked extracellular mucin
• Signet rings cells
• Imaging
➢ Large tumors
➢ Well-defined hypoattenuating
mass
➢ May have calcification
IPMN: Histopathology
• Neoplastic papillary epithelium
• Mucin production
• Duct dilatation
IPMN: MR/MRCP
MCN: Histopathology
• Columnar cell lining
• May have ovarian-type stroma
• Mucin
• Hemorrhage MR showing early capsular enhancement in SPT
• Calcification
MCN: Imaging
• Well-circumscribed cystic mass
➢ Cannot differentiate benign from malignant
• Enhancement
➢ Cyst wall, septations, mural nodules
• Calcifications
➢ Cyst wall, septations, mural nodules
• Cyst fluid
➢ Variable CT attenuation/MR signal intensity
➢ Mucin
➢ Hemorrhage
➢ Proteinaceous fluid
Microcystic Adenoma
• Benign
• Synonyms
➢ Serous cystadenoma
➢ Glycogen-rich cystadenoma
• Variants
➢ Oligocystic adenoma
Microcystic adenoma
Summary: IMPN
• High index of suspicion
• Main duct or side branch
• Imaging
➢ Duct dilatation
➢ Intraductal masses
➢ Bulging papilla
Renal cell metastatic to the pancreas
Summary: Solid
Pseudopapillary Tumor
• Young women
• Imaging features
➢ Capsule
➢ Solid and cystic
➢ Hemorrhage
Adenocarcinoma
1. Vargas R, Nino-Murcia M, Trueblood W, Jeffrey RB, Jr. MDCT in Pancreatic adenocarcinoma: prediction of
vascular invasion and resectability using a multiphasic technique with curved planar reformations. AJR Am J
Roentgenol 2004; 182:419-425.
2. Bronstein YL, Loyer EM, Kaur H, et al. Detection of small pancreatic tumors with multiphasic helical CT. AJR
Am J Roentgenol 2004; 182:619-623.
3. Roche CJ, Hughes ML, Garvey CJ, et al. CT and pathologic assessment of prospective nodal staging in patients
with ductal adenocarcinoma of the head of the pancreas. AJR Am J Roentgenol 2003; 180:475-480.
4. Fletcher JG, Wiersema MJ, Farrell MA, et al. Pancreatic malignancy: value of arterial, pancreatic, and hepatic
phase imaging with multi-detector row CT. Radiology 2003; 229:81-90.
5. Prokesch RW, Chow LC, Beaulieu CF, et al. Local staging of pancreatic carcinoma with multi-detector row CT:
use of curved planar reformations initial experience. Radiology 2002; 225:759-765.
6. Prokesch RW, Chow LC, Beaulieu CF, Bammer R, Jeffrey RB, Jr. Isoattenuating pancreatic adenocarcinoma at
multi-detector row CT: secondary signs. Radiology 2002; 224:764-768.
7. Imbriaco M, Megibow AJ, Camera L, et al. Dual-phase versus single-phase helical CT to detect and assess
resectability of pancreatic carcinoma. AJR Am J Roentgenol 2002; 178:1473-1479.
8. Horton KM, Fishman EK. Adenocarcinoma of the pancreas: CT imaging. Radiol Clin North Am 2002; 40:1263-
1272.
9. McNulty NJ, Francis IR, Platt JF, Cohan RH, Korobkin M, Gebremariam A. Multi--detector row helical CT of the
pancreas: effect of contrast-enhanced multiphasic imaging on enhancement of the pancreas, peripancreatic
vasculature, and pancreatic adenocarcinoma. Radiology 2001; 220:97-102.
10. Tabuchi T, Itoh K, Ohshio G, et al. Tumor staging of pancreatic adenocarcinoma using early- and late-phase helical
CT. AJR Am J Roentgenol 1999; 173:375-380.
11. O'Malley ME, Boland GW, Wood BJ, Fernandez-del Castillo C, Warshaw AL, Mueller PR. Adenocarcinoma of the
head of the pancreas: determination of surgical unresectability with thin-section pancreatic-phase helical CT. AJR
Am J Roentgenol 1999; 173:1513-1518.
12. Hough TJ, Raptopoulos V, Siewert B, Matthews JB. Teardrop superior mesenteric vein: CT sign for unresectable
carcinoma of the pancreas. AJR Am J Roentgenol 1999; 173:1509-1512.
13. Keogan MT, Tyler D, Clark L, et al. Diagnosis of pancreatic carcinoma: role of FDG PET. AJR Am J Roentgenol
1998; 171:1565-1570.
14. Zeman RK, Cooper C, Zeiberg AS, et al. TNM staging of pancreatic carcinoma using helical CT. AJR Am J
Roentgenol 1997; 169:459-464.
15. Raptopoulos V, Steer ML, Sheiman RG, Vrachliotis TG, Gougoutas CA, Movson JS. The use of helical CT and CT
angiography to predict vascular involvement from pancreatic cancer: correlation with findings at surgery. AJR Am
J Roentgenol 1997; 168:971-977.
16. Lu DS, Reber HA, Krasny RM, Kadell BM, Sayre J. Local staging of pancreatic cancer: criteria for unresectability
of major vessels as revealed by pancreatic-phase, thin-section helical CT. AJR Am J Roentgenol 1997; 168:1439-
1443.
17. Lu DS, Vedantham S, Krasny RM, Kadell B, Berger WL, Reber HA. Two-phase helical CT for pancreatic tumors:
pancreatic versus hepatic phase enhancement of tumor, pancreas, and vascular structures. Radiology 1996;
199:697-701.
18. Megibow AJ, Zhou XH, Rotterdam H, et al. Pancreatic adenocarcinoma: CT versus MR imaging in the evaluation
of resectability--report of the Radiology Diagnostic Oncology Group. Radiology 1995; 195:327-332.
19. Megibow AJ. Pancreatic adenocarcinoma: designing the examination to evaluate the clinical questions. Radiology
1992; 183:297-303.
Microcystic Adenoma
1. Buck JL, Hayes WS: From the Archives of the AFIP. Microcystic adenoma of the pancreas. Radiographics 10:313,
1990
2. Healy JC, Davies SE, Reznek RH: CT of microcystic (serous) pancreatic adenoma. J Comput Assist Tomogr
18:146, 1994
3. Hough DM, Stephens DH, Johnson CD, et al: Pancreatic lesions in von Hippel-Lindau disease: prevalence, clinical
significance, and CT findings. AJR Am J Roentgenol 162:1091, 1994
4. Itai Y, Ohhashi K, Furui S, et al: Microcystic adenoma of the pancreas: spectrum of computed tomographic
findings. J Comput Assist Tomogr 12:797, 1988
5. Khurana B, Mortele KJ, Glickman J, et al: Macrocystic serous adenoma of the pancreas: radiologic-pathologic
correlation. AJR Am J Roentgenol 181:119, 2003
6. Minami M, Itai Y, Ohtomo K, et al: Cystic neoplasms of the pancreas: comparison of MR imaging with CT.
Radiology 171:53, 1989
7. Yeh HC, Stancato-Pasik A, Shapiro RS: Microcystic features at US: a nonspecific sign for microcystic adenomas
of the pancreas. Radiographics 21:1455, 2001
Metastases
1. Klein KA, Stephens DH, Welch TJ: CT characteristics of metastatic disease of the pancreas. Radiographics 18:369,
1998
2. Ng CS, Loyer EM, Iyer RB, et al: Metastases to the pancreas from renal cell carcinoma: findings on three-phase
contrast-enhanced helical CT. AJR Am J Roentgenol 172:1555, 1999
Gastric Malignancies
• Adenocarcinoma
• Lymphoma
• Gastrointestinal Stromal Tumors
• Carcinoid
• Kaposi Sarcoma
• Metastases
Gastric Adenocarcinoma
• Fourth most common cancer worldwide1
➢ Lung, breast, colorectum, stomach, liver
1Steward BW and Kleihues P (eds). World Cancer Report. IARC Press. Lyon
2003.
Figure 2-8-3
Signet ring cell adenocarcinoma
produces "linitis plastica"
Figure 2-8-4
Papillary adenocarcinoma produces
intraluminal polypoid masses
Figure 2-8-6
Ulcerated Carcinoma
Lesser Curvature
Gastric Lymphoma
• Increasing incidence
• Up to 10% of gastric malignancies
• Most common site of extranodal lymphoma
• Most common site of GI lymphomas
H. pylori infection
H. pylori gastritis
What is KIT?
• KIT-tyrosine kinase growth factor
• KIT-tyrosine kinase growth factor receptor
• CD117 binds to KIT receptors
• Normally expressed
➢ Hematopoietic stem cells
➢ Germ cells
➢ Interstitial cell of Cajal (gut pacemaker cell)
• KIT-inhibitor therapy
➢ STI-571, Imatinib [Gleevac]
GIST
• Most common sites
➢ Stomach
➢ Small bowel
GIST
• Spindle Cell GIST
• Epithelioid GIST
GIST: Calcification
Differential Diagnosis
Gastric GIST vs. Adenocarcinoma
[Figures 2- 7-19 and 2-7-20]
Gastric Carcinoid
• Type I: autoimmune chronic atrophic gastritis
➢ Hypergastrinemia
➢ Multiple, small
➢ Benign biologic behavior
• Type II: MEN I and Zollinger Ellison syndrome
➢ Hypergastrinemia
➢ Multiple, small
➢ Benign biologic behavior
• Type III: sporadic
➢ Single
➢ Aggressive biologic behavior GIST vs. adenocarcinoma
Metastases
• Melanoma, breast, lung
• Radiologic features
➢ Ulcerating masses
➢ Polyps
GIST vs. lymphoma
➢ Infiltrating
➢ “Linitis Plastica”
Figure 2-8-21
Summary: Adenocarcinoma
• H. pylori
• Chronic atrophic gastritis
• Primary tumor morphology
➢ Polypoid
➢ Ulcerating
➢ Infiltrating
➢ Schirrous
• CT: extragastric spread
Summary: Lymphoma
• H. pylori
• Low grade MALT to high grade B cell
• Compared to adenocarcinoma
➢ Greater wall thickening
➢ Bulky, more extensive adenopathy
Summary: GIST
• Most common mesenchymal neoplasm
• KIT reactivity
➢ Diagnosis
➢ Gleevac therapy
• Classic mural masses on barium
• May have extensive extragastric growth
References
Gastric Carcinoma
1. Balthazar EJ, Siegel SE, Megibow AJ, et al: CT in patients with scirrhous carcinoma of the GI tract: imaging
findings and value for tumor detection and staging. AJR 165:839, 1995
2. Gore RM: Gastric cancer. Clinical and pathologic features. Radiol Clin North Am 35:295, 1997
3. Gore RM, Levine MS, Ghahremani GG, et al: Gastric cancer. Radiologic diagnosis. Radiol Clin North Am 35:311,
1997
4. Levine MS, Kong V, Rubesin SE, et al: Scirrhous carcinoma of the stomach: radiologic and endoscopic diagnosis.
Radiology 175:151, 1990
5. Longmire WP, Jr.: A current view of gastric cancer in the US. Ann Surg 218:579, 1993
6. Miller FH, Kochman ML, Talamonti MS, et al: Gastric cancer. Radiologic staging. Radiol Clin North Am 35:331,
1997
7. Morales TG: Adenocarcinoma of the gastric cardia. Dig Dis 15:346, 1997
8. Parsonnet J: Helicobacter pylori and gastric cancer. Gastroenterol Clin North Am 22:89, 1993
9. Parsonnet J, Friedman GD, Vandersteen DP, et al: Helicobacter pylori infection and the risk of gastric carcinoma.
N Engl J Med 325:1127, 1991
10. Sipponen P, Marshall BJ: Gastritis and gastric cancer. Western countries. Gastroenterol Clin North Am 29:579,
2000
Gastric Lymphoma
1. An SK, Han JK, Kim YH, et al: Gastric mucosa-associated lymphoid tissue lymphoma: spectrum of findings at
double-contrast gastrointestinal examination with pathologic correlation. Radiographics 21:1491, 2001
2. Buy JN, Moss AA: Computed tomography of gastric lymphoma. AJR 138:859, 1982
3. Choi D, Lim HK, Lee SJ, et al: Gastric mucosa-associated lymphoid tissue lymphoma: helical CT findings and
pathologic correlation. AJR 178:1117, 2002
4. Jaffe ES, Harris NL, Stein H, et al (eds): World Health Organization Classification of Tumours: Pathology and
Genetics of Tumours of Haematopoietic and Lymphoid Tissues), Lyon: IARC Press, 2001
5. Kim YH, Lim HK, Han JK, et al: Low-grade gastric mucosa-associated lymphoid tissue lymphoma: correlation of
radiographic and pathologic findings. Radiology 212:241, 1999
6. Levine MS, Elmas N, Furth EE, et al: Helicobacter pylori and gastric MALT lymphoma. AJR Am J Roentgenol
166:85, 1996
7. Levine MS, Rubesin SE, Pantongrag-Brown L, et al: Non-Hodgkin's lymphoma of the gastrointestinal tract:
radiographic findings. AJR Am J Roentgenol 168:165, 1997
8. Megibow AJ, Balthazar EJ, Naidich DP, et al: Computed tomography of gastrointestinal lymphoma. AJR 141:541,
1983
9. Parsonnet J, Hansen S, Rodriguez L, et al: Helicobacter pylori infection and gastric lymphoma. N Engl J Med
330:1267, 1994
10. Wotherspoon AC, Doglioni C, de Boni M, et al: Antibiotic treatment for low-grade gastric MALT lymphoma.
Lancet 343:1503, 1994
11. Yoo CC, Levine MS, Furth EE, et al: Gastric mucosa-associated lymphoid tissue lymphoma: radiographic findings
in six patients. Radiology 208:239, 1998
Gastric Carcinoid
1. Balthazar EJ, Megibow A, Bryk D, et al: Gastric carcinoid tumors: radiographic features in eight cases. AJR Am J
Roentgenol 139:1123, 1982
2. Berger MW, Stephens DH: Gastric carcinoid tumors associated with chronic hypergastrinemia in a patient with
Zollinger-Ellison syndrome. Radiology 201:371, 1996
3. Binstock AJ, Johnson CD, Stephens DH, et al: Carcinoid tumors of the stomach: a clinical and radiographic study.
AJR 176:947, 2001
4. Borch K, Renvall H, Kullman E, et al: Gastric carcinoid associated with the syndrome of hypergastrinemic
atrophic gastritis. A prospective analysis of 11 cases. Am J Surg Pathol 11:435, 1987
5. Ho AC, Horton KM, Fishman EK: Gastric carcinoid tumors as a consequence of chronic hypergastrinemia: spiral
CT findings. Clin Imaging 24:200, 2000
Objectives
• Definition
• Patterns of disease
➢ NHL Adenopathy
➢ Gastrointestinal Lymphoma
• Immunodeficiency-related lymphomas
➢ Post-transplantation Lymphoproliferative Disorder (PTLD)
➢ AIDS-related Lymphomas
Lymphoid Neoplams
• 2001 WHO classification of Hematological Malignancies
• Three major categories
➢ B cell, T and NK (natural killer) cell, Hodgkin lymphoma
• NHL
➢ Large group of diverse diseases
➢ Indolent, aggressive, and very aggressive
Non-Hodgkin Lymphoma
• Rising incidence
➢ True increase in incidence
➢ Improved identification and understanding
➢ HIV infection
➢ Organ transplants
• Immunodeficiency increases risk
➢ Wiskott-Aldrich syndrome
➢ Ataxia telangiectasia
➢ Long-term immunosuppressive therapy
Castleman Disease
• Hyperenhancing masses
➢ Homogeneous or heterogeneous
• May calcify
Carcinoid
• Primary lesion in bowel
• Mesenteric metastasis
➢ Spiculations/tethering of mesentery
➢ May calcifiy
Sarcoid
• Small, discrete nodes
• Retrocural nodes atypical in sarcoid
Gastrointestinal Lymphoma
• Lymphoma that presents with GI disease and no other major site of
involvement
• Most common extranodal site of NHL
➢ 4.4% of all lymphomas
➢ 25% of all extranodal lymphomas
• Almost exclusively NHL
• Stomach is the most common site in US and Western Europe
• Small bowel is the most common site in the Mediterranean, Northern Africa,
Middle East
• B-cell lymphomas
➢ MALT lymphomas
❖ Immunoproliferative small intestinal disease, “alpha-heavy chain
disease”
➢ Mantle cell lymphoma (multiple lymphomatous polyposis)
➢ Burkitt and Burkitt-type lymphoma
➢ Nodal equivalents (diffuse large B-cell lymphomas, follicular, etc)
Figure 2-9-7
Lymphoma histology shows tumor
extension from mucosa to serosa
Figure 2-9-6
Cavitary mass
Figure 2-9-10
Burkitt Lymphoma
• High grade B-cell lymphoma
• More common in males
• Endemic Mural infiltration with luminal
➢ African Burkitt, related to EBV dilatation
➢ Head and neck disease
• Sporadic
➢ Western countries, not related to EBV
➢ ileocecal region of children
• Clinical presentation
➢ Intestinal obstruction
➢ Intussusception
Jejunal Adenocarcinoma
Tuberculosis / Lymphoma
Post-transplantation Lymphoproliferative
Disorder (PTLD)
• Spectrum of benign and malignant disorders
• Variable incidence
➢ 1% renal transplants
➢ 10% combined heart/lung
➢ 10% of patients on cyclosporine and OKT3
• Association with EBV infection
• Lung, GI tract
AIDS-Related Lymphoma
• 25% have GI tract disease
• Higher incidence of mesenteric disease than non-AIDS lymphomas
• Aggressive histology and biologic behavior
➢ Atypical radiologic features
➢ Hemorrhage
➢ Necrosis
• Unique subtypes
➢ Body cavity-based lymphoma (Kaposi’s sarcoma-associated herpes virus
(KSHV))
➢ Anorectal lymphoma Figure 2-9-15
Colonic Lymphoma
Summary
Primary peritoneal lymphoma in AIDS
• Spectrum of Adenopathy
• ➢ GI lymphomas are predominantly
NHL
➢ Unique subtypes involve the bowel
➢ Various patterns: infiltrating masses, luminal dilatation, polyps, cavitary
masses, mesenteric masses
• AIDS-related
➢ Aggressive behavior
➢ Unusual sites, unusual manifestations
• PTLD Figure 2-9-16
➢ Colon, liver
Patterns of Adenopathy
1-Mural Infiltration
2-Polyps
Anorectal lymphoma in AIDS
3-Cavitary Masses
4-Mesenteric Masses
AIDS-Related Lymphomas
Lymphoma Classification
1. Harris NL, Jaffe ES, Diebold J, et al: The World Health Organization classification of neoplasms of the hematopoietic
and lymphoid tissues: report of the Clinical Advisory Committee meeting--Airlie House, Virginia, November, 1997.
Hematol J 1:53, 2000
2. Jaffe ES, Harris NL, Stein H, et al (eds): World Health Organization Classification of Tumours: Pathology and
Genetics of Tumours of Haematopoietic and Lymphoid Tissues), Lyon: IARC Press, 2001
AIDS-related lymphomas
1. Albin J, Lewis E, Eftekhari F, et al: Computed tomography of rectal and perirectal disease in AIDS patients. Gastrointest
Radiol 12:67, 1987
2. Brar HS, Gottesman L, Surawicz C: Anorectal pathology in AIDS. Gastrointest Endosc Clin N Am 8:913, 1998
3. Burkes RL, Meyer PR, Gill PS, et al: Rectal lymphoma in homosexual men. Arch Intern Med 146:913, 1986
4. Ferrozzi F, Tognini G, Mulonzia NW, et al: Primary effusion lymphomas in AIDS: CT findings in two cases. Eur
Radiol 11:623, 2001
5. Gottlieb CA, Meiri E, Maeda KM: Rectal non-Hodgkin's lymphoma: a clinicopathologic study and review. Henry
Ford Hosp Med J 38:255, 1990
6. Ioachimm HL, Antonescu C, Giancotti F, et al: EBV-associated anorectal lymphomas in patients with acquired immune
deficiency syndrome. Am J Surg Pathol 21:997, 1997?
7. Munn S: Imaging HIV/AIDS. Burkitt's lymphoma. AIDS Patient Care STDS 16:395, 2002
Adenoma
• Benign intraepithelial neoplasm composed of
dysplastic cells
➢ Tubular, villous, or tubulovillous histology
➢ May progress to adenocarcinoma
• Locations
➢ 80% are periampullary
• Increased incidence
➢ Familial adenomatous polyposis, FAP
➢ Hereditary nonpolyposis colon carcinoma,
HNPCC
Periampullary Adenocarcinoma
Periampullary adenocarcinoma
• Imaging features
➢ Biliary obstruction
➢ Duodenal mural thickening or polypoid mass
➢ May extend into adjacent pancreas and/ampulla Figure 2-10-5
Adenocarcinoma Duodenum:
Ampullary/Periampullary
[Figures 2-10-4 and 2-10-5]
• May arise from periampullary duodenal mucosa
• May arise from ampulla
• May be mixed location
➢ Origin not clear
Ileal Adenocarcinoma:
Cavitary Mass [Figure 2-10-8]
• Unusual presentation for
adenocarcinoma
• More aggressive histology
➢ Poorly differentiated
➢ Endocrine features mixed
with adenocarcinoma Adenocarcinoma of the ileum manifesting as a cavitary mass
Carcinoid
Carcinoid
• Well-differentiated endocrine neoplasms
• All have malignant potential
• Classification
➢ Foregut, stomach and proximal duodenum
➢ Midgut (60% to 80%), distal duodenum, jejunum, ileum, appendix,
ascending colon, proximal transverse colon Figure 2-10-10
➢ Hindgut, distal transverse colon,
descending colon, rectum
• Spectrum of clinical/imaging features
➢ Population and type of endocrine
cell changes throughout the bowel
➢ Variety of hormones produced
➢ Biologic behavior ranges from
benign to malignant
Carcinoid
Duodenal Carcinoid
• Most common in first and second portion
➢ Low-grade malignancies
➢ Gastrin or somatostatin production most common
➢ Periampullary tumors = somatostatin producing and NF1 association
• Associations
➢ Zollinger-Ellison syndrome
➢ Multiple endocrine neoplasia (MEN 1)
➢ Neurofibromatosis type 1 (NF1) Figure 2-10-11
Duodenal Carcinoid [Figure 2-10-11]
• Imaging features
➢ Solitary or multifocal polyps
➢ Intramural mass
Carcinoid Ileum
• ”Elastic vascular sclerosis”
• Sunburst pattern of mesenteric Ileal carcinoid
vessels
• Multifocal nodules
• Kinking of bowel
• Rigid segment of bowel
Carcinoid Syndrome
• 10% of patients with carcinoids
Figure 2-10-13
• Most common with ileal
carcinoids
• Hepatic metastasis are usually
present
➢ Serotonin and metabolites in
systemic circulation
• Classic syndrome
➢ Paroxysms of sweating,
flushing, cyanosis, wheezing,
abdominal colic, right-sided Metastatic carcinoid shown on CT and 111In-pentetreotide
heart failure, diarrhea scintigraphy
➢ Symptoms precipitated by
ETOH intake, stress, exercise
• Carcinoid heart disease
➢ Right sided valvular dysfunction
➢ Congestive heart failure
Metastatic Disease
• Most common site for metastasis in GI tract
• Metastasis are more common than primary malignancies in the small bowel
• Widespread metastatic disease usually present
• Hematogenous spread
➢ Melanoma
➢ Lung
➢ Breast
➢ Kidney
• Intraperitoneal, direct extension, lymphatic spread
➢ Tumors of GI origin
➢ Ovarian and endometrial carcinoma
• Imaging patterns
➢ Identical to primary neoplasms
➢ Polyps, mural masses, annular strictures, cavitary lesions, association with
mesenteric nodal masses
Metastatic Disease:
Melanoma [Figure 2-10-18]
Summary: Adenoma
• Uncommon
• Most periampullary
• Association Figure 2-10-18
➢ FAP
➢ HNPCC
Summary: Adenocarcinoma
• Periampullary location most
common
• Morphology
➢ Polypoid
➢ Annular
➢ Infiltrating
➢ Cavitary Melanoma metastatic to the small bowel
Summary: Carcinoid
• Endocrine neoplasms
• Midgut most common
➢ Serotonin production
➢ Octreotide scintigraphy
• Key imaging features
➢ Mural wall thickening
➢ Fixation of bowel
➢ Mesenteric mass
➢ Mesenteric retraction
Summary: GIST
• Most common mesenchymal neoplasm
➢ KIT positive
• Mural masses
➢ Intraluminal polyp
➢ Exophytic component
➢ Hemorrhage
➢ Cyst formation
➢ Cavitation
Colorectal Carcinoma
• Third most frequent cancer in the U.S.1
➢ ~150,000 new cases per year
➢ 11% of cancers in men and women
➢ 10% of cancer deaths
1Jemal A et al. CA Cancer J Clin 2005; 55:10-30
Tubular Adenoma
Villous Adenoma
Virtual Colonography
Villous Adenoma
• Higher rate of malignancy
• Recurrence rate 9.3%
• Three types Sessile adenomatous polyp showing
➢ Flat, carpet-like the Bowler Hat sign
➢ Sessile, lobulated
➢ Pedunculated
• Histology
➢ Nonbranching finger-like fronds
Figure 2-11-3
Annular Adenocarcinoma
[Figure 2-11-7]
Infiltrating Adenocarcinoma
[Figure 2-11-8]
Coloduodenal Fistula
Multiple Carcinomas
• Synchronous carcinomas
➢ Diagnosed within 6 months of each Annular adenocarcinoma of the distal transverse colon
other
➢ Incidence 1.5% to 12% Figure 2-11-8
➢ Most are >5 cm away from each
other
• Metachronous carcinomas
➢ Incidence 0.6% to 9.1%
➢ Time interval to second lesion
discovery
❖ 64% within 5 years
❖ 45% within 3 years
❖ 20% within 1 year
Infiltrating adenocarcinoma of the sigmoid colon with
• 8% to 20% of patients with colorectal
pericolonic extension and pericolonic adenopathy
carcinomas have malignancies in other
organs
Figure 2-11-9
Synchronous Carcinomas
[Figure 2-11-10]
Figure 2-11-10
Adenocarcinoma in Ulcerative
Colitis
Colorectal Carcinoma:
Complications Adenocarcinoma in ulcerative colitis
• Bleeding
➢ Occult
➢ Chronic anemia
➢ Massive bleeding, unusual Figure 2-11-12
• Obstruction
➢ Occlusion of the colonic lumen
➢ Colocolic intussusception
• Perforation
➢ Abscess
➢ Fistula
➢ Differential diagnosis, diverticulitis
CT of Obstructing Colon
Colonic ischemia in an obstructing carcinoma of the
Carcinomas
descending colon
• IV contrast
• Identify obstructing lesion Figure 2-11-13
➢ Infiltration of adjacent fat
➢ Adjacent organ invasion
• Evaluate bowel integrity
➢ Obstructive colitis (1% to 7%)
➢ Ischemic changes
➢ Pneumatosis
• Stage
➢ Local extension
➢ Lymph node mets
➢ Liver mets Perforated adenocarcinoma of the transverse colon with
abscess formation
CT of Obstructing Colon Carcinomas
T1 N0 M0
T2 N0 M0 Figure 2-11-15
T3 N2 M0 [Figure 2-11-16]
T3 N10 M0
T3 N8 M1
T4
Figure 2-11-16
Pericolonic Nodes
Intermediate
Principal
Rectal Adenocarcinoma:
Lymphatic Drainage [Figures 2-11-18 and 2-11-
19]
• Pararectal nodes
• Internal iliac nodes
➢ Tumors above dentate line
• Inguinal nodes
➢ Tumors below dentate line
Distribution of
Figure 2-11-18 lymphatic spread for
colon carcinoma
Summary: Complications
• Bleeding
➢ Usually chronic blood loss
➢ Massive GI bleed, unusual
• Obstruction
➢ CT
➢ Identify lesion and bowel wall integrity
• Perforation
➢ Abscess
➢ Fistula
➢ Differential diagnosis inflammatory disorders
Virtual Colonography
1. Fidler JL, Johnson CD, MacCarty RL, et al: Detection of flat lesions in the colon with CT colonography. Abdom
Imaging 27:292, 2002
2. Fletcher JG, Johnson CD, MacCarty RL, et al: CT colonography: potential pitfalls and problem-solving techniques.
AJR Am J Roentgenol 172:1271, 1999
3. Fletcher JG, Johnson CD, Welch TJ, et al: Optimization of CT colonography technique: prospective trial in 180
patients. Radiology 216:704, 20
4. Gluecker TM, Fletcher JG, Welch TJ, et al: Characterization of Lesions Missed on Interpretation of CT Colonography
Using a 2D Search Method. AJR Am J Roentgenol 182:881, 2004
5. Gluecker TM, Johnson CD, Harmsen WS, et al: Colorectal cancer screening with CT colonography, colonoscopy,
and double-contrast barium enema examination: prospective assessment of patient perceptions and preferences.
Radiology 227:378, 2003
6. Johnson CD, Ahlquist DA: Computed tomography colonography (virtual colonoscopy): a new method for colorectal
screening. Gut 44:301, 1999
7. Johnson CD, Harmsen WS, Wilson LA, et al: Prospective blinded evaluation of computed tomographic colonography
for screen detection of colorectal polyps. Gastroenterology 125:311, 2003
8. Johnson CD, Toledano AY, Herman BA, et al: Computerized tomographic colonography: performance evaluation in
a retrospective multicenter setting. Gastroenterology 125:688, 2003
9. Macari M: Virtual colonoscopy: clinical results. Semin Ultrasound CT MR 22:432, 2001
10. Pescatore P, Glucker T, Delarive J, et al: Diagnostic accuracy and interobserver agreement of CT colonography (virtual
colonoscopy). Gut 47:126, 2000
11. Pickhardt PJ: Three-dimensional endoluminal CT colonography (virtual colonoscopy): comparison of three
commercially available systems. AJR Am J Roentgenol 181:1599, 2003
12. Pickhardt PJ, Choi JR, Hwang I, et al: Computed tomographic virtual colonoscopy to screen for colorectal neoplasia
in asymptomatic adults. N Engl J Med 349:2191, 2003
13. Royster AP, Fenlon HM, Clarke PD, et al: CT colonoscopy of colorectal neoplasms: two-dimensional and three-
dimensional virtual-reality techniques with colonoscopic correlation. AJR Am J Roentgenol 169:1237, 1997
14. Spinzi G, Belloni G, Martegani A, et al: Computed tomographic colonography and conventional colonoscopy for
colon diseases: a prospective, blinded study. Am J Gastroenterol 96:394, 2001
15. Taylor SA, Halligan S, Bartram CI: CT colonography: methods, pathology and pitfalls. Clin Radiol 58:179, 2003
16. Taylor SA, Halligan S, Bartram CI, et al: Multi-detector row CT colonography: effect of collimation, pitch, and
orientation on polyp detection in a human colectomy specimen. Radiology 229:109, 2003
17. Taylor SA, Halligan S, Goh V, et al: Optimizing bowel preparation for multidetector row CT colonography: effect of
Citramag and Picolax. Clin Radiol 58:723, 2003
18. Taylor SA, Halligan S, Goh V, et al: Optimizing colonic distention for multi-detector row CT colonography: effect
of hyoscine butylbromide and rectal balloon catheter. Radiology 229:99, 2003
MesentericAnatomy: Definitions
• Mesentery
➢ Double fold of peritoneum
➢ Connects an organ to the
abdominal wall
• Omentum
➢ Specialized mesentery
extending from stomach
to an adjacent organ
Anatomy Mesentery
[Figure 2-12-1]
• Transverse mesocolon
• Small bowel mesentery
• Sigmoid mesentery
• Mesoappendix
Anatomy: Omentum
[Figure 2-12-2]
• Greater omentum Normal posterior attachments of the
➢ Gastrocolic ligament mesentery in sagittal and AP planes
➢ Gastrosplenic ligament
➢ Gastrophrenic ligament
• Lesser omentum
➢ Gastrohepatic ligament
Figure 2-12-2
➢ Hepatoduodenal ligament
Abdominal Lymphangioma:
Lymphangioma of the greater omentum
Pathology
• Interconnecting cysts
• Endothelial lining
• Dilated lymphatic spaces
➢ Proteinaceous fluid
➢ Chyle, low attenuation
➢ Hemorrhage
Differential Diagnosis
• Pancreatic cystic neoplasm
➢ Mucinous cystic neoplasm
➢ Oligocystic adenoma
• Pancreatic pseudocyst
• Mesenteric cyst
➢ Lymphangioma Enteric duplication cyst
➢ Enteric duplication cyst
➢ Enteric cyst
➢ Mesothelial cyst
➢ Pancreatic pseudocyst
• Cystic mesenteric neoplasm
➢ Metastatic disease
➢ Cystic mesothelioma
Differential Diagnosis:
Solid Mesenteric Mass
• Malignant
➢ Soft tissue sarcoma
➢ Lymphoma
➢ Gastrointestinal stromal tumor
➢ Metastatic disease
• Benign Mesenteric fibromatosis
➢ Mesenteric fibromatosis
➢ Sclerosing mesenteritis
➢ Inflammatory pseudotumor Figure 2-12-12
Mesenteric Fibromatosis:
(Intraabdominal Fibromatosis or
Abdominal Desmoid)
• Classified as a deep fibromatosis
➢ Mesenteric, pelvic, retroperitoneal
➢ Abdominal wall
➢ Extraabdominal
• Benign proliferative process Mesenteric fibromatosis with low CT attenuation, located in the
➢ Locally aggressive greater omentum
➢ Recurs following excision
➢ Does not metastasize
• Mesenteric fibromatosis
➢ No gender predilection
➢ Most cases sporadic
➢ 13% associated with FAP
• Abdominal fibromatosis
➢ Most common in young women, 20-30 years of age
Mesenteric Fibromatosis:
Homogeneous Attenuation Mesenteric fibromatosis
Mesenteric Fibromatosis:
Infiltrates small bowel wall Mesenteric fibromatosis in a patient with FAP. The myxoid
stroma creates a “whorled” pattern in this example
Mesenteric Fibromatosis in FAP
• Almost always post operative
➢ Occurs at operative sites
➢ Usually within 4 years of surgery
• Unusual manifestations
➢ Multiplicity
➢ May occur with abdominal wall fibromatosis
➢ Diffuse form may involve mesentery, pelvis, and retroperitoneum
Lymphoma
Sclerosing Mesenteritis
• Rare
• Idiopathic, nonneoplastic
• Chronic inflammation
• Synonyms represent histologic spectrum
➢ Mesenteric panniculitis
➢ Fibrosing mesenteritis
➢ Mesenteric lipodystrophy
Sclerosing Mesenteritis:
Pathologic Features
• Pathologic spectrum
➢ Loose myxomatous to dense
sclerosis Sclerosing mesenteritis
• Histologic features
➢ Sclerosing fibrosis
➢ Fat necrosis
➢ Lipid-laden macrophages
➢ Chronic inflammation
➢ Focal calcification
Summary
• Mesenteric cysts
• Solid mesenteric masses
Summary: Mesothelioma
• Diffuse malignant mesothelioma
➢ Asbestos
➢ Nodules, masses
➢ Bowel encasement
➢ Bowel fixation
• Cystic malignant mesothelioma
➢ Variant of DMM
➢ Cystic masses
➢ Ascites
References
Lymphangioma
1. Kempson RL, Fletcher CDM, Evans HL, Hendrickson MR, Sibley RK. Tumors of the soft tissues: atlas of tumor
pathology, third series, fascicle 30. Washington, DC: Armed Forces Institute of Pathology; 2001
2. Levy AD, Cantisani V, Miettinen M. Abdominal Lymphangiomas: Imaging Features with Pathologic Correlation.
AJR 2004. 182: 1485-1491
3. Ros PR, Olmsted WW, Moser RP, Jr., Dachman AH, Hjermstad BH, Sobin LH. Mesenteric and omental cysts:
histologic classification with imaging correlation. Radiology 1987;164:327-332
Mesenteric Fibromatosis
1. Burke AP, Sobin LH, Shekitka KM, Federspiel BH, Helwig EB. Intra-abdominal fibromatosis. A pathologic analysis
of 130 tumors with comparison of clinical subgroups. Am J Surg Pathol 1990; 14(4):335-341.
2. Levy AD, Rimola J, Mehrotra AK, Sobin LH. Benign Fibrous Tumors and Tumor-like Lesions of the Mesentery:
Radiologic Pathologic Correlation. RadioGraphics 2006; 26: 245- 264
3. Magid D, Fishman EK, Jones B, Hoover HC, Feinstein R, Siegelman SS. Desmoid tumors in Gardner syndrome: use
of computed tomography. AJR Am J Roentgenol 1984; 142(6):1141-1145.
Sclerosing Mesenteritis
1. Emory TS, Monihan JM, Carr NJ, Sobin LH. Sclerosing mesenteritis, mesenteric panniculitis and mesenteric
lipodystrophy: a single entity? Am J Surg Pathol 1997; 21(4):392-398.
2. Sabate JM, Torrubia S, Maideu J, Franquet T, Monill JM, Perez C. Sclerosing mesenteritis: imaging findings in 17
patients. AJR Am J Roentgenol 1999; 172(3):625-629.
3. Valls C. Fat-ring sign in sclerosing mesenteritis. AJR Am J Roentgenol 2000; 174(1):259-260.
Ulcerative Colitis
Differential CT Features
• CT features suggesting UC over Crohn disease
➢ Mural stratification, 61% UC vs. 8% Crohn
➢ Mural thickness less in UC compared to Crohn
➢ Outer colonic contour, smooth in UC and irregular in Crohn
Gore RM et al. AJR 1996: 167:3-15
Crohn Disease
Early Imaging Features
• Distribution
➢ Asymmetric
➢ Segmental
➢ Skip lesions
• Lymphoid hyperplasia
Ulcerative colitis with toxic
• Ulceration
megacolon
➢ Aphthous ulcerations
➢ Linear ulcers
➢ Deep ulcerations (fissuring)
• Cobblestoning
• Mural thickening
• Inflammatory pseudopolyps
Crohn Disease
• Rose thorn ulcers
Figure 2-13-7
Crohn Disease
• Mesenteric hyperemia
• Target sign
➢ Acute inflammation
Crohn Disease
• Linear ulceration
• Mural thickening
• Inflammatory polyps
Figure 2-13-10
Crohn Disease
• Complications
➢ Sinus tracts
➢ Fistula
➢ Abscess
➢ Carcinoma
Crohn Disease
Intramural Fistula
Crohn Disease
Fistulae [Figure 2-13-12]
Chronic Crohn disease with structuring and sacculations
Crohn Disease: Abscess
[Figure 2-13-13]
• Secondary to deep penetrating ulcers
Figure 2-13-12
➢ Sinus tracts
➢ Fistulas
➢ Perforation
• 15% to 20% of patients
• Most frequently associated with small bowel or ileocolic disease
Figure 2-13-13
Neoplasia in IBD
• Adenocarcinoma
➢ Ulcerative colitis, highest incidence
➢ Crohn disease, small and large intestine
• Lymphoma
➢ Increased incidence in Crohn disease
• Features of carcinoma in IBD
➢ Typically do not arise in pre-existing adenomas
➢ Arise in flat mucosa
➢ Carcinomas may be long and flat
➢ May arise in bypassed segments of bowel
Gore RM, Laufer I, Berlin, JW. Ulcerative and granulomatous colitis: idiopathic
inflammatory bowel disease. In: Gore RM, Levine MS (eds), Textbook of
Gastrointestinal Radiology. 2nd ed.
Sarrazin J, Wilson SR. Manifestations of crohn disease at US. RadioGraphics
1996. 16: 499-520.
Summary
• UC vs. Crohn
➢ Similar demographics
➢ UC, contiguous colonic disease
➢ Crohn, entire GI tract with skip areas
➢ UC, mucosal and submucosal disease
➢ Crohn, transmural disease with extension into the mesentery
Objectives
• General approach
• Differential diagnosis of idiopathic IBD
➢ Pseudomembranous colitis
➢ Neutropenic colitis (typhlitis)
➢ Ischemic colitis
➢ Diverticulitis
➢ Infectious colitis
General Approach
• Disease location
➢ Small vs. large bowel
➢ Focal vs. multifocal vs. diffuse
➢ Ascites
• Degree and pattern of mural thickening
➢ How much mural thickening?
➢ Mural enhancement?
➢ Fat attenuation in the submucosa?
• Associated mesenteric disease
➢ Inflammation
➢ Phelgmon/abscess
➢ Mesenteric fat proliferation
• Clinical history
Pseudomembranous Colitis
• Features suggesting PMC
➢ Diffuse colonic involvement
➢ Marked low attenuation mural thickening
➢ Accordion sign
➢ Ascites
Pseudomembranous Colitis
• Onset following antibiotic therapy
➢ Clostridium difficile toxin
• Clinical features
➢ Symptoms within days or weeks following antibiotic therapy
➢ Copious watery diarrhea
➢ Abdominal pain
➢ Fever
➢ Leukocytosis
Pseudomembranous Colitis
• Epithelial necrosis Pseudomembranous colitis
• Inflammatory infiltrate
• Crypt eruption
• Pseudomembranes Figure 2-14-2
Pseudomembranous Colitis:
Thumbprinting = Mural Thickening
Pseudomembranous Colitis:
Low Attenuation Wall with Accordion Sign
Ischemic Colitis
• Most common in elderly
➢ Underlying atherosclerosis, diabetes, hypertension
➢ Low flow states
➢ Occlusive disease
➢ Complicates infectious colitis, especially CMV
• Ischemic Injury
➢ Acute, fulminant
✧ Transmural necrosis and perforation
➢ Transient, reversible
✧ Confined to mucosa and submucosa
➢ Chronic
✧ Submucosal fibrosis
• Locations
➢ Diffuse
➢ SMA and IMA watershed vunerable
Neutropenic colitis
✧ Normal communication through Arc of Riolan (marginal
artery of Drummond)
✧ Absent in 5% Figure 2-14-4
✧ Splenic flexure and rectosigmoid
Ischemic Colitis
• Denuded mucosa
• Pseudomembranes, Hemorrhage
Ischemic colitis
Ischemic Enteritis
• Segmental
• Diffuse
• Segmental, necrotic, ulcerated mucosa
• Mural thickening
➢ Stack of coins
• Thick wall, engorged mesentery
➢ Target sign [Figure 2-14-6]
• Thin wall, infiltrated mesentery
➢ Infiltrated mesentery [Figure 2-14-7]
• Mucosal cast, intramural fistula
• Mucosal ulceration, pneumatosis
• Pneumatosis, mesenteric venous gas
Figure 2-14-7
Ischemic enteritis due to SMV
thrombosis
Figure 2-14-8
. Ischemic enteritis
Diverticular Disease
• Most common disease of the
colon
• Diverticulosis increases with age
➢ 33% to 50% of people over
50
➢ 50% of people over 80
Acute diverticulitis
Diverticular Disease
Etiology of Pulsion Diverticula
• Pressure gradient
➢ Between lumen and serosa
➢ Compartmentalized by haustra
➢ Highest in sigmoid
• Weakness in bowel wall
➢ Intramural vasa recta penetrate wall
➢ Between taenia mesocolica and taenia libera
➢ Between taenia mesocolica and taenia omentalis
Diverticulitis
• Most common complication
➢ 10% to 20% of patients with diverticulosis
• Pathogenesis
➢ Stagnation of fecal material
➢ Inflammatory erosion of the mucosa
➢ Perforation
✧ Intramural abscess
✧ Extramural abscess
Diverticulitis: Complications
• Hemorrhage 25%
• Muscular hypertrophy and obstruction 25%
• Pericolic abscess 20%
• Free perforation 18% Acute diverticulitis with intramural
➢ Debilitated patients fistula and pneumatosis
➢ Corticosteroid therapy
• Vesicocolic fistula 8%
• Small bowel obstruction
• Pyelophlebitis and liver abscess
Diverticulitis: Perforation
Differential Diagnosis
• Colon carcinoma
• Colitis
➢ Infectious
➢ Ischemic
➢ Crohn disease
• Foreign body perforation
• Epiploic appendagitis
Diverticulitis: CT Pitfalls
• Differential diagnosis of colon cancer
➢ Problematic in 10% of cases
➢ If immediate surgery not performed: mucosal evaluation
(endoscopy or BE) to exclude cancer
Diverticular Hemorrhage
• Most common cause of adult rectal bleeding
• Site of hemorrhage
➢ Single diverticulum Giant sigmoid diverticulum
➢ Right side of colon in 2/3 of cases
• Rupture of the vasa recta
Diverticular Hemorrhage
• Clinical features
➢ Elderly patients
➢ Sudden onset
➢ Stops spontaneously in 80%
➢ Rebleeding in 25%
Cecal Diverticulitis
• Congenital or acquired diverticula
➢ Congenital are true diverticula
➢ Acquired are most common
• CT features
➢ Pericolonic inflammation
➢ Mural thickening
➢ Demonstration of diverticula
➢ Intramural or pericolonic abscess
➢ Normal appendix
Summary
• General approach
➢ Location of disease
➢ Degree of mural thickening
➢ Ascites
➢ Mesenteric disease
➢ Clinical history
Summary - Diverticulitis
• Focal disease
• Diverticula
➢ Air filled
➢ Hyperdense
• Adjacent inflammation
Summary
• Infectious colitis
➢ Clinical history
• Right-sided colitis
➢ Campylobacter, yersinia, salmonella
➢ TB
➢ Amebiasis
• Diffuse colitis
➢ PMC
➢ E. Coli
➢ Shigella, campylobacter, salmonella
➢ Amebiasis
➢ CMV
Case 1: 45 year old man with chronic pancreatitis and acute onset
of lower abdominal pain, distension, and constipation
Cecal volvulus
Marked Cecal Dilatation
• Differential diagnosis
➢ Cecal volvulus
➢ Cecal bascule
➢ Pseudoobstruction (Ogilvie
syndrome)
Cecal Volvulus
• Volvulus is an axial twist of at
least 90 degrees
➢ Abnormal fixation to posterior
parietal peritoneum
➢ Freely mobile cecum
• Mechanical obstruction
• Radiographic features
➢ Cecal dilatation
➢ Beak on contrast enema
➢ Whirl on CT
Cecal volvulus
Ogilvie Syndrome
• Colonic pseudo-obstruction
• Marked cecal dilatation
Sigmoid Volvulus
Cecal bascule
Sigmoid volvulus
“Leaping Dolphin”
Cupola Sign
Case 4: 67 year old man with severe chest pain after vomiting
Boerhaave’s Syndrome
• Dr. Hermann Boerhaave
• Emetogenic rupture
➢ Distal esophagus or
➢ Gastric cardia
• Left posterolateral region
➢ 1.5 - 4 cm tear
➢ Reduced muscle fibers
➢ Entrance of nerves, vessels
• Radiographic features
➢ Mediastinal gas
➢ LLL infiltrate, atelectasis
➢ Left effusion
Boerhaave syndrome
Foramen of Winslow
Gastric Volvulus
• Classic Clinical presentation
➢ Severe epigastric pain
➢ Violent retching with production of little vomitus
➢ Inability to pass NG tube into stomach
• Outcomes
➢ Recurrent
➢ Resolve spontaneously
➢ Resolve with NG placement
➢ Complete obstruction
Organoaxial Volvulus
Mesenteroaxial Volvulus
Gastric Bezoar
• Accumulated ingested material
• Trichobezoar
➢ Hair
• Phytobezoar
➢ Vegetable matter
• Pathophysiology
➢ Altered gastric motility
➢ Altered gastric anatomy Gastric Bezoar
➢ Trichotillomania
Imaging findings
• Thick gastric folds
• Thick duodenal wall
• Liver metastasis
• Large, enhancing pancreatic mass
• Positive pentetreotide scan
Zollinger-Ellison Syndrome
• Radiologic features
➢ Multiple ulcers
➢ Increased gastric secretions
➢ Thick gastric folds
• Preoperative localization of gastrinoma
➢ CT
➢ MR
➢ Somatostatin receptor scintigraphy
Menetrier Disease
18 days 22 days
Normal Anatomy
• Minor Papilla
➢ Accessory PD
➢ Duct of Santorini
• Major Papilla
➢ Main PD
➢ Duct of Wirsung
5 weeks 5 weeks
Annular Pancreas
• Bilobed ventral pancreatic bud
• Buds migrate in opposite directions
• Duodenal obstruction
Annular pancreas
Pancreatic Divisum
• Incomplete fusion of dorsal and ventral pancreas
• Body and tail drain through the duct of Santorini, minor
papilla
• Incidence
➢ 4 to 11% (autopsy)
➢ 3 to 4% (ERCP)
• Most asymptomatic
• 12-24% develop idiopathic recurrent pancreatitis
Chronic Pancreatitis
Chronic Pancreatitis
IPMN: Imaging
• Duct dilatation
➢ Focal or diffuse
➢ Main duct or side branch
• Intraductal masses
• Bulging duodenal papilla
• Glandular atrophy
Bulging Papilla
Mediastinal Pseudocyst
Differential Diagnosis:
Complex Hepatic Cyst
• Nonneoplastic
➢ Echinococcal cyst
➢ Simple cyst with
hemorrhage/infection Biliary cystadenoma
➢ Post-traumatic cyst
➢ Abscess
➢ Ciliated hepatic foregut cyst
• Neoplastic
➢ Biliary cystadenoma
➢ Biliary cystadenocarcinoma
➢ Cystic metastasis
➢ Peliosis
➢ Teratoma
Biliary Cystadenoma
Simple Cyst
Echinococcus granulosus
Fibrolamellar Carcinoma
Hemangioma
Hemangioma: Tagged RBC Scan
Intrahepatic cholangiocarcinoma
Differential Diagnosis:
Rim-like Enhancement
• Hemangioma
• Metastatic disease
• Hepatocellular carcinoma
• Intrahepatic cholangiocarcinoma
• Angiosarcoma
• Epithelioid hemangioendothelioma
Intrahepatic Cholangiocarcinoma
Hemangioma
Epithelioid Hemangioendothelioma
Hepatocellular carcinoma
Hepatocellular Carcinoma
Angiomyolipoma
Myelolipoma
Hepatic Teratoma
Fibrolamellar carcinoma
Fibrolamellar Carcinoma
Echinococcus multilocularis
Cases 1-5
• All patients have the same disease
• The underlying disease is a congenital anomaly
• Each presents with a different manifestation Omphalomesenteric
(Vitelline) Duct Anomalies
Meckel Diverticulum
• Most common anomaly of the GI tract
• 2% - 3% of the population
• M=F
• Symptoms more common in males
• 60% of patients present before age 10
• Omphalomesenteric duct anomaly
➢ Improper closure and absorption
Differential Diagnosis
• Inflammatory bowel disease
• Urachal remnant
• Colonic Diverticulitis
• Meckel diverticulitis
• Idiopathic ileal diverticula
Meckel Diverticulitis
Differential Diagnosis
• Neoplasm
• Ulcer
• Vascular ectasia
• Meckel diverticulum
Differential Diagnosis
• Lipoma
• Inverted Meckel diverticula
Inflamed Meckel
with Small Bowel Obstruction
Imaging Features
• Reversal of SMA and SMV
• Swirling vessels about SMA
• Absent colon right side of
abdomen
• Inflammatory process in LLQ
➢ Inflamed tubular structure
➢ Mesenteric inflammation
Differential Diagnosis
• Malrotation
• Inflammation
➢ Diverticulitis
➢ Meckel diverticulum
➢ Inflammatory bowel disease
➢ Appendicitis
Appendiceal Neoplasms
• Uncommon
➢ <0.4% of intestinal tumors
• Histologic subtypes
➢ Carcinoid
➢ Mucinous cystadenoma/cystadenocarcinoma
➢ Adencarcinoma
➢ Non-mucin producing adenocarcinoma
Appendiceal Carcinoid
• Most common location for GI tract carcinoid
➢ 45% of gastrointestinal carcinoids
• Most common appendiceal tumor
➢ 50% to 85% of appendiceal tumors
• Majority benign clinical course
➢ 70% to 90% discovered incidentally
➢ >95% of appendiceal carcinoids have benign biologic behavior
Mucinous Cystadenoma/Cystadenocarcinoma
• Mucin producing epithelial neoplasm
➢ M=F
➢ 27 to 77 years of age
• Presentation
➢ Right lower quadrant pain, nausea, vomiting, abdominal swelling
• Complications
➢ Bowel obstruction, torsion, perforation, intussusception,
appendicitis
• 20% with a synchronous colonic adenocarcinoma
Mucinous Cystadenoma/Cystadenocarcinoma
• Radiologic Findings
➢ RLQ mass on plain film
➢ Rim-like calcification
➢ Mass effect medial cecal wall
➢ Nonfilled appendix on BE
• Cross-sectional imaging
➢ Fluid-filled, complex mass on CT or US
➢ Mass bulges into cecal lumen
➢ Short T1 and long T2 signal on MR
➢ May be the lead point for intussusception
Mucinous Cystadenoma
Epiploic appendagitis
Epiploic Appendagitis
• Appendix epiploica
➢ Torsion
➢ Infarction
➢ Ischemia
• Clinical course
➢ Self limited
➢ Spontaneous resolution
Epiploic Appendagitis
Mesenteric adenitis
Mesenteric Adenitis
• Inflammation of ileocecal nodes
➢ Coexistent inflammation of the TI and cecum may be present
• Children, young adults
• Self limited
• Diagnosis of exclusion
Cecal Adenocarcinoma
Acute Appendicitis: Pathogenesis
• Luminal obstruction followed by infection
➢ Stones
➢ Food, mucus, adhesions
➢ Mucosal edema, lymphoid hyperplasia
➢ Parasites
➢ Tumors
➢ Endometriosis
Cecal Adenocarcinoma
• Mural thickening
➢ Eccentric or asymmetric
• Intraluminal mass
➢ Often near appendiceal orifice if patient presents with appendicitis
• Pericolic lymph nodes
• Peritoneal implants, distant mets
Omental Infarction
Omental Infarction
• Omental torsion
➢ Most commonly site free edge of the right lateral omentum
• CT features
➢ Focal inflammation of omental fat
➢ Normal appendix, colon, terminal ileum
➢ Fatty mass with concentric or swirling lines
Gastrointestinal Radiology 431 Seminar 6: Beyond Appendicitis
Gastrointestinal Seminar 7:
Tumors and Tumor-like Lesions of the
Gallbladder
Angela D. Levy, LTC (P), MC, USA
Adenomyomatous hyperplasia
Sonographic Findings
• Gallbladder wall thickening
• Reverberation artifact
Seminar 7: Tumors and Tumor-like Lesions of the Gallbladder 432 Gastrointestinal Radiology
Differential Diagnosis:
Reverberation (“comet-tail”) Artifact
• Gas in gallbladder wall
• Adenomyomatous hyperplasia
Coronal T2 MR Findings
• Gallbladder wall thickening
• “String of pearls”
Adenomyomatous Hyperplasia
• Gallbladder wall thickening
• “String of pearls”
Adenomyomatous Hyperplasia
• Common
➢ 9% cholecystectomy specimens
➢ More common in women than men
• Gallstones frequently present
• Three variants
➢ Diffuse
➢ Segmental
➢ Localized (fundic adenomyoma)
Gastrointestinal Radiology 433 Seminar 7: Tumors and Tumor-like Lesions of the Gallbladder
Case 2: 47-year-old man complains of fever and right lower
quadrant pain
Xanthogranulomatous cholecystitis
CT Findings
• Gallstone
• Gallbladder wall thickening
• Hypodense nodules in gallbladder wall
• Ill-defined hepatic margin
• Inflammatory change
Differential Diagnosis
• Cholecystitis
➢ Acute
➢ Chronic
➢ Xanthogranulomatous
• Neoplasm
Xanthogranulomatous Cholecystitis
• Aggressive inflammatory process
• Pathophysiology
➢ Intermittent cystic duct obstruction
➢ Bile enters gallbladder wall
• Clinical presentation
➢ RUQ pain, fever, tenderness
• Surgical treatment
➢ Reported association with gallbladder carcinoma
➢ Difficult to preoperative distinguish from carcinoma
➢ Involvement of adjacent organs
Seminar 7: Tumors and Tumor-like Lesions of the Gallbladder 434 Gastrointestinal Radiology
Case 3: 75-year-old woman with RUQ pain and weight loss
MR Findings
• Intraluminal gallbladder mass
• Hepatoduodenal ligament mass
Differential Diagnosis
• Gallbladder carcinoma
• Bile duct carcinoma
• Metastatic disease
Gallbladder Carcinoma
• Sixth most common GI tract malignancy
➢ Worldwide: stomach, colorectal,
liver, esophagus, pancreas,
gallbladder
➢ US: colorectal, pancreas, stomach,
liver, esophagus, gallbladder
• More common in women (3:1)
➢ Mean age 72 years
Gallbladder Carcinoma:
Pathology
• Epithelial malignancies (98%)
➢ Adenocarcinoma (90%), squamous
cell, adenosquamous, small cell
carcinoma
• Other (2%)
➢ Sarcomas, lymphomas, carcinoid,
metastases
Gallbladder adenocarcinoma
Gallbladder Carcinoma
• Imaging patterns
➢ Intraluminal polypoid mass (15% to 25%)
➢ Focal or diffuse wall thickening (20% to 30%)
➢ Mass replacing the gallbladder (40% to 65%)
Gastrointestinal Radiology 435 Seminar 7: Tumors and Tumor-like Lesions of the Gallbladder
Case 4: 30-year-old man with RUQ pain
Metastatic melanoma
Metastatic Melanoma
Seminar 7: Tumors and Tumor-like Lesions of the Gallbladder 436 Gastrointestinal Radiology
Case 5: 35-year-old woman with RUQ pain
Cholesterol polyp
Sonographic Findings
• Small, nonshadowing echogenic mass
• Adherent to gallbladder wall
Cholesterol Polyp
• Common
➢ 50% of polypoid lesions in the gallbladder
• More common in women
➢ 3:1
Cholesterol Polyp
• Lipid laden macrophages
• Normal gallbladder epithelium
Summary
• Look for features to suggest a specific process tumor-like process
➢ Ring-down artifact, pearl necklace sign for adenomyomatous hyperplasia
➢ Focal mural nodules for XGC in the right clinical setting
• Look for features to suggest a malignancy
➢ Gallbladder wall thickening in association with a polypoid mass
➢ Abnormal gallbladder/liver interface
➢ Abnormal liver parenchyma
➢ Hepatoduodenal ligament mass or adenopathy
Gastrointestinal Radiology 437 Seminar 7: Tumors and Tumor-like Lesions of the Gallbladder
Cholelithiasis and Cholecystitis
Robert K. Zeman, MD
Outline/Objectives
• Detection of cholelithiasis
• Gravel versus sludge
• Acute cholecystitis
• Complications of acute cholecystitis
➢ Gangrenous cholecystitis
➢ Emphysematous cholecystitis
➢ Empyema of the gallbladder
➢ Gallbladder perforation
➢ Choledocholithiasis
Premise
• The radiologist plays a central role in identifying the cause of the patient’s
symptoms and…
• Detecting complications of cholecystitis (inflammatory and neoplastic) that will
dictate the therapeutic approach
Cholelithiasis
• 30 million American adults harbor stones
• Should “silent” stones be treated?
• 22% of patients with stones are symptomatic (Sirmione study)
• In symptomatic patients, 50% chance of colic in 1 year; 1–2% cumulative risk
of acute cholecystitis.
Cholelithiasis
• For symptomatic stones, recommend elective laparoscopic cholecystectomy
• For acute cholecystitis:
➢ Delayed surgery allows for better vizualization of surgical field
➢ Early surgery means less adhesions
Solitary Gallstone
Gravel
Acute Cholecystitis
• Uncomplicated vs complicated
• Treatment options if complications
• (do imaging findings influence
operative approach?)
• Cholescintigraphy vs US
Cholescintigraphy In AC
• The only reliable indicator of acute cholecystitis is non-visualization
of the gallbladder – remember the lateral
• High sensitivity, moderate specificity
Intramural Sonolucency
• Described in 11 patients as first specific sign for acute cholecystitis*
• “Consists of a hypo-reflective or sonolucent band, continuous or interrupted,
within the hyper-reflective gallbladder wall” Figure 2-22-5
• Focal lucency or concentric rings (striate)
most suggestive of inflammation**
*Marchal et al, Radiology 133:429, 1979
**Cohen et al, Radiology 164:31, 1987
Acute Cholecystitis-Striate GB
Walls [Figure 2-22-5]
Gangrenous Cholecystitis
• Not always Clostridal infection
• Implies severe inflammation
• Sonography-may see desquamated
mucosa/membranes
• Scintigraphy-increased pericholecystic
activity* due to:
➢ delayed excretion from perihepatitis Two different patients show a band of tracer where the liver
➢ hyperemia with increased tracer abuts the inflamed gallbladder (arrow)
delivery
*Smith et al, Radiology 156:197, 1985
Gangrenous Cholecystitis
• Sloughed membranes
Emphysematous Cholecystitis
• Elderly patients, 20–30% are diabetic
• Male predominance
• 1/3 infected with Clostridia welchii
• Perforation 5 times as common as for non-emphysematous cholecystitis
• “Dirty” shadowing and echogenic GB wall on sonography is suggestive
• Don’t forget plain film – differential diagnosis of RUQ air
Figure 2-22-8
Emphysematous Cholecystitis
• US-echogenic foci=gas
• KUB
Emphysematous Cholecystitis
[Figure 2-22-8]
• US-ring-down
• KUB
Emphysematous Cholecystitis-CT
• Gas confined to GB wall Figure 2-22-9
• Gas in lumen, hepatic ducts
GB Perforation
Figure 2-22-10
Choledocholithiasis
• May occur as primary duct stone (usually pigment),
secondary to gallstones, or following
cholecystectomy
• Most small stones will pass spontaneously. The duct
caliber and dynamics may rapidly change
• CT and US are approx. 70-80% sensitive for
detection of choledocholithiasis
• If you suspect CBD stones…options are MRCP,
ERCP, intraop cholangiogram
MRCP
• T2 wt TSE or FSE, thin sections or “slab”
• Extra sections as needed
References
1. Zeman RK, Garra BS. Gallbladder Imaging: The State-of-the-art. Gastroent Clin N. Am 2:127, 1991.
2. Garra BS, Davros WJ, Lack EE, Horii SC, Zeman RK: Visibility of gallstone fragments at ultrasound and
fluoroscopy. Implications for monitoring of gallstone lithotripsy. Radiology 174:343, 1990.
3. Mathieson JR, So CB, Malone DE, Becker CD, Burhenne HJ: Accuracy of sonography for determining the number
and size of gallbladder stones before and after lithotripsy. AJR 153:977, 1989.
4. duPlessis DJ, Jersky J. Management of acute cholecystitis. Surg Clin North Am 53:1071, 1973.
5. Halasz NA. Counterfeit cholecystitis: A common diagnostic dilemma. Am J Surg 130:189, 1975.
6. Zeman RK, Burrell MI, Cahow CE, Caride V. Diagnostic utility of cholescintigraphy and ultrasonography in acute
cholecystitis. Am J Surg 141:446, 1981.
7. Weissmann HS, Badia J, Sugarman LA et al. Spectrum of 99m Tc-IDA cholescintigraphic patterns in acute
cholecystitis. Radiology 138:167, 1981.
8. Eikman EA, Cameron JL, Colman M et al. A test for patency of the cystic duct in acute cholecystitis. Ann Int Med
82:318, 1975.
9. Fonseca C, Greenberg D, Rosenthall L et al. Assessment of the utility of gallbladder imaging with 99m Tc-IDA.
Clin Nucl Med 3:437, 1978.
10. Freitas JE. Cholescintigraphy in acute and chronic cholecystitis. Semin Nucl Med 12:18, 1982.
11. Shuman WP, Gibbs P, Rudd TG et al. PIDIDA scintigraphy for cholecystitis: False positives in alcoholism and total
parenteral nutrition. AJR 138:1, 1982.
12. Kalff V, Froelich JW, Lloyd R et al. Predictive value of an abnormal hepatobiliary scan in patients with severe
intercurrent illness. Radiology 146:191, 1983.
13. Laing FE, Federle MP, Jeffrey RB et al. Ultrasonic evaluation of patients with acute right upper quadrant pain.
Radiology 140:449, 1981.
14. Ralls PW, Colletti PM, Lapin SA et al. Real-time sonography in suspected acute cholecystitis: Prospective
evaluation of primary and secondary signs. Radiology 155:767, 1985.
15. Cohan RH, Mahony BS, Bowie JD, Cooper C, Baker ME, Illescas FF: Striated intramural gallbladder lucencies on
US studies. Predictors of acute cholecystitis. Radiology 164:31–35, 1987.
16. Teefey SA, Baron RL, Bigler SA: Sonography of the gallbladder. Significance of striated (layered) thickening of
the gallbladder wall. AJR 156:945, 1991.
17. Shaler WJ, Leopold GR, Scheible FW: Sonography of the thickened gallbladder wall. A nonspecific finding. AJR
136:337, 1981.
18. West MS, Garra BS, Horii SC, Zeman RK et al. Gallbladder varices: Imaging findings in patients with portal
hypertension. Radiology 179:179, 1991.
19. Weissmann HS, Berkowitz D, Fox MS et al. The role of technetium-99m iminodiacetic acid (IDA)
cholescintigraphy in acute acalculous cholecystitis. Radiology 146:177, 1983.
20. Shuman WP, Rogers JV, Rudd TG et al. Low sensitivity of sonography and cholescintigraphy in acalculous
cholecystitis. Radiology 142:531, 1984.
21. Swayne LC. Acute calculous cholecystitis: Sensitivity in detection using technetium-99m iminodiacetic acid
cholescintigraphy. Radiology 160:33, 1986.
22. Mirvis SE, Vainright JR, Nelson AW, et al. The diagnosis of acute acalculous cholecystitis: A comparison of
sonography, scintigraphy, and CT. AJR 147:171, 1986.
23. Jeffrey RB, Laing FC, Wong W, Callen PW. Gangrenous cholecystitis: Diagnosis by ultrasound. Radiology
156:797, 1985.
24. Wales LR. Desquamated gallbladder mucosa: Unusual sign of cholecystitis. AJR 139:810, 1982.
25. Smith R, Rosen J, Gallo LN, Alderson PO. Pericholecystic hepatic activity in cholescintigraphy. Radiology
156:797, 1985.
26. Siskind B, Hawkins M, Cinti D, Zeman RK, Burrell MI. Perforation of the gallbladder: Radiologic-pathologic
correlation. J Clin Gastroenterol 9:670–78, 1987.
27. Clemett AR, Lowman RM. The roentgen features of the Mirizzi syndrome. AJR 94:480, 1965.
28. Weltman D, Zeman RK. Imaging of acute diseases of the gallbladder and bile ducts. Radiological Clinics of North
America 32:933-950, 1994.
29. Fulcher AS, Turner MA, Capps GW. Technical Advances and Clinical Applications. RAdiographics 19:25-41,
1999.
Reflux Esophagitis
• Most common inflam condition
• Purpose of Ba study not simply to show HH/GER but to R/O morphologic
sequelae of GERD
Pathogenesis
• Frequency of GER
➢ Decreased LES tone
➢ Mult trans LES relaxations
• Duration of GER
➢ Abnormal motility
➢ (scleroderma)
Pathogenesis
• Acidity of refluxate
➢ ZES (increased acid)
➢ Billroth II (bile or panc)
• Resistance of mucosa
➢ Age
➢ Debilitation
Clinical Findings
• Heartburn and regurg Reflux esophagitis with
• Epigastric or RUQ pain granular mucosa
• Upper GI bleeding
• Dysphagia (peptic stx)
Figure 2-23-2
Hiatal Hernia and GER
• Occur independently
• Spont GER at fluoro:
➢ 30–60% in esophagitis
➢ 40–50% in volunteers
Schatzki Ring
• Variant of peptic stx
• Episodic dysphagia (meat)
➢ (Steakhouse syndrome)
• Symm ringlike constriction
• Vertical height 2–4 mm
• Usually sx if < 13 mm diam
• Best seen on prone views
Barrett’s Esophagus
• Prog columnar metaplasia from GER and esophagitis
• Prevalence:
➢ 10% with esophagitis
➢ 40% with peptic stx
Clinical Findings
• Men > Women, W > B
• Reflux sx, dysphagia
• 40% asymptomatic
• Tx of GER may not cause Barrett’s to regress
Histologic Findings
• Projections or islands of columnar epith separated by squam epith
• Foveolar epith > 3 cm above LES or intestinal metaplasia with goblet cells
Figure 2-23-3
Premalignant Condition
• Risk of adenocarcinoma
• Dysplasia-Ca sequence
• Endoscopic surveillance
Classification of Risk
• High: High stx or ulcer or reticular pattern
• Mod: Distal stx or reflux esophagitis
• Low: None of above
Radiologic vs Endoscopic Dx
Risk Endo
• High 10 9 (90%)
• Moderate 73 12 (16%)
• Low 117 1 (1%)
Barrett esophagus
Radiologic Diagnosis with mid esophageal stricture
• Less sensitive than endoscopy
and reticular pattern
• Most false negative exams in mild disease
• Vast majority do not have Barrett’s esophagus
Figure 2-23-4
Candida Esophagitis
• Most common type
• Immunocompromised (75%)
• Local esophageal stasis (25%)
➢ (achalasia, scleroderma)
Clinical Findings
• Dysphagia/odynophagia
• OP Candidiasis (50%)
• Marked clinical response to antifungal agents (ketoconazole)
Candida esophagitis
Radiographic Findings [Figures 2-23-4 and 2-23-5] with plaques
• Mucosal Plaques (90%)
➢ Linear Figure 2-23-5
➢ Etched in white
• “Shaggy” esophagus (AIDS)
➢ Plaques and membranes
➢ Superimposed ulcers
Herpes Esophagitis
• 2nd most common type
• Herpes simplex virus type 1
• Immunocompromised
• Viral Cx or Bx (intranuclear inclusions in cells adjacent to ulcers)
Clinical Findings
• Dysphagia/odynophagia
• Oropharyngeal herpes
• Marked clinical response to antiviral agents (acyclovir)
Herpes esophagitis
with tiny ulcers
HIV Esophagitis
• Odynophagia and giant ulcers
• Palatal ulcers
• Maculopapular rash
• Recent seroconversion
• Dx of exclusion (No CMV)
• Treatment with steroids
Radiation Esophagitis
• 2–5000 rad: self-limited esophagitis (1 – 2 weeks)
• 5000 or more rad: stx, progressive dysphagia (4–8 months)
• Adriamycin potentiates XRT (only 500 rad)
Radiographic Findings
• Acute
➢ Ulceration
➢ Granular mucosa
➢ Decreased distensibility Tetracycline-induced
• Chronic esophagitis with three ulcers
➢ Abnormal motility
➢ Strictures
Caustic Esophagitis
• Strong acids or alkali (liquid lye)
• Three phases of injury: Figure 2-23-10
➢ Acute necrosis
➢ Ulceration and granulation
➢ Cicatrization
• Chest pain, odynophagia, hematemesis,
shock
Esophageal Intramural
Pseudodiverticulosis
• Dilated excretory ducts
• Ductal obstruction
• Candida, diabetes, alcohol
• High strictures classic
• Peptic stx more common
Radiographic Findings
[Figures 2-23-10 and 2-23-11]
• Flask-shaped outpouchings
• “Floating” outside wall
• Associated strictures
Diffuse esophageal Localized esophageal
➢ (especially peptic stx)
intramural intramural
pseudodiverticulosis with pseudodiverticulosis with
high stricture peptic stricture
Location Cause
• Uphill Distal Portal HTN
• Downhill Mid SVC obst
Diffuse Nodules/Plaques
Cause Finding
• Reflux Granularity
• Candida Plaques
• Glycogenic acanthosis Nodules/plaques
Localized Nodules/Plaques
Cause Finding
• Candida Plaques
• Sup spr Ca Coalesce nodules
• Barrett’s Reticular pattern
Ulcers
Cause Finding
• Reflux Distal
• Herpes Small, mid
• Drugs Small, mid
• CMV Giant
• HIV Giant
Thickened Folds
• Esophagitis
• Varices
• Varicoid Ca
High Strictures
• Barrett’s esophagus
• Mediastinal irradiation
• Caustic ingestion
• Primary or metastatic tumor
Distal Strictures
• Peptic stricture
• Lower esoph ring
• Barrett’s Ca
Mucosal Lesions
• Squamous papilloma
• Adenoma
• Glycogenic acanthosis
Clinical Findings
• Usually asymptomatic
• Malignant degeneration rare
• Multiple papillomas (papillomatosis)
Figure 2-24-1
Radiographic Findings
• Small, sessile polyp
• Lobulated mass
• Bubbly appearance
• Diff Dx – early Ca
Glycogenic Acanthosis
• Accum of cytoplasmic glycogen
• White nodules/plaques
• Rarely causes esophageal sx
• No risk of malignant degeneration
Intramural Lesions
• Fibrovascular polyp
• Leiomyoma
• Granular cell tumor
• Duplication cyst
• Idiopathic varix
Clinical Findings
• Most pts asx
• Dysphagia
• GI bleed rare
• Enucleation
Unusual Findings
• Annular lesion
• Giant intraluminal mass
• Gastric involvement
• Multiple lesions
• Leiomyomatosis
Leiomyomatosis
• Proliferation of smooth m.
• Children/adolescents
• Long-standing dysphagia
• Familial – autosomal dominant
• Alport’s syndrome (nephritis, deafness, ocular lesions)
Esophageal leiomyoma in
profile
Radiographic Findings
• Ba – tapered narrowing of distal esophagus (1° achalasia?)
• Length > achalasia
• Symmetric fundal defects Figure 2-24-3
• CT – thickened wall (2° achalasia?)
Pathologic Findings
• Arises in cervical esophagus
• Loose submucosal conn tiss
• Dragged inf by peristalsis
• Occas prolapses into fundus CXR with right superior mediastinal mass
• Pedicle in cervical esophagus caused by fibrovascular polyp
Duplication Cyst
• Abnl embryo development
• Sequest from prim foregut
• Ciliated columnar epith
• Most pts asymptomatic
• Occas bleeding/infection
Malignant Tumors
• Squamous cell carcinoma
• Adenocarcinoma
• Spindle cell carcinoma
• Small cell carcinoma
• Leiomyosarcoma
• Kaposi’s sarcoma
• Malignant melanoma
• Lymphoma
• Metastases
Predisposing Factors
• Achalasia
• Lye strictures
• Head and neck tumors
• Celiac disease
• Plummer-Vinson
• Tylosis
Definitions
• Early: mucosa or submucosa without lymph node mets
• Superficial: mucosa or submucosa with or without lymph node mets
• Small: < 3.5 cm regardless of depth of invasion or lymph node mets
Routes of Spread
• Direct extension – trachea, bronchi, lungs, pericard, aorta, diaphragms
• Lymphatic spread – nodes in med, neck, upper abdomen (paracardiac, lesser
curv, celiac)
• Hematogenous – lungs, adrenals, liver
Clinical Findings
• Dysphagia and wt loss
• Odynophagia (if ulcerated)
• Chest pain (poor sign)
• Paroxysmal coughing (if TEF)
• 5-year survival < 10%
Adenocarcinoma
• Arises in Barrett’s mucosa
• Dysplasia-Ca sequence (low-grade, high-grade, ca-in-situ, invasive)
• Comprises 20–50% of esoph Ca’s
• Predominantly in distal esophagus
• Often invades proximal stomach
Figure 2-28-9
• Prevalence 10% in Barrett’s esoph
• 30–40X greater risk than gen pop
• Dysphagia and weight loss
• Same prognosis as squamous Ca
• Endoscopic surveillance
Figure 2-28-8
Duodenitis
• Spastic bulb NSAID-induced erosive gastritis with
• Thickened folds linear erosions clustered in gastric
• Nodules body near greater curvature
• Erosions
Benign posterior wall gastric ulcer Anterior wall gastric ulcer seen as ring shadow on
double contrast view
Ulcer fills with barium on prone compression Giant NSAID greater curvature ulcer
Upper GI vs Endoscopy
• More than 95% GUs Dx in North America are benign
• 6–16% of benign-app GUs on S/C studies are
malignant
• Is endo always necessary?
Equivocal Ulcers
• Irregularity of ulcer shape
• Asymmetry of mass effect
• Nodularity, irregularity, or clubbing of radiating folds
• Enlarged areae gastricae
• Location on greater curve
Malignant lesser curvature ulcer with clubbed folds
abutting ulcer on prone compression
Radiologic Dx of Gastric Ulcers
Rad Dx No Pts Endo Final Dx
• Benign 191 164 All ben
• Equiv 69 63 56 ben / 7 malig
• Malig 72 68 2 ben / 66 malig
AJR 141:331–333, 1983
Upper GI vs Endoscopy
Cost
• D/C upper GI $218
• Endoscopy procedure $540
• Pathology $180
• Hospital $102
• Total $822
Ulcer Scar
• Central pit or depression
• Radiating folds
• Retraction of adjacent wall
Risk of Ulcers
Prevalence
Gastric ulcer 60-80%
Duodenal ulcer 95-100% Gastric MALT lymphoma with confluent nodules in
gastric body
Detection of H.Pylori
• Endoscopic bx
• Urea breath test
• Serum Ab test
Normal Pancreas
Acute Pancreatitis
• (Marseilles 1985)
• Sudden onset abdominal pain
• Increased pancreatic enzymes, blood, urine
• Pancreatic edema, fat and gland necrosis, hemorrhage
• Variable involvement of regional or remote tissues (Atlanta 1992)
Chronic Pancreatitis
• (Marseilles 1985)
• Recurrent or persistent abdominal pain
• +/- increased enzymes
• Irreversible morphologic change in pancreas
➢ Fibrosis
➢ Acinar destruction
➢ Calcification
• Diffuse, Focal
• Loss of function
Acute Pancreatitis: CT
• Best overall modality
• Global view
• Prognosis & followup
• Understand widespread nature of pancreatitis
• Routes for intervention Large, well-encapsulated pseudocyst
adjacent to pancreatic tail
Acute Pancreatitis: Terminology
Atlanta Symposium 1992
• Confusion of terms
• Acute pancreatitis
➢ Mild = minimal organ involvement, uncomplicated recovery w. supportive
Rx
➢ Severe = organ failure or complications eg. pseudocyst, necrosis, infected
necrosis, abscess
Figure 2-26-2
Acute Pancreatitis: Acute Fluid Collections
• Extravasated pancreatic fluid
• Anterior pararenal space, lesser sac
• Not loculated
• No capsule
• 40% patients w. acute pancreatitis
• 50% resolve spontaneously
• May develop into pseudocyst
Figure 2-26-3
• APACHE II
➢ Vitals signs
➢ PO2
➢ pH
➢ Electrolytes
➢ Creatinine
➢ HCT; WBC
➢ Glasgow coma score
Chronic Pancreatitis
• Definition (Marseilles 1985)
➢ Recurrent or persistent abdominal pain
➢ May or may not see increase enzymes
➢ Irreversible morphological change in pancreas
❖ Fibrosis
❖ Acinar destruction
❖ Calcification, duct /parenchyma
➢ Focal, segmental, diffuse
➢ Progressive loss of exocrine/endocrine function
Chronic Pancreatitis
• Who Gets It?
➢ Chronic alcohol abuse (60–70%)
➢ Idiopathic (30%) Balthazar Classification of severity of acute
➢ Biliary tract disease pancreatitis
➢ Hereditary (top). Mild Pancreatitis: CTSI = 0-1. Small amount
➢ Hyperlipidemia of peripancreatic stranding. No fluid collections.
➢ Hyperparathyroid Entire gland enhances.
➢ Pancreas divisum
• Clinical (bottom). Severe Pancreatitis: CTSI = 8-9.
➢ Recurrent abdominal pain (95%), Pancreas outlines are obliterated with necrosis.
➢ Pancreatic insufficiency , No enhancement with contrast
❖ Malabsorption,
❖ Diabetes,
➢ Amylase/Lipase levels +/– abnormal
Chronic Pancreatitis: CT
• Not as useful as in acute pancreatitis
• Gland enlargement (30%)
• Mass (30%) ? Cancer
• Atrophy (15%)
• Sens. 50-90%: Spec. 55-85%
• Acute + chronic w. exacerbation of disease
Pancreatic Pseudocyst
References
GI Bleeding: Demographics
• Older
• Male
• Use alcohol, tobacco
• Aspirin, non-steroidal anti-inflammatory
• Anticoagulants
Peura et al, Am.J.Gastro. 1997
GI Bleeding: Endoscopy
• First line procedure in UGI bleed
➢ 90–95% accurate Dx
➢ Useful for prognosis, treatment
• Performed immediately
➢ Alcoholics,
➢ Large volume loss
➢ Aorto-enteric fistula
• Performed more “electively”
➢ Young, no evidence of hypovolemia
Nuclear Scintigraphy
• Most sensitive non-invasive test
• Detects bleeding rates 0.1ml/min
• Two techniques
➢ Tc 99m sulfur colloid
➢ Tc 99m labeled red blood cells
• Used to
➢ Delineate obscure sources – small bowel, intermittent bleeding
➢ Enhance the efficacy of angiography
Gastritis
• Hemorrhage, erythema, erosions
• Erosion = superficial break in mucosa w. punctate bleeding, fibrin base
• Causes
➢ Non-steroidals -> antral erosions, ulcer
❖ bleeding usually not severe, resolve w. D/C
➢ Alcohol ingestion
❖ Direct toxin? ->erythema
Gastritis
• Portal hypertension
➢ Diffuse or patchy erythema, punctate bleeding, vascular ectasia
• Requires reduction of portal hypertension
• Stress Erosions
➢ ICU patients
➢ One or more bleeding erosions
❖ Bleeding may be severe
Esophageal Varices
• 50% cirrhotics develop esoph. varices.
• 1/3 of these bleed
• Portal v. pressure >12 mmHg. above Hep.v
• At risk to bleed
➢ Large size
➢ Located near GE Junct.
➢ Vascular ectasia on the varices
• Rapid bleeding
• Emergent endoscopy
• 50% of cirrhotics w. bleed = non-variceal
• Poor prognosis
➢ 30–50% mortality for first bleed
➢ 2/3 die within one year
Mallory-Weiss Tear
• 5–10% GI bleeds
• Hx of retching; 40% no retching
• Non-penetrating linear tear(s) near GEJ
➢ 25% multiple lesions; 75% have o. pathol.
• 90% resolve spontaneously
• Rx ->endo.oversewing
Gut Hemangioma
• Rare
• Described in young and old
• Esophagus, stomach, sm. bowel, colon
• Classification
➢ Capillary – collection of thin-walled vess.
➢ Cavernous – large, dilated channels w. thrombosis -> Ca++
❖ Tendency to bleed
➢ Angiomatosis – large area of hemangioma
Gut hemangioma
• Cavernous hemangioma
➢ Phleboliths on plain film
➢ UGI = Submucosal mass
• CT
➢ Thick wall
➢ Early enhancement – network of vessels & sinuses thickening the wall
➢ Late enhancement – confluent sinus fill-in
• Endoscopy
➢ Soft, submucosal mass or thickened folds, blue-red discoloration
Nuclear Scintigraphy
• Most sensitive non-invasive test
• Detects bleeding rates of 0.1 ml/min
• Two techniques
➢ Tc 99m sulfur colloid
➢ Tc 99m labeled RBC′s
• Used to
➢ Delineate obscure sources – small bowel, intermittent bleeding
➢ Enhance the efficacy of angiography
Aortoenteric Fistula
• Erosion of aorta into 3rd portion of duod,
• Dacron graft, atheroma, mycotic aneurysm
• “Herald bleed” stops spontaneously followed by exsanguinating bleed
• High index of suspicion
• Preemptive surgery
Pill Endoscopy
• Ingestible capsule
• 7 hour recording
• 2 images per second
• Localizing surface antennae
• View in “real-time”
• Contraindicated w. obstruction
• 22% Capsule vs. 3% barium-positive in 52 pts w. occult gi bleed
Hara AK, Radiol 2004, 230: 260-265)
Colonic Diverticulosis
• Colon Diverticula = herniations of mucosa and submucosa through muscular
layers at site of penetration of vasa recta through bowel wall.
Angiodysplasia
• 20–40% acute LGI bleeding
• Vascular ectasia
➢ 2/3 in pts >70 yrs old
➢ Aortic valve disease
❖ Von Willebrand factor depletion?
• < 5mm vascular tufts
• Cecum & right colon
• Bleeding
➢ Not massive, intermittent
➢ Stop spontaneously, 85% bleed again
• Pathogenesis
➢ Increased tension in cecal wall
➢ Repeated, intermittent obstruction of submucosal veins -> dilation &
tortuosity
➢ Develop small A-V malformation
• Colonoscopy 80–90% sensitive
• Angiography
➢ early tangle of vessels
➢ early filling & slow emptying dilated veins
• Treatment
➢ Abnormal vessels – poor response to vasoconstrictors; may temporize
➢ Endoscopic electrocoagulation
➢ Embolo Rx
➢ Diffuse disease – estrogen-progesterone
➢ Surgery
References
1. Peura DA, Lanza FL, et al. The American College of Gastroenterology Bleeding Registry: Preliminary Findings.
Am J Gastroenterol. 1997, Jun: 92(6): 924-8.
2. Reinus JF, Brandt LJ. Upper and lower gastrointestinal bleeding in the elderly. Gastroenterology Clinics of North
America. 1990 Jun; 19(2): 293-318.
3. Mitros FA, Atlas of Gastrointestinal Pathology. Gower Medical Publishing.
4. Elta GH, Approach to the patient with gross gastrointestinal bleeding. In Textbook of Gastroenterology, Lippincott,
Williams and Wilkins. Philadelphia, 1999, Yamada T, et al eds.
5. Fritscher-Ravens A, Swain CP. The wireless capsule: new light in the darkness. Dig. Dis. 2002;20(2): 127-33.
6. Hara, AK et al. Small bowel: preliminary comparison of capsule endoscopy with barium study and CT
Radiology 2004, 230: 260-265.
7. Hara AK. Capsule endoscopy: the end of the barium small bowel examination?Abdom Imaging, 2005, Jan.
SBO
• Review
➢ Mechanical
➢ Classic Acute “Complete” SBO
❖ Simple SBO
❖ Closed Loop Obstruction (CLO)
- Urgent Emergency !
➢ Classic Appearances
❖ Intermittent “Chronic” SBO
❖ Partial SBO
➢ Motility
❖ Common Ileus
❖ Unusual dysmotilities
Acute mechanical SB obstruction
SBO showing uniformly distended bowel
• Motility
➢ Paralytic Ileus
➢ Scleroderma “Collagen Vasc Disease”
➢ Sprue, MAB diseases Figure 2-28-2
➢ Radiation enteritis, earliest stage
➢ Hypothyroidism, metabolic
➢ Chronic Intestinal Pseudo-obstruction
➢ DYSMOTILITY is a FUNCTIONAL Obstruction !
➢ Slow passage acts / looks obstructive
Simple SBO
• A tapered distension meandering back toward Treitz.
• A single transition point
Scleroderma SB shows dilated loops
Chronic Intermittent SBO
with segments whose diameter are
• Dilated but not distended
greater than last case of acute SBO.
Loops are not uniformly distended
Chronic vs Acute SBO [Figures 2-28-1 to 2-28-3]
with segments that are partly
• Distention vs Dilatation
collapsed
• Distended, not (XS) Dilated:
➢ Acute, initial SBO
• Dilated, not Distended:
➢ Chronic, intermittent SBO or
➢ DYSMOTILITIES !
Bloating, Obstruction
• Prior Colectomy for constipation with
• Ileo-rectal anastomosis
• Idiopathic Intestinal Pseudoobstruction [Figure 2-28-4]
• Myopathic type
MNGIE = POLIP
• Mitochondrial Neuro Gastro Intestinal Encephalopathy MNGIE
• Polyneuropathy, Ophthalmoplegia, Leukoencephalopathy,
Intestinal Pseudo-obstruction. P-O-L-IP
• Rarenth power (73 cases up to 2005)
• Familial, Autosomal Recessive
Blondon H, et al Digestive smooth muscle mitochondrial myopathy in
pts with mitochondrial-neuro-gastro-intestinal encephalomyopathy
(MNGIE), 3 cases & review of literature; Gastroenterologie 2005 Aug. SB appears both dramatically dilated
VOL 29 - N 8-9,p. 773 - 778 and uniformly distended.(double
arrow). This suggests acute
Simon et al, Polyneuropathy, Ophthalmoplegia, obstruction in a patient with chronic
Leukoencephalopathy, Pseudoobstruction: POLIP Syndrome; Ann recurring obstruction from Crohns
Neurol 1990;28:349-360 Disease (arrow)
Figure 2-28-4
Adhesion
• MAJOR CAUSE SBO:
• Benign Adhesions
➢ Surgical
➢ Inflammatory -itis
➢ Radiation
➢ Endometriosis
➢ Ischemia
• Neoplastic Adhesions
➢ (Carcinoid)
Abdominal Hernias
• By Location
➢ External vs Internal
Figure 2-28-8
➢ Inguinal, Femoral, Sciatic, Hiatal, Spigelian, etc
• By Type
➢ Complete vs Partial (Richter)
• By Content
➢ Littre (pre-existing tic), Amyand (appendix)
• By Severity
➢ Reducible
➢ Non-Reducible or “Incarcerated”
➢ Ischemic or “Strangulated”
➢ Infarcted Figure 2-28-9
Obturator Hernia
[Figure 2-28-9]
• Elderly F 10 to 1 M
• R >> L
• Assoc w recent wt loss
• Not palpable
• SBO in Obturator
Pectineal Space
• Howship Romberg Sign
➢ Pain medial thigh +/-
50%
• Hannington Kiff
➢ Absent thigh adductor
reflex
Ijiri R, et al Oburator H:
usefulness of CT in DX.:
Surg.1996 Feb;119(2):137-40.
SB “Bezoars” are useful to point to a
site of obstruction. They are
composed of residual fibrous material
that begins fermentation. Carrots,
mushrooms, and other fibrous foods
Obturator Hernias are unusual may cause transient symptomatic
hernias difficult to detect by obstruction in normal patients when
simple physical examination. the bolus reaches the ileocecal valve.
Special maneuvers are Poor peristaltic tone may play a role
needed. Tiny barely visible in pts with dysmotility disorders
hernias may produce
significant obstruction
Figure 2-28-10
Figure 2-28-11
Mesenteric Volvulus
• Assoc w
➢ Malrotation
❖ Left Colon
❖ Right SB
❖ “Weak” Treitz
➢ Internal Hernia
➢ External Hernia
➢ Post operative
• Short / bunched mesentery
Figure 2-28-14
Figure 2-28-16
Paraduodenal Hernia
• 50% IH = Paraduodenal
• Mortality pre-CT era (20%)
• Clinically:
➢ Asymptomatic,
➢ Pain,
➢ SBO,
• Left 3X > R; M > F
• SB entrapment =
➢ Congenital anomaly
J Comp. Assist. Tomo. 10:542, 1986
Figure 2-28-18
Bilio
Pancreatic Alimentary
Limb Limb
Desc Meso-colon H
• “Left PDH”
• Descending mesocolic H
• Ligament of Treitz OK
• Cecum OK
• Stomach displaced to right
• Neck contains IMVein & Left Colic Art.
displaced anteriorly by hernia
• CT: IMV ant to SB loops
Treatment with percutaneous draininage will allow elective
surgery if the obstruction does not resolve
Desc Meso-colon Hernia
[Figure 2-28-22]
• 1. Ligament of Treitz OK Figure 2-28-21
• 2. IMV in front of SB
• 3. SMA, V’s into hernia
• 4. Bunched SB possible
• If you want to diagnose a Left PDH, look for the IMV
Figure 2-28-22
Foramen of Winslow
• “Epiploic Foramen”
• SB above antrum
ascending
Cecal Volvulus into lesser sac
• SBO
➢ Potential in Cecal Volvulus
➢ SB follows IC Valve
SB Obstruction
• Common disease.
• Mechanical: Acute, Chronic, Internal, External
• Dysmotilities
• Critical
➢ Diagnose
➢ Stage
➢ Establish etiology
descending
SBO The Paraduodenal Hernia will
• Reviewed remain in our literature and our
➢ Mechanical Board Examinations even
❖ Classic Acute “Complete” SBO though they are not hernias but
Simple SBO errors of rotation in which the
Closed Loop Obstruction (CLO) SB is trapped behind the
Urgent Emergency !!!!!!!! returning meso-colon.
❖ Classic Appearances Because there is a wide arc of
Intermittent “Chronic” SBO returning colon, from the
Partial SBO ascending, the transverse,and
➢ Paralytic the descending colon, there will
❖ Common be variation in radiographic
❖ Unusual appearance depending on
where the SB is trapped.
Above one can see ascending,
transverse, and descending
retro-meso-colic entrapment
1. Balthazar et al Closed-loop & strangulating intestinal obstruction: CT signs. Radiology. 1992 Dec
2. Blondon H, et al Digestive smooth muscle mitochondrial myopathy in pts with mitochondrial-neuro-gastro-
intestinal encephalomyopathy (MNGIE), 3 cases & review of literature. Gastroenterologie 2005 Aug. 29N, 8-
9:773-778
3. Frager D, Medwid SW, et al . CT of SBO: Value in Establishing Diagnosis and Determining Degree and
Cause.AJR 1994;162: 37-41.
4. Ljiri R et al. Oburator H: usefulness of CT in DX.:Surg. 1996 Feb; 119(2): 137-40
5. Luedke, Scholz. Larsen CT of Spigelian H. Comp Med Imag Graph. 198812(2):123-9.
6. Maglinte, Herlinger, Nolan. Rad of CLO: 25 confirmed cases. Radiology. 1991 May;179(2):383-7 (Chronic)
7. Mayo-Smith WW, Wittenberg, et al. CT SB faeces sign: description & clinical significance. Clin Radiol. 1995
Nov;50(11):765-7.
8. Megibow A, Balthazar E, Cho K, et al. Bowel Obstruction: evaluation with CT. Rad 1991;180:313-318.
9. Passas V, Karavias D, Grilias D, Birbas A. Computed tomography of left paraduodenal hernia. J Comput Assist
Tomogr. 1986 May-Jun;10(3):542-3.
10. Sandrasegaran K, Maglinte DD, et al CT of acute bilio-pancreatic limb obst. AJR 2006 Jan;186(1):104-9
11. Scheirey C, Scholz F, et al. Radiology Lap Roux-Y Gastric Bypass: Conceptualization and Precise Interpretation
Radiographics in press Sept 2006.
12. Simon et al, Polyneuropathy, Ophthalmoplegia, Leukoencephalopathy, Pseudoobstruction: POLIP Syndrome; Ann
Neurol 1990;28:349-360
13. Zalcman et al Helical CT Signs in Dx of Intestinal Ischemia in SBO; AJR 2000;175:1601-1607
14. Zalcman M, et al Helical CT signs in Dx of intestinal ischemia in SBO. AJR 2000 Dec;175(6):1601-7.
Bowel Ischemia
• Small Bowel or “Mesenteric” ischemia
➢ SMA distribution: SB and Right Colon
• ”Colonic Ischemia” - a different disease
➢ Watershed: Sigmoid, Splenic
• ESD: never: unless
➢ Surgery
➢ Radiation
➢ Vasculitis
Pathophysiology of Ischemia
• Initial Damage to Endothelial cells of pre-capillary arteriole and capillaries.
• Blood vessels leak fluid, then cells
• Mucosa & submucosa
➢ Most sensitive, high metabolism
➢ Edema, hemorrhage, & slough
• Muscularis propia
➢ Initial spasm
➢ Then atonia
➢ Then perforation / death
(healing with stricture)
• Serosa
➢ Petechiae, Ascites
➢ With healing may see adhesions
Ischemia
• Rad Findings, Symptoms & Prognosis depend on:
➢ Duration
❖ Momentary to Permanent
➢ Degree
❖ 1%-100%
➢ Extent
❖ % of SB
Fast Ischemia
• Cell, Tissue, Organ & Organism death -24-48 H
➢ Eg. Embolus to SMA
➢ Eg. Hypotension: Profound & prolonged
Ischemia
• Chronic - recurrent - slow
• Acute - sudden - fast
• Often both
➢ Chronic for months then Acute
Figure 2-29-6
Figure 2-29-8
A regular stack of coins with relatively
uniform appearance of folds is
suggestive of recent bleeding into
wall. A stack of coins appearance
can be due to blood or fluid. It is a
longitudinal image of cross sectional
“target sign”. Pts with coagulopathies
or with leaking capillaries due to
vasculitis will have a similar
appearance
Ischemic Pneumatosis
[Figure 2-29-10]
Intramural and
Intravenous Air [Figure 2-29-
11]
Figure 2-29-11
Figure 2-29-10
Figure 2-29-14
Figure 2-29-16
J Tube Jejunitis
• Schunn CD, Daly JM. SB necrosis associated w post-op jejunal tube feeding.
J Am Coll Surg. 1995 Apr;180(4):410-6.
• Lawlor DK, et al SB necrosis assoc w jejunal tube feeding. Can J Surg. 1998
Dec;41(6):459-62.
• Rai J, et al SB necrosis in assoc w jejunostomy tube feedings. Am Surg. 1996
Dec;62(12):1050-4.
• Munshi IA, et al.SB necrosis assoc with early post-op jejunal tube feeding in a
trauma pt.J Trauma. 2000 Jul;49(1):163-5.
• Schloerb PR, et al. Bowel necrosis caused by water in jejunal feeding. J
Parenter Enteral Nutr. 2004 Jan-Feb;28(1):27-9.
• Brenner DW, Schellhammer PF. Mortality assoc w feeding catheter
jejunostomy after radical cystectomy. Urology. 1987 Oct;30(4):337-40.
• Gaddy MC, et al . SB ischemia: consequence of feeding jejunostomy? South
Med J. 1986 Feb;79(2):180-2.
• Jorba R, et al. SB necrosis in assoc w early post-op enteral feeding after
pancreatic resection. Surgery. 2000 Jul;128(1):111-2.
Figure 2-29-19
Luxury
Reperfusion with
gray mucosa and
hyperemic
muscularis and
mesentery
Figure 2-29-22
Figure 2-29-26
Peripheral focal lesion [Figure 2-29-26] A SB series (Image A) shows a stack of coins
appearance (within circle). An angiogram (Image
Ulcerating Plaque [Figure 2-29-27] B) shows a bulging segment of SMA (arrow), an
ulcerating plaque showering cholesterol emboli.
Dysplasia [Figure 2-29-28] (This could also be a mycotic aneurysm if patient
were septic.)
Becker Duodenal necrosis as presenting manifestation of
polyarteritis nodosa.
Clin Rheumatol. 2002 Aug;21(4):314-6 Chronic Radiation Enteritis
Degos Disease
• “Malignant atrophic papulosis”
• Porcelain-white, atrophic papules
➢ Peripheral erythema
➢ Telangiectases.
• Small vessel thromboses
• M3 X F, all ages
• Skin presentation
• May rarely remain dermal
• When systemic, 2-4 yr prognosis
Coskun B Benign Cutaneous Degos' Disease:
case report and review of literature. J Dermatol. 2004 Aug;31(8):666-70
Degos GI Path
• GI - Any portion, but SB predominant
• 60% Degos: GI perfs lead to death Figure 2-29-28
• Sub-serosal white or yellow plaque, transmural bowel
inflam., ulcers, hemorrhage, infarction
Etiologies of Ischemia
• Arterial Occlusive
➢ Atherosclerosis
➢ Embolus
• Venous Occlusive 5%-10%
➢ Proximal Obstruction
➢ Distal Disease
• Arterial Non-Occlusive
Figure 2-29-31
Figure 2-29-33
Figure 2-29-34
Shock Bowel
• Dense persistent enhancement:
➢ Bowel Wall, solid organs
• Delayed pyelogram
• Small aorta, IVC, Spleen
• Ascites
• Variable Distension - Wall Thickness
• Periportal extravasation of fluid
• Major trauma with
➢ Resuscitation
➢ Volume repletion
• 2° to Reflex vasoconstriction
Mirvis SE, et al Diffuse SB ischemia in hypotensive
adults after blunt trauma (shock bowel): CT findings &
clinical significance. AJR Am J Roentgenol. 1994
Dec;163(6):1375-9
Shock Bowel
• May develop:
➢ Ischemia
➢ Infarction
• SB = Low Flow State usually caught in time CT images (A-F) show wall thickening with fluid
density in pt with angioedema, a process where
Ischemia Mimic: Angioedema capillaries leak serum. It may be due to allergies
[Figure 2-29-35] to food, drugs, or other exogenous allergens. A
• Enhancement of mucosa hereditary form occurs without specific causation.
• Submucosa edema Angiotensin Converting Enzyme inhibitor drugs
• Fluid in lumen may produce this finding alone or in association
• Ascites with glottic or generalized edema. It may be dose
• Etio related or seen with certain ACE inhibitors. Those
➢ Allergic reaction, with bowel angioedema from ACE inhibitors may
➢ Hereditary, present with a rad and clin picture suggesting
➢ ACE inhibitors. mesenteric ischemia. Pts on hypertensive or
cardiac medications should be questioned about
DeBacker AI, et al; CT of Angioedema of the Small
antihypertensive medication to exclude this as an
Bowel, AJR 2001; 176: 649-52
etiology. Cessation of offending ACE inhibitor may
3 cases: 3 different etiologies
provide relief and rad return to normal within 24 to
1 case report of 1 pt
48 hrs
1 NEJM Images in Clinical Medicine
Ischemia CT Mimics
• Vascular or Mucosal Barrier Interruption
➢ Ischemia
➢ Vasculitides HSP
➢ Coagulopathies
❖ Bleeders - Purpuras, anticoags
❖ Clotters - P Vera, S,C defic
➢ Angioedema - ACE inhibitors
➢ Regional Inflammation - tic appy itis
➢ Crohns
➢ Infectious Enteritis
➢ Neutropenic Enterocolitis
Mesenteric Ischemia
• Diagnosis
➢ Imperative in Acute & Chronic Ischemias
➢ Now earlier Dx by CT - study vessels
➢ Think of it in every abd pain CT.
• Physiological understanding is critical
• Remember Steals
• Surgeons undercall some, be brave, stay bold
• We undercall some, explain plums & prunes
References
General References
1. Becker Duodenal necrosis as presenting manifestation of polyarteritis nodosa. Clin Rheumatol. 2002 Aug;
21(4):314-6.
2. Carucci LR, Levine MS, Rubesin SE, Laufer I, Assad S, Herlinger H. Evaluation of pts with jejunostomy tubes:
imaging findings. Radiology. 2002 Apr; 223(1): 241-7.
3. Coskun B. Benign Cutaneous Degos' Disease: case report and review of literature. J Dermatol. 2004
Aug;31(8):666-70
J Tube Jejunitis
1. Brenner DW, Schellhammer PF. Mortality assoc w feeding catheter jejunostomy after radical cystectomy. Urology.
1987 Oct;30(4):337-40.
2. Gaddy MC et al. SB ischemia: consequence of feeding jejunostomy? South Med J. 1986 Feb; 79(2):180-2.
3. Jorba R, et al. SB necrosis in assoc w early post-op enteral feeding after pancreatic resection. Surgery. 2000
Jul;128(1):111-2.
4. Lawlor DK, et al SB necrosis assoc w jejunal tube feeding. Can J Surg. 1998 Dec; 41(6):459-62.
5. Munshi IA, et al.SB necrosis assoc with early post-op jejunal tube feeding in a trauma pt.J Trauma. 2000 Jul;
49(1):163-5.
6. Rai J, et al SB necrosis in assoc w jejunostomy tube feedings. Am Surg. 1996 Dec; 62(12):1050-4.
7. Schloerb PR, et al. Bowel necrosis caused by water in jejunal feeding. J Parenter Enteral Nutr. 2004 Jan-
Feb;28(1):27-9.
8. Schunn CD, Daly JM. SB necrosis associated w post-op jejunal tube feeding. J Am Coll Surg. 1995 Apr;
180(4):410-6.
Celiac Disease
• Vessel cloaking nodes, fluid in pelvic SB loops
Entero-Enteric Circulation
• Crypts secrete fluid into lumen
• Villi absorb fluid + nutrients from lumen
• Nutrients into portal veins, lymphatics
• Crypts recycle fluid back into lumen
The MAB pattern results in part from loss of normal peristalsis. Long
arrow in A is normal feathery or fish-tail appearance of jejunal
peristalsis. Short arrows in B show normal contractile pattern of
Ileum with parallel folds in tapered segments mimicking esophageal
contraction
Figure 2-30-6
Image A shows a smooth fold-free segment of the
jejunum, called “toothpaste” or “moulage” caused
by atrophy of mucosal villi and thickening of the
wall by crypt hyperplasia.
Image B shows a bald jejunum in the LUQ and a
feathery abundant fold pattern in the ileum RLQ.
Chronic increase in the nutrient mix presented to
the ileum because of lack of jejunal absorption
cause compensatory hypertrophy of ileal mucosa,
hence “Reversal of Fold Pattern”
Figure 2-30-9
Figure 2-30-11
Figure 2-30-13
Figure 2-30-14
Figure 2-30-16
Nutritional Collapse
• Hypoproteinemia
➢ Hypoalbulminemia
➢ Ascites
• Vitamin deficiencies
➢ K (Coagulation defects)
• Iron Deficiency Anemia
➢ Jejunum absorbs Fe
➢ Slowwww bleeding
• Electolyte Disturbances
➢ Tetany
➢ Seizures Multiple small and moderate sized lymph nodes
are seen in the SB mesentery (arrows)
Sprue = “Immune Disease” surrounding mesenteric vessels. They are
• Lymphatic activity reactive lymph nodes chronically stimulated by the
➢ Reactive mesenteric nodes low grade SB autoimmune inflammatory process.
➢ Para-aortic LNs They are notable for number but rarely for size
➢ Large cavitating nodes = poor prognosis
➢ Peripheral lymphadenopathy
➢ Splenic atrophy & clinical hyposplenism
• Antibody Tests define “Autoimmunity”
“Genetic Disease”
• Unique histo-compatability complex in 80% of sprue HLA B8 , DR3
➢ (vs 20% of “normal” population)
➢ Increased prevalence of Sprue in families
➢ 10% latent Sprue in 1st order relatives
Determinants of Severity
• Genetic “Dose” +
• Gluten “Dose” +
• Time +
• Other Factors
Adapted from Marsh, Gastroenterology 1992: 102:330-54
Dermatitis Herpetiformis
• Pruritic papulovesicular lesions
• IG A deposits - dermal-epidermal junction
• Goes away with gluten restriction
Healing Sprue
• Folds slowly return, first
• Diameter slowly shrinks
• May take 3-4 years
Sprue
• Occult Marsh 1
➢ Nl SB exam, Asympt,
➢ bx +, labs +
➢ Intraepithelial lymphocytes
➢ 1° relatives of sympt pts: 5%-15 %
• Nodular Marsh 2
➢ Sandy Nodules, irritable
• Classic MAB pattern Marsh 3, 4
➢ Wet, wide, way late
• Non-responsive
➢ Diet errors, misdiagnosis
➢ Recalcitrant 5%-20% - Bact Overgr; Panc Insuffic
➢ Lymphoma
Recalcitrant Sprue
• Responsive to initial Rx 8+yrs
• Loss of responsiveness
• Smoldering symptoms
• Thick folds
• “Ulcerative Jejunitis”
• High incidence Lymphoma
Think Physiologically
[Figures 2-30-19 and 2-30-20]
• Maldigestion (no enzymes, no mixing)
➢ Biliary - panc insuff, ZE, bacterial
overgrowth, SB diverticulosis
“Luminal”
• Cellular MAB (columnar C uptake
failure)
➢ Sprue, ischemia, villous tip
infiltration
• Malassimilation (columnar cell exit
failure) A patient with bloating, cramps, gas, indigestion, occasional
➢ Lymphangiectasia, diarrhea for yrs. CT Scan shows a big gassy colon, fluid filled
abetalipoproteinemia, mesenteric loops of pelvic small bowel, and baggy proximal SB. The
diseases “Mesenteric” diagnosis was made because of these findings and because of
obvious findings in upper slices evident in the first two images
Figure 2-30-21
Figure 2-30-23
Figure 2-30-22
Figure 2-30-25
ZE
• Excess fluid Figure 2-30-26
• Thick folds
• Hyperemic mucosa
Tropical Sprue
• Villous and Crypt Atrophy
• Malabsorption
• Glossitis, wt loss, diarrhea, skin changes
• Folate & B12 deficiency prominent
➢ Rx folate, B12 improves partly
• Antibiotic Rx cures
• Relapses common in tropics
Westergaard H.Tropical Sprue Curr Treat Options
Gastroenterol. 2004 Feb;7(1):7-11.
Haghighi P, Wolf PL. Tropical Sprue and subclinical
enteropathy.. Crit Rev Clin Lab Sci. 1997 Aug; 34(4):
313-41.
Malabsorption
• Radiologists may still be first on scene in pts with
Sprue & MAB diseases
• MAB major radiographic pattern
• Fluid is the hallmark of MAB pattern
➢ Increased production +/or
➢ Decreased absorption
Figure 2-30-34
References
1. Farrell RJ, Kelly CP. Celiac Sprue. N Engl J Med. 2002 Jan 17;346(3):180-8
2. Fine KD, Prevalence of occult GI bleeding in Celiac Sprue. NEJM. 1996 334: 1163-7
3. Haghighi P, Wolf PL. Tropical Sprue and subclinical enteropathy. Crit Rev Clin Lab Sci. 1997 Aug; 34(4): 313-41.
4. Johnston SD et al. A comparison of antibodies to tissue transglutaminase with conventional serological tests in the
diagnosis of coeliac disease. Eur J Gastroenterol Hepatol. 2003 Sep; 15 (9): 1001-4.
5. Jones B, Bayless TM, Hamilton SR, Yardley JH. "Bubbly" duodenal bulb in celiac disease: radiologic-pathologic
correlation. Am J Roentgenol. 1984 Jan; 142(1): 119-22
6. Lomoschitz F et al. Enteroclysis in adult celiac disease: diagnostic value of specific radiographic features. Eur Radiol.
2003 Apr;13(4):890-6.
7. Lomoschitz F et al. Enteroclysis in adult celiac disease: diagnostic value of specific radiographic features. Eur Radiol.
2003 Apr;13(4):890-6.*
8. Marsh MN. Gluten, major histocompatibility complex, and small intestine. A molecular and immunobiologic approach
to spectrum of gluten sensitivity ('celiac sprue'). Gastroenterology 1992 Jan;102(1):330-54)*
9. Marsh M N, Gluten, major histocompatibility complex, and the small intestine. A molecular and immunobiologic
approach to the spectrum of gluten sensitivity ('celiac sprue'). Gastroenterology 1992 Jan;102(1):330-54)
10. Rubesin SE, Herlinger H, Furth EE." Bubbly" duodenal bulb in clinically unsuspected or refractory adult celiac
disease. Abdom Imaging. 1998 Jul-Aug; 23 (4): 449-52.
11. Schweiger GD, Murray JA. Postbulbar duodenal ulceration and stenosis associated with celiac disease. Abdom
Imaging. 1998 Jul-Aug; 23(4):347-9.
12. Tomei E et al. CT of SB in adult celiac disease: jejunoileal fold pattern reversal. Eur Radiol. 2000; 10(1):119-22.*
13. Trier J. Celiac Sprue. NEJM. 1991
14. Westergaard H. Tropical Sprue. Curr Treat Options Gastroenterol. 2004 Feb; 7(1): 7-11.
54 y/o M, Vomiting
• 2003: Vomiting 2-3 hrs p meals
• Liquid diet wks
• 30 lb wt loss - 4 mos
• Mother deceased, colon CA.
• 1996 Proctocolectomy, end-ileostomy
• 2001 Laparotomy, gastrotomy: 3 big gastric polyps removed
Figure 2-31-1
2 yrs earlier
Endoscopy
• Many gastric polyps, Large obstructing duodenal
polyp(s)
• Gastrectomy:
➢ Stomach: inflamm, mucosal papillary
hyperplasia with atypia.
• Duodenum : Hyperplastic mucosa, foci suggestive of
adenomatous change
FAP
• Usually:
➢ Dx known clinically ~75%
➢ Colonoscopic Dx, not BE, not CT
➢ Not Dx challenge except: Only a small percentage of Colorectal Cancers are
❖ ~25% de novo mutation related to FAP
❖ Professor’s quiz
➢ Differential important:
➢ More things look like FAP than are FAP
Figure 2-31-2
Colorectal Cancer CRC Perspective
[Figure 2-31-1]
• 150,000 new CR CA / yr, only ~ 1% = FAP
Barely Countable
Countable, Pedunculated
Figure 2-31-7
Figure 2-31-8
Ampullary tumor and stoma: a link worthy of being
an Aunt Minnie
Mandibular Osteomas
Figure 2-31-12
Figure 2-31-13
FAP Skin
• Sebaceous Cysts
• Pigment Changes
Desmoids
• Rare benign “tumors”,
• Never metastasize, invade locally,
• FAP associated, occ spontaneous
• In FAP pts:
Desmoid
NOTE: Colectomy, Hazy Dense Mesentery Desmoid tumors may be
geometric or infiltrative
NON FAP DESMOID: TUMORAL & INFILTRATIVE with
Ischemia
Infiltrative / Tumoral
FAP Mimics
• Numerically, more things resemble FAP than the cases of FAP that
we see.
• More common entities mimic classic polyposis syndromes
Peritoneal Inclusion Cysts are a
complication produced by pelvic
peritoneal adhesions in
premenopausal women.
Classification of Hereditary GI
Polyposis Syndromes (Gene)
• Familial adenomatous polyposes
➢ Born Adenomas -> Malignant transformation
• Hamartomatous polyposes HPs
➢ Born Hamartomas of varying types
➢ Some undergo epithelial atypia from “overwork”
➢ Some adenomas may develop, at risk CA
➢ Bowel CA can occur in all HPs
✧ More than general population
✧ Far less than FAP
Non-Hereditary GI Polyposes
• Inflammatory and post inflammatory
➢ CUC, Crohns, Infectious colitides Peritoneal Inclusions Cyst (s) progressively
• Lymphoid enlarge unless cycle suppression therapy is
➢ Reactive nodular lymphoid hyperplasia instituted. Reoccurrence may occur after lysis of
➢ Lymphoma adhesions
• Pneumatosis cystoides intestinalis
• Lipomatosis
• Angiomatosis Figure 2-31-17
• Leiomyomatosis
• Cronkhite-Canada syndrome
Figure 2-31-18
Peutz Jeghers
• One 5 X 8 mm, many 1-2 mm polyps
Figure 2-31-21
Figure 2-31-22
Cowdens Syndrome
Ruvalcaba-Myhre-Smith
• “Bannayan-Riley-Ruvalcaba syndrome (BRRS)”
• “Riley - Smith syndrome”
• “Bannayan - Zonana syndrome”
• “R M S” is best
• “Macrocephaly hamartoma papilledema syn”
RMS Syndrome
• Rare2, autosomal dominant ? (80% male)
• Men more common
• Ileal & Colonic polyps in 45%
• Other:
➢ Colonic tumors
➢ GI tumor/polyp/hemangioma
➢ Lobulated tongue (including hamartomas)
➢ Skin
❖ Abnormal genital pigmentation
Large Juvenile Polyps in the SB
❖ Acanthosis nigricans
❖ Cafe au lait spots
❖ Nevi or lentigines Figure 2-31-24
❖ Lipomata
❖ Capillary hemangioma
❖ Cavernous hemangioma
❖ Other tumors of skin
❖ Supernumerary nipples
➢ Bones
❖ Delayed bone age
❖ Asymmetric limbs
❖ Joint laxity
❖ Muscle weakness/myopathy
➢ Brain
❖ Tumors/cysts
❖ Intra-cranial calcification
❖ Vascular malformations of brain Ruvalcabre Myhre Smith in SB and Colon
❖ Macrocephaly
❖ Papilledema
➢ Eye
❖ Anterior chamber abnormalities, Figure 2-31-25
❖ Visible nerve fibers on cornea
❖ Palpebral fissures slant down
➢ High birth wt (> 90th %centile)
Lymphoma
[Figure s 2-31-27 and 2-31-28]
• Nodularity one form of
Lymphoma.
• Remember L is a “PoLyposis+
Nodular Lymphoid
Hyperplasia Colon [Figure 2-31-29]
• Can be:
➢ Related to GI infection
➢ Assoc w
hypogammaglobulinem
➢ Assoc w Giardia
➢ Diff to histo diff from
Lymphoma
➢ TI most frequent Cronkhite Canada Syndrome
➢ Anywhere in GI tract
Figure 2-31-30
Nodular Lymphoid
Hyperplasia
Small Bowel [Figure 2-31-30]
• Radiology
➢ Uniform, 1-4 mm
➢ May be umbilicated
➢ Diffuse
➢ Regional
➢ Clustered -”patches”
Nodular Lymphoid
Hyperplasia
Colon
• Radiology
➢ Uniform, 1-4 mm
➢ May be umbilicated
➢ Diffuse Nodular Lymphoid Hyperplasia
➢ Regional may mimic a polyposis syndrome
➢ Clustered or Lymphoma
NLH of SB
Figure 2-31-33
Figure 2-31-34
Figure 2-31-37
Familial Polyposis
• Protean manifestations
• Multiple mimics
• Worthy of further study:
➢ For itself
➢ As starting point for Bumps of the
Bowel Pneumatosis Cystoides Coli may fool the unwary
References
1. Carl, W. Herrera, L. Dental and bone abnormalities in patients with familial polyposis coli; Semin Surg Oncol
73-83, 1987
2. Knudsen AL, Bulow S. Desmoid tumour in familial adenomatous polyposis. A review of literature. Fam Cancer.
2001;1(2):113-21.
3. Offerhaus GJA et al. Gastroenterology 1992;102:1980
Embryology
• Formed from the mesenchymal cells between the layers of the dorsal
mesentery, which lies between the stomach and pancreas
• Rotates to the left pulling the mesentery with it and forming the lesser sac
between the stomach and pancreas. Left side of the dorsal mesentery fuses
with the parietal peritoneum covering the left kidney and adrenal to form
Gerota’s fascia. This fusion brings the splenic vessels and the pancreas into
the retroperitoneum.
• Hilum of the spleen is retroperitoneal, while most of the spleen is
intraperitoneal, with a bare area similar to that of the liver, along posterior
surface adjacent to the left kidney
Anatomy
• Crescent shaped, convex toward the diaphragm and concave medially, located
in the LUQ
• Bounded by ribs, stomach, left kidney and splenic flexure of the colon.
• Splenic hilum contains splenic vessels and tail of pancreas (retroperitoneal)
➢ Splenic artery-tortuous, often containing aneursyms
➢ Splenic vein-straight. Confluence with SMV forms the portal vein. Splenic
vein often enlarges with splenomegaly. Upper normal is 1.5cm
Important Connections
• Splenorenal ligament (retroperitoneal)
➢ Connects the splenic hilum to the left kidney
➢ Contains the pancreatic tail, and splenic artery and vein
• Gastrosplenic ligament (peritoneal)
➢ Peritoneal fusion of the lesser and greater sacs, connecting the splenic
hilum to the stomach
• Phrenicocolic ligament (peritoneal)
➢ Connects the lower pole of the spleen to the splenic flexure of the colon
and to the diaphragm
Histopathology
• Stroma supports functional red and white pulp
• White pulp: the functional cells of the spleen; lymphocytes, plasma cells and
macrophages.
• Red pulp: surrounds white pulp and is comprised of arteries and sinuses filled
with blood. Also contains chords which slowly filter the blood, removing aging
cells
Splenic Function
• Adult: filtration of aged rbc’s, sequesters platelets, removes foreign particles
with macrophages.
• Childhood: adult functions plus production of lymphocytes and monocytes.
• Fetal hematopoesis
• Maintains immunity against bacterial pathogens (streptococcus D)
Normal Size
• Long axis from diaphragm to inferior pole
• Usual size (US and CT and MRI) length 12cm, width 7cm and thickness 3-
4cm. (you can allow greater length if the spleen is thinner)
• Spleen may be horizontal or longitudinal in orientation
Normal Variants
• The spleen is formed from multiple cell aggregates
which coalesce.
• This gives rise to:
➢ Accessory spleens
➢ Clefts Normal accessory spleen
➢ Splenosis Left: normal spleen in left upper quadrant
➢ Splenic rests Right: Isoattenuating 2cm enhancing nodule
lateral to the left kidney and adjacent to the splenic
Accessory Spleens [Figure 2-32-4] flexure is a normal accessory spleen
• 30%-40% incidence in normal population and 10% of
patients have >1 focus
• Frequently (75%) in splenic hilum
Figure 2-32-7
Asplenia
• Bilateral right-sidedness
➢ 2 right lungs in 2/3
➢ Midline liver
➢ More complex cardiac anomalies including single AV valve, pulmonary
stenosis or atresia, TAPVR, transposition of the great vessels, ASD, single
ventricle
➢ Mortality is as high as 80% in first year.
• Impaired immune response due to asplenia
➢ May present with serious bacterial infections
“Wandering Spleen”
• Long mesentery if dorsal mesentery fails to fuse with the posterior peritoneum.
• Diagnosis made by US, CT or MR showing classic splenic tissue in abnormal
location
• May torse and lead to acute or chronic abdominal pain. Lack of enhancement
is present in complete infarction.
• Chronic torsion may lead to hypersplenism, splenomegaly, or gastric varices
Enlarged Spleen
• Moderately large
➢ Portal hypertension most common (check for cirrhosis and collaterals)
➢ Anemia
➢ Infection
➢ AIDS
• Very large (17 cm or more)
➢ Leukemia or lymphoma
➢ Infectious mononucleosis
➢ Myelofibrosis
➢ Portal hypertension
Figure 2-32-12
36 yo female with 3 days of LUQ and flank
pain. Cysts occupy the spleen (left and
center) and the gastric wall and supcapsular
regions of the spleen (right). Surgery
revealed multiple pseudocysts. The
pseudocyst in the gastric wall is a clue to
the origin of the cysts
Malignant Lesions
• Lymphoma Figure 2-32-14
• Metastases
• Angiosarcoma
Lymphoma
• Most common splenic malignancy
• Rarely as isolated lesion, usually as part
of diffuse disease
• Low grade lymphomas usually diffuse
enlargement
• Hodgkins and higher grade NHL cause Splenic hemangiomas. Left: early phase dynamic CT shows
discrete low attenuation/echogenicity markedly enhancing smooth round nodules. Right: Delayed CT
nodules. image at the same level shows delayed washout, characteristic
• Accuracy of CT prediction of splenic of a benign lesion. On CT splenic hemangiomas often show
involvement ranges from 30%-70%. diffuse bright enhancement, more than the puddling peripheral
Marked splenomegaly the best predictor enhancement seen in hepatic hemangiomas
of involvement. FDG PET reported
98%-100% accuracy in predicting splenic lymphoma
Warshauer, D. Spleen: Computed Body Tomography with MRI Correlation. Lee
JKT, Sagel SS, Stanley RJ, Heiken JP eds. Lippincott, Williams and Wilkins.
Philadelphia, PA. 2006 pp 973-1006
Lymphoma
• Often presenting with splenic enlargement, LUQ pain or fever, weight loss,
malaise.
• US: nodules are hypoechoic
• CT or MR, nodules usually not seen without contrast, but can be low signal on
T2w MRI.
Figure 2-32-15
• Post contrast (CT or MR) are less intense than normal spleen but fill in quickly
(2 min).
• Look for adjacent adenopathy
Hodgkins Lymphoma
• A 35 yr old man with past left seminoma presents
with new lymphadenopathy and focal splenic lesions.
Lymph node biopsy yielded Hodgkins lymphoma
Metastases
• Common at autopsy difficult to image except on early
arterial phase contrast imaging (CT or MR)
Diffuse Non-Hodgkins lymphoma. 22 yo male with
• Sources include islet cell tumors, melanoma, breast
fever and LUQ mass. Left: Longitudinal US shows
carcinoma and lung carcinoma
massive splenomegaly with multiple diffuse
hypoechoic lesions. Right: US guided biopsy of a
Angiosarcoma [Figure 2-32-18]
focal lesion returned non-Hodgkins lymphoma.
• Most common primary nonlymphomatous splenic
The patient died within 2 weeks of splenic rupture
malignancy
and hemorrhage
• Single or multifocal
• Aggressive growth with hemorrhage and necrosis.
• Very vascular and enhance intensely with contrast in arterial phase Figure 2-32-17
Figure 2-32-18
Abscess Evolution
• 2 weeks later
• 6 weeks later TB in the spleen. Left: original US
Right: repeat US 5 years later shows persistant splenomegaly,
Abscess now with inumerable calcifications. Patient was treated
• What caused the abscess? successfully and was assymptomatic
• How did it get to the spleen?
• Dx: Diverticulitis extending along the phrenicocolic ligament
• What else do you see? Figure 2-32-21
• Splenic artery aneurysm
Sarcoidosis
• Splenic involvement common on biopsy
(24%-59%)
• Most patients asymptomatic
• May show splenomegaly, or diffuse
hypoattenuating nodules on CT and MR
which lack peripheral enhancement Splenic abscess. 27 yo male with Crohn’s disease presents 3
• Associated abdominal weeks status post ileal and cecal resection with LUQ pain and
lymphadenopathy common fever. Left CT shows portal vein thrombus. Center CT shows
splenic vein thrombosis. Right CT shows typical rosette shaped
Trauma abscess, in this case from septic thrombophlebitis from the GI
• Spleen most frequently affected organ tract
in blunt abdominal trauma.
• Highly associated with left lower rib fractures.
• Four appearances:
➢ Lacerations (check for splenic hilar involvement) are decreased
attenuation on contrast enhanced CT-perisplenic blood or clot often more
apparent than the laceration.
➢ Intrasplenic hematoma (contusion) may be low attenuation or contain
higher attenuation clot
➢ Subcapsular hematoma: non-enhancing fluid with crescentic compression
of underlying splenic tissue.
➢ Infarcts-non-enhancing wedge shaped areas extending to the capsule.
• Severe trauma shatters the spleen into fragments.
• Active bleeding is identified as focal extravascular enhancement similar in
intensity to the aorta
Trauma
• Clinically important injury is accompanied by hemoperitoneum
Active bleeding identified as area of contrast enhancement with arterial intensity.
Surgical intervention is based on clinical stability/hypotension, lacerations involving
the hilum, and presence of pseudoaneurysms or arteriovenous fistulae
Molina PL, Quinn MT, Bouchard EW, Lee JKT. Computed Tomography of
Thoracoabdominal Trauma; Computed Body Tomography with MRI Correlation,
4th ed, Lippincott, Williams and Wilkins, Philadelphia 2006, pp1440-1429
Trauma
• Massive splenic trauma with fragmentation of the spleen, active arterial
extravasation of contrast and hemoperitoneum
Splenic Angiosarcoma
• Exceedingly rare
• Most common nonlymphoid primary malignant tumor
of the spleen
• More common in patients with thorotrast exposure Trauma. Initial CT shows tiny low attenuation
• Splenomegaly with well defined nodules or diffuse lesion (top left ) without fluid, and subtle low
involvement attenuation lesions (lower right) in an otherwise
normal spleen (lower left and upper right
Delayed Splenic Rupture
• Not predicted by degree of splenic injury
• Actual incidence unknown, but not uncommon.
• May occur days to weeks after initial injury Figure 2-32-23
Molina PL, Quinn MT, Bouchard EW, Lee JKT.
Computed Tomography of Thoracoabdominal Trauma.
Computed Body Tomography with MRI Correlation, Lee
JK, Sagel SS, Stanley RJ and Heiken JP, eds. 4th
Edition, Lippincott Williams and Wilkins, Philadelphia,
2006: 1417-1480
Sequelae of Trauma
• Injuries (lacerations, infarcts and hematomas) may
take months to a year to heal and may leave scars,
deformed splenic margins, or splenic pseudocysts.
• Uncommon injuries requiring intervention include
pseudoaneurysms or arteriovenous fistulae
Trauma. Eleven days later patient presents with
Blunt Splenic Trauma diffuse abdominal pain. Top left CT shows medial
• Initial CT for blunt trauma shows a bright area of contusion and perisplenic blood and ascites
extravasation superiorly (left) and multiple around the liver. Lower left and upper right show
lacerations more caudally (right). The patient was additional lesions. Lower right CT in the pelvis
discharged shows marked hemoperitoneum (high attenuation
ascites)
Splenic Trauma
Vascular Abnormalities
• Portal hypertension
➢ Enlarged splenic vein and/or collaterals
• Splenic vein thrombosis
➢ Infection (Crohn’s, diverticulitis)
➢ Pancreatitis
• Splenic artery thrombosis (embolic)
• Splenic artery aneurysms
• Pseudoaneurysms ((trauma, pancreatitis)
Infarcts
• Common due to arterial emboli
• Common in lymphomatous spleens which outgrow their blood supply
• Autoinfarction with sickle cell disease
Infarct Appearance
• Focal wedge-shaped peripheral lesions
• Invisible on US
• Decreased attenuation on contrast enhanced CT and low signal on T1
weighted post-Gd enhanced MRI
• May rupture with peripsplenic hematoma
Healing Infarcts
• Several months later the splenic contour is
diminished and the areas of infarction still lack
enhancement
12 Hours Later
Conclusion
• The spleen is easily evaluated on cross-sectional
imaging modalities.MRI is most sensitive for iron and
for small lesions such as diffuse Candidiasis. Round, hemoorhagic splenic infarcts. Top left US
• Anatomic variants (splenules, clefts) are common shows a large heterogenous mass with through
and should not be mistaken for pathologic transmission. The mass is avascular (upper right).
processes. Lower left Ultrasound 2 weeks later shows less
• Splenomegaly is non-specific, but usually related to fluid in the lesion with smaller diameter, indicating
hematologic abnormalities or portal hypertension. some clot retraction. Pathology specimen (lower
• Infection is acquired by hematogenous or direct right) shows 2 infarcts, the larger one
spread (splenic vein, colon, pancreas) corresponding to the US images
• Splenic infarction is often the sequelae to other
disease processes and should encourage you to
search harder to make the diagnosis
Figure 2-32-27
Classical infarcts going from superior spleen (left) to hilum (center) to inferior spleen (right)
show varying shapes of infarcts which all extend to the periphery of the spleen and lack
enhancement
References
1. Vos PM, Mathieson JR, Cooperberg PL. The Spleen In: Diagnostic Ultrasound; Rumack CM, Wilson SR, and
Charbonneau JW eds.Elsevier Mosby 2005, St Louis, pp 147-170
2. Kelekis NL, Burdeny DA, and Semelka RC. Spleen In: MRI of the Abdomen and Pelvis. Semlka RC, Ascher SM
and ReinholdC, eds. 1997, Wiley-Liss New York, NY. Pp 239-256
3. Warshaer DM. Spleen; In: Computed Body Tomography with MRI Correlation, Lee JK, Sagel SS, Stanley RJ and
Heiken JP, eds. 4th Edition, Lippincott Williams and Wilkins, Philadelphia, 2006: 973-1006
4. Molina PL, Quinn MT, Bouchard EW, Lee JKT. Computed Tomography of Thoracoabdominal Trauma; Computed
Body Tomography with MRI Correlation, 4th ed, Lippincott, Williams and Wilkins, Philadelphia 2006, pp1440-1429.
5. Molina PL, Quinn MT, Bouchard EW, Lee JKT. Computed Tomography of Thoracoabdominal Trauma. Computed
Body Tomography with MRI Correlation, Lee JK, Sagel SS, Stanley RJ and Heiken JP, eds. 4th Edition, Lippincott
Williams and Wilkins, Philadelphia, 2006: 1417-1480
SCANNING PARAMETERS
• 3MHz transducer-small footprint often preferred for intercostal approaches
• Doppler gain as high as possible without image or spectral noise
• Wall filter as low as possible to avoid false diagnosis of thrombosis
• Scale (PRF) as low as possible to localize vessels quickly with color, then
sample and angle correct for spectral Doppler
PORTAL HYPERTENSION
• Most commonly caused by cirrhosis, but may also be caused by diffuse
metastatic disease and by venous outflow obstruction.
• Color flow Doppler and spectral doppler are used in the evaluation of portal
hypertension to detect portal vein thrombosis, the presence of collaterals and
to assess bypass shunts (portocaval, splenorenal, mesocaval, and TIPS) for
patency.
• A positive diagnosis can be made by reversed (hepatofugal) flow on Doppler
or by presence of porto-systemic collaterals
eMedicine - Portal Hypertension : Article by Ali Nawaz Khan, MBBS ...
Wilson SR, Withers CE. The Liver in Diagnostic Ultrasound, Rumack, Wilson and
Charboneau eds.2005, Mosby, Inc. pp 77-146
CASE 2
• Patient with AML and rising liver function tests. Baseline examination
CASE 3 :Explain the spectral tracings in the right and left lobes
• Dx: Liver metastases with localized left-sided portal hypertension
ATYPICAL PORTAL
HYPERTENSION
• While portal hypertension is most
commonly the sequelae of cirrhosis, it
can be caused by any process which
obstructs the sinusoids including Veno-
occlusive disease, Budd Chiari
syndrome, and metastases.
• Focal flow reversal should prompt a CASE 3: 61 year old female with rising liver function tests and
search for localized disease, including jaundice. Prior Doppler ultrasound was normal.
analysis of the gray scale images Left: Doppler tracing of the right HA and PV.
Center: Gray scale transverse image of the left lobe
PORTOSYSTEMIC COLLATERALS Right: Spectral Doppler tracing of the left HA and PV. Explain
• These are diagnostic of portal the difference between the left and right lobe.
hypertension Diagnosis: Metastatic breast carcinoma with localized left portal
• Frequent locations include the hypertension
gastroesophageal junction,
paraumbilical vein in the falciform ligament, splenorenal and gastrorenal in the
left upper quadrant, intestinal veins in the retroperitoneum, and hemorrhoidal
veins in the pelvis. Visualization of the paraumbilical vein is specific for the
diagnosis of portal hypertension.
• Visualization of collaterals requires slow flow settings, and a good sonographic
window, unobscured by bowel gas
CASE 4: Can you account for the alternate flow directions in the
left and right portal veins? What is your diagnosis?
• Portal hypertension with a patent umbilical collateral vein
PORTO-SYSTEMIC SHUNTS
• These are used to decompress portal hypertension
to control bleeding
• Color Doppler is useful to assess shunt patency,
providing an adequate acoustic window is present
(may be limited in mesocaval and splenorenal
shunts)
• Intrahepatic portal venous flow should be hepatofugal
if the shunt is working properly
CASE 8: TIPS shunt. Is the portal vein flow normal
PORTOSYSTEMIC SHUNTS: TIPS or abnormal?
• These are the most common portosystemic shunt now used.
• The entrance is percutaneous from the jugular vein into the right hepatic vein
through the liver to the main portal vein.
• Spectral Doppler TIPS peak velocity is obtained in the proximal (portal venous
end), mid and distal (hepatic end) shunt. Absent flow indicates shunt occlusion
• Color flow in the intrahepatic portal veins should be toward the TIPS, and the
involved hepatic vein flow should be toward the IVC
NORMAL TIPS
ABNORMAL TIPS
• 28mm gradient between TIPS and right atrium due to tight
stenosis at the hepatic venous end which was balloon
angioplastied. Note monophasic portal wave form
Proximal TIPS Shunt Velocity
TIPS Shunt Stenosis Doppler signal from the proximal end
• Increased shunt velocity at the distal end of the shunt indicated by of the TIPS shunt. Note the increase
color Doppler aliasing in flow velocity as the cursor is
• Spectral Doppler signal demonstrates the focal distal shunt moved from the main portal vein into
stenosis, velocity is 256.7 cm/sec the shunt
CONCLUSION
• Portal venous Doppler US is an effective way to
assess the patency and function of the hepatic portal
TIPS Shunt Stenosis. (Right) Increased shunt
system.
velocity at the distal end of the shunt indicated by
• It permits rapid identification of portal flow direction
color Doppler aliasing. (Left)Spectral Doppler
and can identify collaterals, specific to portal
signal demonstrates the focal distal shunt
hypertension.
stenosis, velocity is 256.7 cm/sec
• It is particularly useful to serially monitor TIPS shunt
function
eMedicine - Portal Hypertension : Article by Ali Nawaz Khan, MBBS ...
Wilson SR, Withers CE. The Liver in Diagnostic Ultrasound, Rumack, Wilson and Charboneau eds.2005,
Mosby, Inc. pp 77-146.
References
Uterus
• Fundus
• Corpus
• Cervix
Uterine Corpus
• Serosa
➢ peritoneal reflection
• Myometrium
➢ involuntary smooth muscle
• Endometrium
➢ stratum basalis
➢ stratum functionalis
Normal cervix
Cervix [Figure 3-1-1]
• Internal os
• Endocervical canal
➢ columnar epithelium
➢ plicae palmatae
➢ surrounded by fibrous stroma and muscular layer
• External os Figure 3-1-2
➢ squamocolumnar junction
Uterine Ligaments
• Broad ligaments
➢ double sheet of peritoneum
• Cardinal ligaments
• Uterosacral ligaments
• Uterovesical ligaments
• Round ligaments
Endometrium, proliferative phase Before ovulation (days 1 – 14), the ovary is in the
follicular phase and the endometrium is in the
proliferative phase. After ovulation (days 14-28)
Figure 3-1-5b the ovary is in the luteal phase and the
endometrium is in the secretory phase
Hysterosalpingography: HSG
• First ten days of menstrual cycle
• Active PID contraindication
• Radiation dose 75–750 mrad
• Only visualizes internal contour
• Primary use tubal patency
Pelvic Protocol
• Pelvic Coil
• Coronal localizer – FMSPGR
➢ Always include kidneys
• FSE T2 – sagittal, axial,
coronal, oblique
➢ TR 4,000–5,000
➢ TE 90–130
➢ ETL 16
➢ FOV 20–24 cm
Normal Uterus: Sagittal T2WI and HSG view
➢ Thickness 4–5 mm, 1
mm gap
Figure 3-1-7
➢ Matrix 256x256
➢ 2–4 NEX
• T1 SE
➢ Axial
➢ TR 300–500
➢ TE min
• T1 Fat Sat with Gd
Uterus
• T1 – uniform intermediate
signal
• T2 – zonal anatomy
➢ Endometrium – high
signal Normal Cervix: sagittal and donut view
➢ Junctional zone – low
signal Figure 3-1-8
➢ Myometrium – intermediate signal
Normal Uterus
[Figure 3-1-6]
Normal Cervix
[Figure 3-1-7]
Embryology
[Figures 3-1-8 and 3-1-9]
Figure 3-1-9
Unicornuate / Didelphys
[Figure 3-1-11]
• Low rate of pregnancy loss
• Limited surgical options
• Unicornuate – highest rate of renal
agenesis
• Didelphys – 75% have vaginal
septum
Figure 3-1-13
Bicornuate, unicollis
Figure 3-1-15
Arcuate Uterus
[Figure 3-1-17]
Figure 3-1-16
Figure 3-1-17
At least 1 cm of remaining
myometrium should be present for
hysteroscopic resection
Arcuate uterus is a normal variant. 1 -
1.5 cm indentation
Leiomyoma
• Benign smooth muscle tumor
• Dysmenorrhea, hypermenorrhea, fertility problems
• 25% of premenopausal women
DES exposure
Leiomyoma
[Figure 3-1-19]
• Submucosal, intramural, subserosal
• Well circumscribed
• US – generally hypoechoic
• MRI – low signal on T1 and T2 unless they have
undergone degeneration
Figure 3-1-19
Adenomyosis
[Figures 3-1-21 and 3-1-22]
• Heterotopic implants of endometrium within the
myometrium
• Dysmenorrhea, hypermenorrhea
• 25% of hysterectomy specimens
Endometrial Thickness
• < 15 mm in premenopausal patient (secretory phase)
• ≤ 8mm in asymptomatic post-menopausal patient (if on hormones
scan after withdrawl bleeding)
• ≤ 4mm postmenopausal and bleeding
Figure 3-1-24
Figure 3-1-25
Endometrial Carcinoma
• Most common GYN malignancy- 33,000
cases/year
• Risk factors:
➢ unopposed estrogens, tamoxifen
➢ nulliparous
➢ diabetes
➢ obesity
MRI Findings
• Intermediate signal mass Figure 3-1-28
• Expands endometrial cavity
• Enhances less than myometrium
• Not for screening
Prognostic Factors
• Histology
• Tumor grade
• Depth of myometrial invasion
• Lymph node involvement
Endometrial carcinoma extending to serosa
Cervical Carcinoma
• 14,000 cases/year, 4,900 deaths/year
• Begins at squamocolumnar junction
• 90% are squamous cell
• Association with papilloma virus, herpes, and HIV
Cervical Carcinoma
Stage Description
0 Carcinoma in situ
I Confined to cervix
II Invades beyond cervix but not to pelvic sidewall or lower third of vagina
IIa No parametrial invasion
IIb Parametrial invasion
III Extension to pelvic sidewall / lower third of vagina / causes
hydronephrosis
IVa Invasion into bladder / rectum
IVb Distant metastases
MRI
• Intermediate signal T2WI
• Check list
➢ tumor size
➢ depth of stromal invasion
➢ parametrial invasion
➢ hydronephrosis
➢ lymphadenopathy
References
1. Bazot M, Cortez A, Darai E, et al. Ultrasonography compared with magnetic resonance imaging for the diagnosis
of adenomyosis: correlation with histopathology. Hum Reprod 2001; 16:2427-2433.
2. Davis PC, O'Neill MJ, Yoder IC, Lee SI, Mueller PR. Sonohysterographic findings of endometrial and
subendometrial conditions. Radiographics 2002; 22:803-816.
3. Nicolet V, Carignan L, Bourdon F, Prosmanne O. MR imaging of cervical carcinoma: a practical staging approach.
Radiographics 2000; 20:1539-1549.
4. Reinhold C, Khalili I. Postmenopausal bleeding: value of imaging. Radiol Clin North Am 2002; 40:527-562.
5. Reinhold C, Tafazoli F, Mehio A, et al. Uterine adenomyosis: endovaginal US and MR imaging features with
histopathologic correlation. Radiographics 1999; 19 Spec No:S147-160.
6. Scheidler J, Heuck AF. Imaging of cancer of the cervix. Radiol Clin North Am 2002; 40:577-590, vii.
7. Troiano RN, McCarthy SM. Mullerian duct anomalies: imaging and clinical issues. Radiology 2004; 233:19-34.
8. Ueda H, Togashi K, Konishi I, et al. Unusual appearances of uterine leiomyomas: MR imaging findings and their
histopathologic backgrounds. Radiographics 1999; 19 Spec No:S131-145.
Intravenous Urography
• Only good for expansile masses
• Misses 1/3 of masses <3cm
• All lesions require further work up
➢ US, CT, MRI
Ultrasound
• Cyst
➢ anechoic
➢ acoustic enhancement
➢ sharp posterior wall
• RCCA
➢ can be hypo, iso, or hyperechoic
Computed Tomography
• 94% sensitive for lesions 3 cm or less
• 90%-95% accuracy in staging
• Pre and post contrast of lesion
• Scan in both corticomedullary and nephrographic phase
Phases of Excretion
• Corticomedullary phase 25 –80 sec
• Nephrographic phase 90–120 sec
• Excretory phase 3 –5 min
➢ Varies with injection rate, cardiac output, and renal
function
Nephrographic Phase
• Renal lesions are best seen in the nephrographic phase
• 1.1 > 2.4 more masses detected Contiguous vs. overlapping
reconstruction
Venous extension
[Figure 3-2-4] Figure 3-2-3
Excretory Phase
• Decreasing density of nephrograms
• Worsening streak artifact especially with non-ionic contrast
Excretory Phase
• Decreasing density of nephrograms
• Worsening streak artifact especially with non-ionic contrast
• New role in CT urography
Enhancement
• < 10 HU no enhancement
• > 15 HU enhancement
• 10–15 HU gray zone
Calculating % Enhancement
• (Post SI – Pre SI) / Pre SI x 100 = % enhancement
Malignant Neoplasms
• Adenocarcinoma
• Uroepithelial tumors
➢ Transitional cell
➢ Squamous cell
• Lymphoma
• Metastases
Histology
• Clear cell – 70%–80%
➢ Deletion on chromosome 3p
➢ Lipid rich
• Papillary – 10%–15%
➢ Slower growing, less vascular, calcification more common, often
encapsulated, better prognosis
• Other – chromophobe, sarcomatoid, medullary, etc.
“Cystic” Changes
• 15–25% of RCCA
➢ Necrosis 75%
➢ Cystic 25% – often papillary histology
❖ Mural nodule or septations [Figure 3-2-7]
❖ Malignant cell lining (VHL)
Benign Lesions
• Simple Cyst
➢ Water density
➢ Thin (1-2 mm) wall
➢ No enhancement
• Minimally Complicated Cyst VHL with multiple RCCA
➢ High density cysts (protein or blood)
➢ Thin septations
➢ Thin curvilinear calcifications Figure 3-2-7
Surgical Lesions
• Enhancing lesions
• Nodularity
• Thick wall (>2mm)
• Thick septations
• Irregular or central calcifications
➢ Less important
Nephron-sparing Surgery
• Margins of at least 5 mm normal tissue
• < 4cm
• Away from renal hilum (polar, cortical)
• Survival rates comparable to radical nephrectomy
• RF ablation non-surgical alternative
Figure 3-2-11
Stage III
Stage IV
Abdominal CT Checklist
• Renal vein, IVC
• Regional lymph nodes
• Adrenal glands
• Contralateral kidney
• Review lung and bone windows Stage IV with invasion into the descending colon
Uroepithelial Neoplasms
• 5%–10% of all urinary tract malignancies
• Transitional cell 85%– 95%
• Squamous cell carcinoma 5%–10%
• Rare – adenocarcinoma, sarcoma, metastases
Figure 3-2-17
Sqaumous cell carcinoma with a staghorn calculus and large soft tissue
mass. SCCA often has overlapping features with XGP
Figure 3-2-18
Figure 3-2-19
Perirenal
lymphoma with
capsular
invasion
Oncocytoma
[Figure 3-2-22]
• Oncocyte – Greek “swollen cell”
• Large epithelial cells with granular eosinophilic cytoplasm (abundant
mitochondria)
• Found in kidney, salivary glands, thyroid, parathyroid, and pancreas
Multilocular cystic nephroma
Oncocytoma with herniation into the renal
• Usually asymptomatic pelvis
• Large – 7 cm avg. at detection Figure 3-2-22
• Older males
• Solid exophytic enhancing mass
• Can not distinguish from RCCA
Oncocytoma
• Helpful features – all non-specific
➢ Central scar
➢ “Spoke wheel” angio appearance
➢ Necrosis, hemorrhage, calcification rare
➢ No adenopathy or metastases
• Gross – tan/brown tumor with pale central scar
Angiomyolipoma: AML
• Renal hamartoma with blood vessels, smooth muscle, and fat
• Prevalence 0.3%–3%
• 80% sporadic
➢ Females 30–50 yo
➢ Usually solitary
• 20% tuberous sclerosis
Low-signal, non-enhancing
Angiomyolipoma: Imaging leiomyoma (capsuloma)
• Ultrasound non-specific [Figure 3-2-24]
• AML
➢ Shadowing Figure 3-2-24
➢ Markedly hyperechoic
• RCCA
➢ Hypoechoic rim
➢ Cystic spaces
• Must prove with CT or MRI
Angiomyolipoma: Imaging
• CT
➢ HU < –10 will detect 85% of AMLs
➢ No calcifications
➢ Vascular phase imaging can detect aneurysms
• MRI
➢ fat bright on T1 and T2
➢ fat saturation sequence
• Angiography
➢ Tortuous, abnormal vessels with small
aneurysms
➢ Embolization AML with shadowing
Tuberous Sclerosis
[Figure 3-2-25]
• Renal involvement
➢ Approx 3/4 will have AML
❖ 75% multiple
❖ 50% bilateral
➢ Cysts can also be seen especially in children
➢ 1%–2% develop RCCA Tuberous sclerosis with large bilateral
AMLs
References
1. Catalano C, Fraioli F, Laghi A, et al. High-resolution multidetector CT in the preoperative evaluation of patients
with renal cell carcinoma. AJR Am J Roentgenol 2003; 180:1271-1277.
2. Choyke PL, Glenn GM, Walther MM, Zbar B, Linehan WM. Hereditary renal cancers. Radiology 2003; 226:33-
46.
3. Khan A, Thomas N, Costello B, et al. Renal medullary carcinoma: sonographic, computed tomography, magnetic
resonance and angiographic findings. Eur J Radiol 2000; 35:1-7.
4. Rendon RA, Stanietzky N, Panzarella T, et al. The natural history of small renal masses. J Urol 2000; 164:1143-
1147.
5. Sheth S, Scatarige JC, Horton KM, Corl FM, Fishman EK. Current concepts in the diagnosis and management of
renal cell carcinoma: role of multidetector ct and three-dimensional CT. Radiographics 2001; 21 Spec No:S237-
254.
6. Agrons GA, Wagner BJ, Davidson AJ, Suarez ES. Multilocular cystic renal tumor in children: radiologic-
pathologic correlation. Radiographics 1995; 15:653-669.
7. Israel GM, Bosniak MA, Slywotzky CM, Rosen RJ. CT differentiation of large exophytic renal angiomyolipomas
and perirenal liposarcomas. AJR Am J Roentgenol 2002; 179:769-773.
8. Urban BA, Fishman EK. Renal lymphoma: CT patterns with emphasis on helical CT. Radiographics 2000; 20:197-
212.
9. Wong-You-Cheong JJ, Wagner BJ, Davis CJ, Jr. Transitional cell carcinoma of the urinary tract: radiologic-
pathologic correlation. Radiographics 1998; 18:123-142; quiz 148.
10. Yamakado K, Tanaka N, Nakagawa T, Kobayashi S, Yanagawa M, Takeda K. Renal angiomyolipoma: relationships
between tumor size, aneurysm formation, and rupture. Radiology 2002; 225:78-82.
GU Trauma
• Evaluate lower tract before upper tract if both may be injured Figure 3-3-1
• Males always perform retrograde urethrogram before foley is inserted if there
is blood at the meatus or pubic rami fx/diastasis
Figure 3-3-2
Normal urethral anatomy
Figure 3-3-3
Intact urethra
Urethral Trauma
[Figures 3-3-3 to 3-3-8]
Type 1 - Stretch injury
• Posterior – pelvic fractures
I – stretch
II – rupture above UGD Figure 3-3-4 Figure 3-3-5
➢ retropubic extravasation
III – rupture above and below
UGD
➢ perineal/scrotal
extravasation
IV – bladder neck and urethra
Figure 3-3-8
Type V – Anterior urethral trauma [Figures 3-3-9 and 3-3-10]
• Bony injury uncommon
• Partial/complete
➢ Corpora/venous extravasation
• Associated scrotal trauma
Complications
• Strictures
• Fistulas
Bladder Trauma
• Blunt or penetrating
• 5%–10% of pubic rami fx
• Pelvic fractures in 80% of ruptures
➢ 83% of extraperitoneal
➢ 62% of intraperitoneal
Intraperitoneal Bladder
Rupture
[Figures 3-3-13 and 3-3-14]
• 40%
• free flowing extravasation,
outlines intraperitoneal
organs
• surgical therapy Extaperitoneal bladder rupture
Figure 3-3-15
Figure 3-3-16
Ureteral Injury
• Least common site of injury (<3%) Extraperitoneal bladder rupture on CT cystogram
• Penetrating trauma – anywhere
• UPJ disruption
Figure 3-3-19
Hematoma
Figure 3-3-22
Laceration breaks through
renal capsule and causes a
perinephric hematoma
Figure 3-3-23
Segmental infarction
Figure 3-3-26
Figure 3-3-29
Figure 3-3-27
Figure 3-3-28
Figure 3-3-30
Figure 3-3-31
Figure 3-3-32
UPJ disruption
Conclusion
• If there is blood at the meatus, perform urethrogram first
• A normal bladder on CT does not rule out a leak
• Post-drainage films are key for small leaks
• Don’t forget delayed images
References
1. Ali M, Safriel Y, Sclafani SJ, Schulze R. CT signs of urethral injury. Radiographics 2003; 23:951-963; discussion
963-956.
2. Blankenship B, Earls JP, Talner LB. Renal vein thrombosis after vascular pedicle injury[clin conference]. AJR Am
J Roentgenol 1997; 168:1574.
3. Fishman EK, Horton KM. CT evaluation of bladder trauma: a critical look. Acad Radiol 2000; 7:309-310.
4. Goldman SM, Sandler CM, Corriere JN, Jr., McGuire EJ. Blunt urethral trauma: a unified, anatomical mechanical
classification. J Urol 1997; 157:85-89.
5. Herschorn S, Radomski SB, Shoskes DA, Mahoney J, Hirshberg E, Klotz L. Evaluation and treatment of blunt
renal trauma. J Urol 1991; 146:274-276; discussion 276-277.
6. Kamel IR, Berkowitz JF. Assessment of the cortical rim sign in posttraumatic renal infarction. J Comput Assist
Tomogr 1996; 20:803-806.
7. Kawashima A, Sandler CM, Corriere JN, Jr., Rodgers BM, Goldman SM. Ureteropelvic junction injuries
secondary to blunt abdominal trauma. Radiology 1997; 205:487-492.
8. Kawashima A, Sandler CM, Corl FM, et al. Imaging of renal trauma: a comprehensive review. Radiographics
2001; 21:557-574.
9. McAndrew JD, Corriere JN, Jr. Radiographic evaluation of renal trauma: evaluation of 1103 consecutive patients.
Br J Urol 1994; 73:352-354.
10. Nunez D, Jr., Becerra JL, Fuentes D, Pagson S. Traumatic occlusion of the renal artery: helical CT diagnosis. AJR
Am J Roentgenol 1996; 167:777-780.
11. Roberts JL. CT of abdominal and pelvic trauma. Semin Ultrasound CT MR 1996; 17:142-169.
Treatment
• Stents
• Steroids
• Immunosuppression
• Surgery
Neurogenic Tumors
• Nerve sheath
➢ Schwannoma (neurilemmoma), neurofibroma,
malignant nerve sheath tumor
• Ganglionic
➢ Ganglioneuroma, ganglioneuroblastoma,
neuroblastoma
• Paraganglionic
➢ Paraganglioma (pheochromocytoma)
Neurogenic Tumors
• Paraspinal masses
• Mass often elongated and well-defined
• Smooth or mildly lobular RPF with low signal on T2WI
• Generally benign
• Rapid growth, increased vascularity, poorly circumscribed suggest malignancy
Paraganglioma
(Extra-adrenal pheochromocytoma)
• About 10% of pheochromocytomas
• Most (60%–80%) have known catecholamine excess
➢ Hypertension, palpitations, sweating, tremor, diarrhea,
nausea
• More commonly malignant than adrenal pheochromocytomas
Figure 3-4-9
Figure 3-4-11
Lymphangioma
Teratoma
• Most are mature (benign) and are cured by surgery
• Children (less than 6 months) and young adults
(15–25 years)
• Female:male = 3:1
Figure 3-4-15
References
1. Engelken JD, Ros PR. Retroperitoneal MR imaging. Magn Reson Imaging Clin N Am 1997; 5:165-178.
2. Granstrom P, Unger E. MR imaging of the retroperitoneum. Magn Reson Imaging Clin N Am 1995; 3:121-142.
3. Kim T, Murakami T, Oi H, et al. CT and MR imaging of abdominal liposarcoma. AJR Am J Roentgenol 1996; 166:829-
833.
4. Nishimura H, Zhang Y, Ohkuma K, Uchida M, Hayabuchi N, Sun S. MR imaging of soft-tissue masses of the
extraperitoneal spaces. Radiographics 2001; 21:1141-1154.
5. Nishino M, Hayakawa K, Minami M, Yamamoto A, Ueda H, Takasu K. Primary retroperitoneal neoplasms: CT and
MR imaging findings with anatomic and pathologic diagnostic clues. Radiographics 2003; 23:45-57.
6. Morton A. Meyers. Dynamic Radiology of the Abdomen. Springer-Verlag. A must read book in your residency
Embryology
• Sex is chromosomally determined at fertilization
• No morphologic differentiation until week 7 (“indifferent stage”) Figure 3-5-1
• Testis determining factor on short arm of Y chromosome
➢ induces formation of seminiferous tubules
Embryologic Remnants
• Mullerian
➢ appendix testis
• Wolffian
➢ appendix epididymis
Epididymis
• Form single convoluted tubule in head (600 cm)
• Tail loosely attached inferiorly
• Exits as single tube Normal testis
Ultrasound
• Testes
➢ homogeneous low level echoes
➢ linear echogenic mediastinum testis
• Epididymis
➢ globus major (head), body, tail
➢ iso- to slightly hyperechoic
MRI
• T1WI - homogeneous intermediate signal
• T2WI - high signal with low signal mediastinum testis and linear
septations
Non Seminomatous Germ Cell Tumor MGCT with large amount of teratoma
• Mixed germ cell tumors much more common than
any pure tumor
• Heterogeneous, ill-defined
• Peak age 20’s
• Not radiosensitive
• Often higher stage and less favorable prognosis than seminoma
Tumor Markers
• Alpha-fetoprotein (AFP)
➢ from fetal liver, GI tract, and yolk sac
➢ elevated in tumors with yolk sac elements
• Human chorionic gonadotropin (HCG)
➢ produced by syncytiotrophoblasts from developing placenta
➢ elevated in tumors with choriocarcinoma (occasional seminoma)
• LDH
➢ Non-specific, correlates with bulk of disease
• Elevated in 80% of non-seminomatous tumors
Testicular Microlithiasis
• 0.6% in general population
• Present in 40% of germ cell tumors
• Usually bilateral
• Consider annual screening
Concentric rings in a
epidermoid cyst
Hydrocele
• Fluid between the parietal and visceral layers of the tunica vaginalis
• Small amount is normal
Scrotal Calculi
• Torsion of appendix or inflammatory deposits
• Repeated microtrauma
➢ bikers
• Variable size and calcification
• Mobile
Epididymal Masses
• Cyst, Spermatocele [Figure 3-5-19]
• Infection Epididymal cyst
➢ Bacterial (acute)
➢ TB (chronic)
• Tumors
Figure 3-5-20
➢ Adenomatoid tumor
➢ Papillary cystadenoma (von Hippel-Lindau)
➢ Lymphoma
• Sarcoidosis
Papillary Cystadenoma
• Associated with VHL (70%)
• 40% bilateral
• Benign
Adenomatoid tumor
Tuberculosis
• Epididymis primary site with testis secondarily
involved Sarcoidosis with marked epididymal enlargement
• 30% bilateral
• 50% will have abscess or fistulas
Acute Scrotum
• Trauma
• Epididymitis/orchitis
• Torsion
Acute Epididymitis
• Bacterial infection from lower urinary tract - chlamydia, gonococcus, E coli
• US findings - enlarged, hypoechoic, hyperemia, hydrocele, skin thickening
• 20% have associated orchitis
Orchitis
• Usually secondary to epididymitis
• May rarely be focal
• US findings - enlarged, heterogeneous echogenicity, hyperemia
• May lead to focal ischemia/infarction
Fournier Gangrene
• Diabetics or other immunosuppression
• Scrotal abscess with necrotizing infection of the perineum
• Surgical emergency
Torsion
• Gray scale US may be normal early
• Decreased or absent flow with Doppler
➢ Compare with normal side
➢ Venous compromise occurs first
• Look for mass in inguinal canal
• Testis becomes enlarged and hypoechoic with time
Torsion
• < 6 hrs at diagnosis salvage rate 80%-100%
• 12 hr salvage rate 20%
Paratesticular masses
• Varicocele
• Fibrous pseudotumors
• Polyorchidism
• Neoplasms
➢ Lipomas
✧ Half of all spermatic cord tumors
➢ Liposarcoma
➢ Rhabdosarcoma, leiomyosarcoma, MFH
➢ Mesothelioma
Varicocele
• 15% of general population
• 40% of men with infertility
• ? increased temperature
• Improved pregnancy rates (35%-50%) with repair even if
subclinical
Large varicocele
Fibrous Pseudotumor [Figure 3-5-23]
• Hylanized collagen and granulation tissue Figure 3-5-23
• Attached to tunica albuginea
• US non-specific
• MRI low signal intensity
Polyorchidism
• Abnormal division of genital ridge
• Often abnormal spermatogenesis
• Increased risk of torsion
Paratesticular Neoplasms
• Lipomas [Figure 3-5-24]
• Liposarcoma [Figure 3-5-25]
• Rhabdosarcoma
• Leiomyosarcoma
• MFH
• Mesothelioma
References
1. Black JA, Patel A. Sonography of the abnormal extratesticular space. AJR Am J Roentgenol 1996; 167:507-511.
2. Black JA, Patel A. Sonography of the normal extratesticular space. AJR Am J Roentgenol 1996; 167:503-506.
3. Bostwick DG. Spermatic cord and testicular adnexa. In: Bostwick DG, Eble JN, eds. Urologic surgcial pathology.
St. Louis: Mosby, 1997; 647-674.
4. Chung JJ, Kim MJ, Lee T, Yoo HS, Lee JT. Sonographic findings in tuberculous epididymitis and epididymo-
orchitis. J Clin Ultrasound 1997; 25:390-394.
5. Cramer BM, Schlegel EA, Thueroff JW. MR imaging in the differential diagnosis of scrotal and testicular disease.
Radiographics 1991; 11:9-21.
6. Doherty FJ. Ultrasound of the nonacute scrotum. Semin Ultrasound CT MR 1991; 12:131-156.
7. Feuer A, Dewire DM, Foley WD. Ultrasonographic characteristics of testicular adenomatoid tumors. J Urol 1996;
155:174-175.
8. Frates MC, Benson CB, DiSalvo DN, Brown DL, Laing FC, Doubilet PM. Solid extratesticular masses evaluated
with sonography: pathologic correlation. Radiology 1997; 204:43-46.
9. Geraghty MJ, Lee FT, Jr., Bernsten SA, Gilchrist K, Pozniak MA, Yandow DJ. Sonography of testicular tumors
and tumor-like conditions: a radiologic-pathologic correlation. Crit Rev Diagn Imaging 1998; 39:1-63.
10. Grebenc ML, Gorman JD, Sumida FK. Fibrous pseudotumor of the tunica vaginalis testis: imaging appearance.
Abdom Imaging 1995; 20:379-380.
11. Heaton ND, Hogan B, Michell M, Thompson P, Yates-Bell AJ. Tuberculous epididymo-orchitis: clinical and
ultrasound observations. Br J Urol 1989; 64:305-309.
12. Horstman WG, Middleton WD, Melson GL. Scrotal inflammatory disease: color Doppler US findings. Radiology
1991; 179:55-59.
13. Kassis A. Testicular adenomatoid tumours: clinical and ultrasonographic characteristics. BJU Int 2000; 85:302-
304.
14. Kim ED, Lipshultz LI. Role of ultrasound in the assessment of male infertility. J Clin Ultrasound 1996; 24:437-
453.
15. Kutchera WA, Bluth EI, Guice SL. Sonographic findings of a spermatic cord lipoma. Case report and review of the
literature. J Ultrasound Med 1987; 6:457-460.
16. Mattrey RF. Magnetic resonance imaging of the scrotum. Semin Ultrasound CT MR 1991; 12:95-108.
17. Ragheb D, Higgins JL, Jr. Ultrasonography of the scrotum: technique, anatomy, and pathologic entities. J
Ultrasound Med 2002; 21:171-185.
18. Sudakoff GS, Quiroz F, Karcaaltincaba M, Foley WD. Scrotal ultrasonography with emphasis on the
extratesticular space: anatomy, embryology, and pathology. Ultrasound Q 2002; 18:255-273.
19. Tessler FN, Tublin ME, Rifkin MD. Ultrasound assessment of testicular and paratesticular masses. J Clin
Ultrasound 1996; 24:423-436.
20. Woodward PJ, Schwab CM, Sesterhenn IA. From the archives of the AFIP: extratesticular scrotal masses:
radiologic-pathologic correlation. Radiographics 2003; 23:215-240.
21. 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; 22:189-216.
Gestational Sac
• Visualized as early as 4 - 4.5 wks (TV)
• Intradecidual sac sign [Figure 3-6-1]
• Double decidual sac sign [Figure 3-6-2]
➢ Basalis [DB]
➢ Capsularis [DC]
➢ Parietalis [DP]
Figure 3-6-2
Figure 3-6-3
a b
c d
Multiple Gestations
• # of chorions equals
# of placentas
➢ sharing is bad
➢ risk for twin/twin Normal 6.5 week embryo with
transfusion “double bleb” or “diamond ring” sign
• # of amnions equals
# of separate sacs 8 week embryo surrounded by
➢ sharing is really bad amnion
➢ risk for cord accidents
Figure 3-6-9
Figure 3-6-13
• Gestational Sac 2 mm 5 mm
• Yolk Sac TV 4 mm TV10 mm
TA 20 mm
• Embryo TV 8 mm TV 18 mm
TA 25 mm
• Heartbeat 2 mm (CRL) 5 mm (CRL)
Major: Discriminators
• MSD > 10 mm must have a yolk sac
• MSD > 18 mm must have an embryo
• CRL > 5mm must have a heartbeat
Cardiac Activity
• Must be present if embryo is > 5 mm
• 5–6 weeks 100–110 bpm
• 8–9 weeks 150–170 bpm
Yolk Sac
• First landmark in gestational sac
• In the chorionic cavity
• Abnormal findings: Anembryonic pregnancy
➢ >6mm with empty amnion
➢ irregular shape
➢ calcifications
➢ multiple yolk sacs
Ectopic pregnancy
• Tubal 95%
• Unusual locations 5%
➢ Interstitial
➢ Cervix
➢ Ovary
➢ Abdominal
• 1:50-1:200 live births
• Risks factors: IUD, prior ectopic, PID, tubal surgery,
infertility treatment
Perigestational hemorrhage
Figure 3-6-17
Figure 3-6-18
Heterotopic Pregnancy
• 1 in 30,000 spontaneous pregnancies
• 1 in 4,000 assisted pregnancies
Systemic Methotrexate
• Preserves fallopian tube
• Non-invasive
• Outpatient
• Criteria
➢ Mass < 4cm
➢ No bleeding Figure 3-6-20
➢ hCG <3,000 IU/L (2IS)
➢ No formed fetal parts
Cutting Edge
• Sonoembryology
• Early diagnosis of major malformations
• Screen for aneuploidy
➢ nuchal translucency
➢ hypoplastic nasal bone
➢ abnormal flow in ductus venosus
Nuchal Translucency
Screen for Trisomy 21 [Figure 3-6-20]
• Accredited lab
• 11-14 weeks
Increased nuchal translucency in
• >3mm abnormal
Down syndrome
• Risk assessment based on age, NT, serum screen
• High detection rates (75%-90%)
References
1. Ackerman TE, Levi CS, Dashefsky SM, Holt SC, Lindsay DJ. Interstitial line: sonographic finding in interstitial
(cornual) ectopic pregnancy. Radiology 1993; 189:83-87.
2. Brown DL, Emerson DS, Felker RE, Cartier MS, Smith WC. Diagnosis of early embryonic demise by endovaginal
sonography. J Ultrasound Med 1990; 9:631-636.
3. Brown DL, Doubilet PM. Transvaginal sonography for diagnosing ectopic pregnancy: positivity criteria and
performance characteristics. J Ultrasound Med 1994; 13:259-266.
4. Dickey RP, Olar TT, Curole DN, Taylor SN, Matulich EM. Relationship of first-trimester subchorionic bleeding
detected by color Doppler ultrasound to subchorionic fluid, clinical bleeding, and pregnancy outcome. Obstet Gynecol
1992; 80:415-420.
5. Frates MC, Brown DL, Doubilet PM, Hornstein MD. Tubal rupture in patients with ectopic pregnancy: diagnosis
with transvaginal US. Radiology 1994; 191:769-772.
6. Frates MC, Benson CB, Doubilet PM, et al. Cervical ectopic pregnancy: results of conservative treatment. Radiology
1994; 191:773-775.
7. Frates MC, Laing FC. Sonographic evaluation of ectopic pregnancy: an update. AJR Am J Roentgenol 1995; 165:251-
259.
8. Jarjour L, Kletzky OA. Reliability of transvaginal ultrasound in detecting first trimester pregnancy abnormalities.
Fertil Steril 1991; 56:202-207.
9. Jurkovic D, Gruboeck K, Campbell S. Ultrasound features of normal early pregnancy development. Curr Opin Obstet
Gynecol 1995; 7:493-504.
10. Nyberg DA, Mack LA, Laing FC, Patten RM. Distinguishing normal from abnormal gestational sac growth in early
pregnancy. J Ultrasound Med 1987; 6:23-27.
Fetal MRI
• Fast T2WI (SSFSE, HASTE)
• Safety issues
➢ No known deleterious effects
➢ Do not perform in the first trimester
➢ Do not give gadolinium
➢ Obtain informed consent
Hydranencephaly
• Absent cerebral hemispheres
• Occlusion of ICA -? etiology
➢ infection
➢ vasculitis
➢ emboli
• Falx
• Normal facial development
Figure 3-7-3
Alobar, semilobar lobar
holoprosencephaly
compared to normal.
Hydrocephalus
• Dilated ventricles and enlarged head
Ventriculomegaly
• Dilated ventricles
Signs
• Lateral ventricle > 10mm
• Medial ventricular wall to choroid > 3mm
• Dangling choroid
Figure 3-7-6
Figure 3-7-7
3-7-9
3-7-10
Hydrocephalus: Differential
• Aqueductal Stenosis
• Dandy-Walker Malformation
• Chiari II
• Communicating Hydrocephalus
Figure 3-7-13
Figure 3-7-14
1st trimester anencephaly
Occipital encephalocele
Figure 3-7-15
References
1. Chang MC, Russell SA, Callen PW, Filly RA, Goldstein RB. Sonographic detection of inferior vermian agenesis in
Dandy-Walker malformations: prognostic implications. Radiology 1994; 193:765-770.
2. Chatzipapas IK, Whitlow BJ, Economides DL. The 'Mickey Mouse' sign and the diagnosis of anencephaly in early
pregnancy. Ultrasound Obstet Gynecol 1999; 13:196-199.
3. Coleman BG, Adzick NS, Crombleholme TM, et al. Fetal therapy: state of the art. J Ultrasound Med 2002; 21:1257-
1288.
4. d'Ercole C, Girard N, Cravello L, et al. Prenatal diagnosis of fetal corpus callosum agenesis by ultrasonography and
magnetic resonance imaging. Prenat Diagn 1998; 18:247-253.
5. Ghidini A, Strobelt N, Locatelli A, Mariani E, Piccoli MG, Vergani P. Isolated fetal choroid plexus cysts: role of
ultrasonography in establishment of the risk of trisomy 18. Am J Obstet Gynecol 2000; 182:972-977.
6. Goldstein RB, LaPidus AS, Filly RA. Fetal cephaloceles: diagnosis with US. Radiology 1991; 180:803-808.
7. Johnson SP, Sebire NJ, Snijders RJ, Tunkel S, Nicolaides KH. Ultrasound screening for anencephaly at 10-14 weeks
of gestation. Ultrasound Obstet Gynecol 1997; 9:14-16.
8. Levitsky DB, Mack LA, Nyberg DA, et al. Fetal aqueductal stenosis diagnosed sonographically: how grave is the
prognosis? AJR Am J Roentgenol 1995; 164:725-730.
9. McGahan JP, Nyberg DA, Mack LA. Sonography of facial features of alobar and semilobar holoprosencephaly. AJR
Am J Roentgenol 1990; 154:143-148.
10. Pilu G, Romero R, Rizzo N, Jeanty P, Bovicelli L, Hobbins JC. Criteria for the prenatal diagnosis of holoprosencephaly.
Am J Perinatol 1987; 4:41-49.
11. Ulm B, Ulm MR, Deutinger J, Bernaschek G. Dandy-Walker malformation diagnosed before 21 weeks of gestation:
associated malformations and chromosomal abnormalities. Ultrasound Obstet Gynecol 1997; 10:167-170.
12. Vergani P, Ghidini A, Strobelt N, et al. Prognostic indicators in the prenatal diagnosis of agenesis of corpus callosum.
Am J Obstet Gynecol 1994; 170:753-758.
Neck Masses
• Neural Tube Defects Figure 3-8-1
• Cystic Hygroma
• Teratoma (Epignathus)
• Thyroid
Figure 3-8-5
Figure 3-8-4
Chest Masses
• Congenital Diaphragmatic Hernia
• Cystic Adenomatoid Malformation
• Extralobar Sequestration
• Teratoma
Figure 3-8-8
Figure 3-8-9
Sagittal scan of the fetal chest and neonatal CXR
showing type II CCAM
AIUM: Abdomen
• Stomach
• Kidneys
• Bladder
• UC insertion site Extralobar sequestration with feeding vessel from
• Umbilical cord vessel number the aorta.
Oligohydramnios
• Never normal
• A “DRIP” of fluid
➢ Demise Double bubble, oblique view confirms
➢ Renal, also bladder duodenal atresia
often anhydramnios
➢ IUGR Figure 3-8-11
➢ PROM, post dates
Fetal GI Tract
• Atresias
• Abdominal Wall Detect
Gastroschisis
Atresias
• Esophageal
• Duodenal
• Small Bowel
• Anorectal
Esophageal Atresia
• Stomach may be present but small
• Polyhydramnios after 20 wks Figure 3-8-12
• IUGR common
➢ ingested fluid important for nutrition
Jejunal/Ileal Atresia
• 1/3 have cystic fibrosis
• 5%-10% may perforate Omphalocele
• Meconium peritonitis
➢ ascites Figure 3-8-13
➢ calcifications
➢ pseudocyst formation
Bowel
• Normal bowel herniation at 8 weeks
• Rotates counterclockwise 270°
• Returns to abdomen in 12 weeks
Associations
• VACTERL Syndrome
➢ Vertebral, anal atresia, cardiac, TE fistula, renal, limb
• Inherited Disorders
➢ Meckel-Gruber (renal cystic dysplasia, encephalocele,
polydactyly)
• Chromosomal Abnormalities
➢ Trisomy 13
Autosomal recessive polycystic
Hydronephrosis kidney disease
• UPJ Obstruction
• UVJ Obstruction
• Duplications Figure 3-8-16
• PUV, Urethral Atresia
• Reflux
Figure 3-8-18
Figure 3-8-20
Figure 3-8-21
Severe posterior urethral valves
with oligohydramnios
Sacral Mass
• Sacrococcygeal teratoma
• Myelomeningocele
Ovarian cyst
Figure 3-8-22
Sacrococcygeal teratoma
References
1. Leung JW, Coakley FV, Hricak H, et al. Prenatal MR imaging of congenital diaphragmatic hernia. AJR Am J
Roentgenol 2000; 174:1607-1612.
2. Coleman BG, Adzick NS, Crombleholme TM, et al. Fetal therapy: state of the art. J Ultrasound Med 2002;
21:1257-1288.
3. Adzick NS, Harrison MR, Crombleholme TM, Flake AW, Howell LJ. Fetal lung lesions: management and
outcome. Am J Obstet Gynecol 1998; 179:884-889.
4. Lopoo JB, Goldstein RB, Lipshutz GS, Goldberg JD, Harrison MR, Albanese CT. Fetal pulmonary sequestration: a
favorable congenital lung lesion. Obstet Gynecol 1999; 94:567-571.
5. Dalla Vecchia LK, Grosfeld JL, West KW, Rescorla FJ, Scherer LR, Engum SA. Intestinal atresia and stenosis: a
25-year experience with 277 cases. Arch Surg 1998; 133:490-496; discussion 496-497.
6. Nyberg DA, Resta RG, Luthy DA, Hickok DE, Mahony BS, Hirsch JH. Prenatal sonographic findings of Down
syndrome: review of 94 cases. Obstet Gynecol 1990; 76:370-377.
7. Corteville JE, Gray DL, Langer JC. Bowel abnormalities in the fetus--correlation of prenatal ultrasonographic
findings with outcome. Am J Obstet Gynecol 1996; 175:724-729.
8. Stringer MD, McKenna KM, Goldstein RB, Filly RA, Adzick NS, Harrison MR. Prenatal diagnosis of esophageal
atresia. J Pediatr Surg 1995; 30:1258-1263.
9. Meizner I, Levy A, Katz M, Maresh AJ, Glezerman M. Fetal ovarian cysts: prenatal ultrasonographic detection and
postnatal evaluation and treatment. Am J Obstet Gynecol 1991; 164:874-878.
10. Muller-Leisse C, Bick U, Paulussen K, et al. Ovarian cysts in the fetus and neonate--changes in sonographic
pattern in the follow-up and their management. Pediatr Radiol 1992; 22:395-400.
11. Hutton KA, Thomas DF, Davies BW. Prenatally detected posterior urethral valves: qualitative assessment of
second trimester scans and prediction of outcome. J Urol 1997; 158:1022-1025.
12. James CA, Watson AR, Twining P, Rance CH. Antenatally detected urinary tract abnormalities: changing incidence
and management. Eur J Pediatr 1998; 157:508-511.
13. Abuhamad AZ, Horton CE, Jr., Horton SH, Evans AT. Renal duplication anomalies in the fetus: clues for prenatal
diagnosis. Ultrasound Obstet Gynecol 1996; 7:174-177.
ADPKD
• Occurs in 1:1000 Individuals
• Genetics: Autosomal Dominant
• ESRD in 50%
• Risk of Cancer = Not increased
Clinical Manifestations
• Pain
• Hypertension
• Infection (Women > Men)
• Stones
• Loss of Renal Function
• Renal Failure
Figure 3-9-2
Figure 3-9-3
MRI of ADPKD
Complications [Figure 3-9-6] Figure 3-9-6
• Acute Infection
Manifestations of ADPKD
• Intracranial Aneurysms
• Cardiovascular Disease: Mitral, Aortic
valve, aortic aneurysm
• Cysts: Hepatic, Pancreatic, Spleen
• Diverticula: Colon
Intracranial Aneurysms [Figure 3-9-7] Gas forming organism requiring percutaneous drainage
• ICA
➢ 18–26% of ADPKD
Figure 3-9-7
➢ Rupture ~2–11%
➢ 46–61% Mortality Rate
➢ Mean age 39–47 years of rupture
• Screening (MRA) performed periodically in patients
with ADPKD
Extrarenal Cysts
• Occur in 70–75% of ADPKD
• Complications (liver):
➢ Pain
➢ Biliary Obstruction
➢ IVC compression
Dissecting aneurysm of the abdominal aorta in
Screening ADPKD
• US Screening begins in teenage years
• ~ 2/3 of affected children will show cysts Figure 3-9-8
between 11–20
• ~ 95% by age 30
Tuberous Sclerosis
• Prevalence: 1:10,000
• Genetics: Autosomal Dominant**
• Produces hamartomas throughout the body:
• ESRD: 15% (cystic/AML bleeding)
• Risk of Cancer: 1-2% (slight increase)
➢ ** mostly new mutations; not hereditary
Types of TSC
• TSC 1
➢ 9q34
➢ ~1/3 TSC
➢ “Hamartin”
➢ Assoc with severe MR
• TSC 2
➢ 16p 13.3 !!
➢ 2/3 of TSC Typical appearance of increased
➢ “Tuberin” echogencity within the kidneys and
➢ Assoc with worse renal disease increased signal on T2W MRI in
ARPKD
Pathogenesis
• Tuberous= nodular, Sclerosis= hard
➢ Skin: Adenoma Sebaceum, Angiofibromas
➢ CNS: Tubers, Subependymal nodules, Giant Cell Astrocytoma
➢ Kidneys: Cysts, Angiomyolipomas
➢ Heart: Rhabdomyomas
➢ Lungs: Lymphangiomyomatosis (LAM)
➢ Bone: Islands
Figure 3-9-10
Renal Involvement
[Figure 3-9-12]
• Angiomyolipoma predominant
➢ Mild to severe
➢ Risk of Hemorrhage
➢ Treat conservatively
❖ Partial nephrectomy
❖ Angioembolization
❖ Radiofrequency ablation
Renal Manifestations
• Carcinoma of the Kidney
➢ 1–2% of TS patients Cystic predominant form of TSC
➢ Heterogenous solid lesions
➢ Faster growing than AMLs Figure 3-9-12
➢ No screening recommendations
Management
Risk of Metastases - 3 cm rule - Risk of Renal Failure
Figure 3-9-13
Illustrates features of non fatty angiomyolipomas; hyperdense lesions that enhance uniformly
Figure 3-9-15
Figure 3-9-17
Cystic lesions of the pancreas in VHL
Pathogenesis
• Theory 1: Dialysis Toxin
• Theory 2: Uremic Milieu Bilateral pheochromocytomas
➢ Mutations which lead to cysts, adenomas, tumors and
metastatic cancers
Figure 3-9-18
Screening
• “Screening is not routinely justified”
➢ Relatively low risk of cancer
➢ High risk of dying from other causes
➢ Reserve screening for pts with good long term prognosis
Levine E, Abdom Imaging 1995 20:569-71
References
1. Witzgall R. New developments in the field of cystic kidney diseases. Curr Mol Med 2005; 5:455-465.
2. Tahvanainen E, Tahvanainen P, Kaariainen H, Hockerstedt K. Polycystic liver and kidney diseases. Ann Med 2005;
37:546-555.
3. Adeva M, El-Youssef M, Rossetti S, et al. Clinical and molecular characterization defines a broadened spectrum of
autosomal recessive polycystic kidney disease (ARPKD). Medicine (Baltimore) 2006; 85:1-21.
4. Okumura M, Bunduki V, Shiang C, Schultz R, Zugaib M. Unusual sonographic features of ARPKD. Prenat Diagn
2006.
5. Choyke PL, Glenn GM, Walther MM, Zbar B, Linehan WM. Hereditary renal cancers. Radiology 2003; 226:33-
46.
6. Sessa A, Righetti M, Battini G. Autosomal recessive and dominant polycystic kidney diseases. Minerva Urol
Nefrol 2004; 56:329-338.
7. Herring JC, Enquist EG, Chernoff A, Linehan WM, Choyke PL, Walther MM. Parenchymal sparing surgery in
patients with hereditary renal cell carcinoma: 10-year experience. J Urol 2001; 165:777-781.
8. Seizinger BR, Smith DI, Filling-Katz MR, et al. Genetic flanking markers refine diagnostic criteria and provide
insights into the genetics of Von Hippel Lindau disease. Proc Natl Acad Sci U S A 1991; 88:2864-2868.
9. Choyke PL, Glenn GM, Walther MM, Patronas NJ, Linehan WM, Zbar B. von Hippel-Lindau disease: genetic,
clinical, and imaging features. Radiology 1995; 194:629-642.
10. Ishikawa I, Saito Y, Asaka M, et al. Twenty-year follow-up of acquired renal cystic disease. Clin Nephrol 2003;
59:153-159.
Prostate Cancer
• Diagnosis
• Staging
• Image guided Therapy
Epidemiology
• ~220,000 new diagnoses per year
➢ ~29,000 cancer deaths (USA)
➢ 2nd most common cause of cancer deaths in males
➢ 21% decrease in cancer deaths in the PSA era
Anatomy
• Zonal Anatomy of Prostate
➢ Peripheral Zone
❖ Glandular
❖ 70% of Cancers
➢ Transitional Zone
❖ Stromal/Glandular
❖ 25% of Cancers, 90% of Hyperplastic nodules
➢ Central Zone
Treatment
• A1, 2 T1 a-c Surg/XRT/WW
• B1, 2 T2 a,b Surg/XRT/WW
• C1, 2 T3 a-c XRT/WW/Hormonal
• D1 T4 XRT/WW/Hormonal
• D2 Tx, N+, M+ Hormonal/Chemotherapy
Radioactive Ablation
• Strontium-89 (Metastron)
➢ ~80% response rate
➢ Up to 6 months relief of Examples of nodal metastasis due to prostate cancer. Percutaneous biopsy
bone pain can be performed to determine if a node is positive
➢ Samarium and
Rhenium
Figure 3-10-7
Image Guided Treatment
• Brachytherapy
• Cryotherapy
References
1. Adusumilli S, Pretorius ES. Magnetic resonance imaging of prostate cancer. Semin Urol Oncol 2002; 20:192-210.
2. Campbell T, Blasko J, Crawford ED, et al. Clinical staging of prostate cancer: reproducibility and clarification of
issues. Int J Cancer 2001; 96:198-209.
3. el-Gabry EA, Halpern EJ, Strup SE, Gomella LG. Imaging prostate cancer: current and future applications. Oncology
(Huntingt) 2001; 15:325-336; discussion 339-342.
4. Engelbrecht MR, Barentsz JO, Jager GJ, et al. Prostate cancer staging using imaging. BJU Int 2000; 86 Suppl 1:123-
134.
5. Harisinghani MG, Barentsz J, Hahn PF, et al. Noninvasive detection of clinically occult lymph-node metastases in
prostate cancer. N Engl J Med 2003; 348:2491-2499.
6. Hocht S, Wiegel T, Bottke D, et al. Computed tomogram prior to prostatectomy. Advantage in defining planning target
volumes for postoperative adjuvant radiotherapy in patients with stage C prostate cancer? Strahlenther Onkol 2002;
178:134-138.
7. Hernandez J, Thompson IM. Prostate-specific antigen: a review of the validation of the most commonly used cancer
biomarker. Cancer 2004; 101:894-904.
8. Konety BR, Bird VY, Deorah S, Dahmoush L. Comparison of the incidence of latent prostate cancer detected at
autopsy before and after the prostate specific antigen era. J Urol 2005; 174:1785-1788; discussion 1788.
9. Karakiewicz PI, Eastham JA, Graefen M, et al. Prognostic impact of positive surgical margins in surgically treated
prostate cancer: multi-institutional assessment of 5831 patients. Urology 2005; 66:1245-1250.
10. Kumar R, Zhuang H, Alavi A. PET in the management of urologic malignancies. Radiol Clin North Am 2004; 42:1141-
1153, ix.
11. Mathews D, Oz OK. Positron emission tomography in prostate and renal cell carcinoma. Curr Opin Urol 2002; 12:381-
385.
12. Ravery V, Boccon-Gibod L. T3 prostate cancer: how reliable is clinical staging? Semin Urol Oncol 1997; 15:202-
206.
13. Raja J, Ramachandran N, Munneke G, Patel U. Current status of transrectal ultrasound-guided prostate biopsy in the
diagnosis of prostate cancer. Clin Radiol 2006; 61:142-153.
14. Sanchez-Chapado M, Angulo JC, Ibarburen C, et al. Comparison of digital rectal examination, transrectal
ultrasonography, and multicoil magnetic resonance imaging for preoperative evaluation of prostate cancer. Eur Urol
1997; 32:140-149.
15. Sodee DB, Nelson AD, Faulhaber PF, Maclennan GT, Resnick MI, Bakale G. Update on fused capromab pendetide
imaging of prostate cancer. Clin Prostate Cancer 2005; 3:230-238.
Learning Objectives
• Pathogenesis of renal stone disease
• Highlight CT as the modality of choice
• Alternative modalities
• Reinforce the critical role of Radiology
AFIP
• Limited Rad-Pathology
• Stone Dz
➢ Major nuisance
➢ Med/Urologic Advances
➢ Previously Debilitating
• Annual 2-3% incidence
• White male LTR is 1 in 3-8
➢ 14% @ 1yr
➢ 35% @ 5yr
➢ 52% @ 10yr
• Multi Billion $$ Cost
Genetics
• Family Hx (3 X)
• M : F : 3: 1
• Recognized D/O
➢ Familial RTA
➢ Mutations in CLCN5 gene
Extrinsic
• Climate
• Water
• Diet
• Occupation
• Stress
Predisposing Factors
• Family Hx
• Bone/GI Dz
• Gout
• Chronic UTI
• Nephrocalcinosis
• Stasis
Stone Makeup
• Composition Percent of all stones
• Ca Oxalate/phosphate 75
• Struvite/matrix 10-15
• Uric Acid 6
• Cystine 1-2
• Other (incl indinavir) <5
Heterogeneous Nucleation
• Epithelial cells
• Urinary Casts
• RBC’s
• Homogeneous Nuc---
Promoters
• Glycosaminoglycans
• Tamm-Horsfall
Aggregation
• Free crystals need to grow (2-5 min transit fm glomerulus to nephron)
• Anatomic Abnl
➢ UPJ
➢ MSK
• Lack of inhibitors Figure 3-11-1
➢ Light chain proteins
Formation Product
• Real question?
• Why don’t we all form stones
• Kf is 7-11 X Ksp
Calcium Stones
• Hyperoxaluria
➢ Crohn disease
➢ Celiac sprue
➢ Pancreatic insufficiency Figure 3-11-2
➢ Small intestinal bypass surgery for obesity
• CaPhos
➢ PTH or RTA
Cystine Stone
• Hereditary Cystinuria
➢ Three Types
➢ Auto Recessive
➢ Abnormal renal tubule transport
➢ Large amounts of cystine are excreted in the urine (10 X normal)
➢ Younger Patients
Presentation
• Autonomic System
➢ Celiac ganglion
➢ Confusion about source
➢ Diaphragm to testicle
➢ GI sx
❖ N/V
❖ Diarrhea
❖ Ileus
Figure 3-11-3
Films
• Visualize
• Characterize
• Sens 45%
• Spec 50%
IVP
• Sensitivity: 64-97%
• Specificity: 92-94%
• Still 10-15% false negative rate
CT-Radiation
4 by 2.5, 120 KVP, 120mAs,1-1.5
• 500 mrem
• 150-350 mrem for full IVP
• 13 mrem for one image
Comet Tail Sign [Figure 3-11-4] Calcifications in right pelvis demonstrating the
Comet Tail Sign
Secondary Signs
Perinephric/ureteral edema [Figure 3-11-7]
Secondary Signs
Unilateral absence of the white pyramid
[Figures 3-11-8 to 3-11-10]
Figure 3-11-6
Figure 3-11-7
Figure 3-11-8
Figure 3-11-9
Figure 3-11-10
Urologist
• Size
• Number
• Location
• Complications
Hydronephrotic Kidney
References
Testicular Torsion
• Defined as a twist of the spermatic cord or of the testis itself on its
attachments.
• Degree of ischemia relative to the amount of twisting, beginning with venous
compromise, and progressing to arterial occlusion. A 360 degree twist may still
have arterial inflow.
• Torsion most common in puberty (ages 12-18), but also occurs in neonates
and adults
Dogra VS, Gottlieb RH, Oka M, Rubens DJ. Sonography of the scrotum.
Radiology 2003;227:18-36
Bell-Clapper Deformity
Figure 3-12-3
Figure 3-12-4
TORSION/DETORSION
• History is critical-classically that of intermittent acute and sharp pain
with long symptom-free intervals
• Know which side hurts and if it still hurts during the examination.
• If scanned immediately after detorsion, the affected testis may show
increased blood flow
Figure 3-12-8
Figure 3-12-10
Figure 3-12-11
Figure 3-12-14
RT LT CASE 7: Repeat spectral Doppler
exam 10 hours later. What is your
diagnosis?
Top: Bilateral normal testes with
inadequate Doppler on initial
examination
Figure 3-12-15
Imaging Methods
• Doppler examination is 86% sensitive, 100% specific and 97% accurate* when
using absent flow in the symptomatic side as the single diagnostic criteria. If
assymmetric abnormal spectral tracing were also used for diagnosis,
sensitivity would improve
• In children, power Doppler is more sensitive than color Doppler to detect
normal flow, with rates of 97% vs 88% respectively **
*Burks DD, Markey BJ, Burkhard TK, Balsara ZN Haluszka MM, Canning DA.
Suspected testicular torsion and ischemia: evaluation with color Doppler
sonography. Radiology 1990;175:815-21
** Barth RA, Shortliffe LD. Normal pediatric testis: comparison of power Doppler
and color Doppler US in the detection of blood flow. Radiology 1997;204:389-93
Torsion Mimics/Variants
• Infarction may present with pain which mimics torsion
• Partial infarction may occur from torsion/detorsion, from vasculitis, or from
variant arterial anatomy. In some patients, the epidydimal artery, a branch of
the testicular artery, supplies the superior and anterior pole of the testis. If this
artery is hypoplastic, a small twist may result in focal infarction involving the
superior pole
• Total infarction is more unusual, but should be suspected in patients with
underlying vasculitides such as polyarteritis nodosa and systemic lupus
Artery to Epididymis
• In some patients, the epidydimal artery, a branch of the testicular artery,
supplies the superior and anterior pole of the testis. If this artery is hypoplastic,
a small twist may result in focal infarction
References
1. Barth RA, Shortliffe LD. Normal pediatric testis: comparison of power Doppler and color Doppler US in the
detection of blood flow. Radiology 1997;204:389-93.
2. Burks DD, Markey BJ, Burkhard TK, Balsara ZN Haluszka MM, Canning DA. Suspected testicular torsion and
ischemia: evaluation with color Doppler sonography. Radiology 1990;175:815-21
3. Dogra VS, Bhatt S, Rubens, DJ. Sonographic Evaluation of Testicular Torsion. Ultrasound Clin 2006; 1:55-66 with
permission.
4. Dogra VS, Gottlieb RH, Oka M, Rubens DJ. Sonography of the Scrotum. Radiology 2003;227:18-36
5. Dogra VS, Sessions A, Mevorach R, Rubens DJ Reversal of diastolic plateau in partial testicular torsion. J Clin
Ultrasound 2001; 29:105-108
6. Donohue RE, Utley WL. Urology 1978 11:33
7. Middleton WD, Middleton MA, Dierks M, et al. Sonographic prediction of viability in testicular torsion:
preliminary observation. J Ultrasound Med. 1997;16:23–27.
Ovarian Masses
• Non-neoplastic
➢ physiologic cyst, endometriosis, etc.
• Neoplastic
➢ epithelial tumors 65%
➢ germ cell tumors 25%
➢ sex-cord stromal tumors 5%
➢ secondary malignancies 5%
➢ gonadoblastoma <1%
Figure 3-13-5
Serous
cystadenocarcinoma Serous cystadenoma (LMP)
Ovarian Masses
• Non-neoplastic
➢ Physiologic cyst, endometriosis, etc.
• Neoplastic
➢ Epithelial tumors 65%
➢ Germ cell tumors 25%
➢ Sex-cord stromal tumors 5%
➢ Secondary malignancies 5%
➢ Gonadoblastoma <1%
Doppler sonography*
• ideally, should allow more specificity and sensitivity for malignancy
• based on low resistance flow (high diastolic flow) in malignant neovascularity
• significant overlap with benign processes, especially in pre-menopausal
women
* = controversial
Post-menopausal patient
• simple cyst <16 mm: ignore
• simple cyst 16–50 mm: follow-up 4 months
➢ presumed serous inclusion cyst vs. benign neoplasm
• simple cyst > 50 mm OR any complex lesion: consider surgery
1. Gajewski W, Legare RD. Ovarian cancer. Surg Onc Clin N Am 1998; 7:317.
2. Hricak H, Chen M, Coakley FV. Complex adnexal masses: detection and characterization with MR imaging --
multivariate analysis. Radiology 2000; 214:39.
3. Jung SE, Lee JM, Rha SE, Byun JY, et al. CT and MR Imaging of Ovarian Tumors with Emphasis on Differential
Diagnosis. Radiographics 2002; 22:1305.
4. Kawamoto S, Urban BA, Fishman EK. CT of epithelial ovarian tumors. Radiographics 1999; 19:S85.
5. Kinkel K, Lu Y, Mehdizade A, et al. Indeterminate ovarian mass at US: incremental value of second imaging test
for characterization – meta-analysis and Bayesian analysis. Radiology 2005; 236:85-94.
6. Koonings PP, Campbell K, Mishell DJ, Grimes DA. Relative frequency of primary ovarian neoplasms: a 10-year
review. Obstet Gynecol 1989; 74:921-926.
7. Kurtz AB, et al. Diagnosis and Staging of Ovarian Cancer: Comparative Values of Doppler and Conventional US,
CT, and MR Imaging Correlated with Surgery and Histopathologic Analysis—Report of the Radiology Diagnostic
Oncology Group. Radiology 1999; 212:19.
8. Outwater EK, Wagner BJ, Mannion C, McLarney JK, Kim B. Sex-cord stromal and steroid cell tumors of the ovary.
RadioGraphics 1998; 18:1523.
9. Patel MD, Feldstein VA, Lipson SD, Chen DC, and Filly RA. Cystic teratomas of the ovary: diagnostic value of
sonography. Am J Roentgenol 1998; 171:1061-1065.
10. Siegelman ES, Outwater, EK. Tissue Characterization in the Female Pelvis by Means of MR Imaging. Radiology
1999; 212:5.
11. Sironi S, Messa C, Mangili G, Zangheri B, et al. Integrated FDG PET/CT in Patients with Persistent Ovarian Cancer:
Correlation with Histologic Findings. Radiology 2004; 233:433.
12. Tanaka YO, Tsunoda H, Kitagawa Y, Ueno T, et al. Functioning Ovarian Tumors: Direct and Indirect Findings at
MR Imaging. RadioGraphics 2004; 24:S147.
13. Wagner BJ, Buck JL, Seidman JD, McCabe KM. Epithelial Neoplasms of the Ovary: Radiologic-Pathologic
Correlation. RadioGraphics 1994; 14:1351.
14. Woodward PJ, Hosseinzadeh K, Saenger JS. Radiologic Staging of Ovarian Carcinoma with Pathologic Correlation.
RadioGraphics 2004; 24:225.
Neoplastic
• Adenoma
• Metastasis
• Lymphoma
• Pheochromocytoma
• Adrenocortical Carcinoma
• Myelolipoma
• Hemangioma (rare)
Non-neoplastic
• Hemorrhage
• Inflammation
• Hyperplasia
• Cyst
• Pseudocyst*
*may be secondary to neoplasm (adenoma)
Adrenal adenoma
Adenoma radiology
• CT findings (NCCT):
➢ small, homogeneous
➢ hypodense due to lipid content (< 18HU?, <15HU?,
<10HU?) Degenerating adenoma
• CT findings (CECT):
➢ decreased enhancement compared to metastasis, etc.
➢ rapid wash-out of contrast? Figure 3-14-3
• Some adenomas are “lipid poor”
• A mass that does not satisfy the density requirements for an
adenoma may still be an adenoma (biopsy or washout study
required?)
• A mass that does not decrease in signal on an opposed phase
image may still be an adenoma
• MR (opposed phase imaging) [Figure 3-14-3]
➢ spleen used as internal reference
➢ visual assessment is generally adequate, although signal
intensity ratios of lesion:spleen may be used
• Opposed phase MRI operates on the same principle (lipid
content) as non-contrast CT, therefore will generally add little to
the patient work-up* (i.e. an indeterminate lesion by CT will likely
be indeterminate on opposed phase MRI).
* controversial
Myelolipoma Myelolipoma
Algorithm
• NCCT:
➢ If less than 10 HU, it’s an adenoma [STOP]
➢ If more than 10 HU, proceed to:
• CECT: (dynamic and 15* minute delay)
❖ If less than 30* HU on delayed scan = adenoma ?
❖ If more than 30 HU on delayed scan, what is washout value
* = controversial
• Opposed phase MRI (OPMRI)
➢ decrease in signal relative to spleen = adenoma → no further evaluation
needed
➢ no decrease → biopsy
➢ indeterminate → consider CT evaluation [will probably need
“washout”/delay scans because the lipid content is probably too small to
make the lesion sufficiently hypodense]
References
1. Blake MA, Kalra MK, Sweeney AT, et al. Distinguishing beinign from malignant adrenal masses: multi-detector
row CT protocol with 10-minute delay. Radiology 2005; 238:578-85.
2. Blake MA, Slattery JMA, Kalra MK, et al. Adrenal lesions: characterization with fused PET/CT image in patients
with proved or suspected malignancy – initial experience. Radiology 2006; 238:970-77.
3. Caoili EM, Korobkin M, Francis IR, et al. Adrenal masses: characterization with combined unenhanced and delayed
enhanced CT. Radiology 2002; 222:629-33.
4. Elsayes KM, Narra VR, Leyendecker JR, et al. MRI of adrenal and extraadrenal pheochromocytoma. Am J Roentgenol
2005; 184:860-67.
5. Haider MA, Ghai S, Jhaveri K, Lockwood G. Chemical shift MR imaging of hyperattenuating (>10 HU) adrenal
masses: does it still have a role? Radiology 2004; 231:711.
6. Kenney PJ, Wagner BJ, Rao P, Heffess CS. Myelolipoma: CT and pathologic features. Radiology 1998; 208: 87-
95.
7. Korobkin M. CT characterization of adrenal masses: the time has come. Radiology 2000; 217:629.
8. Mayo-Smith WW. CT characterization of adrenal masses (letter). Radiology 2003; 226:289.
9. Savci G, Yazici Z, Sahin N, et al. Value of chemical shift subtraction MRI in characterization of adrenal masses. Am
J Roentgenol 2006; 186:130-53.
Outline
• Bladder Figure 3-15-1
➢ filling defects
➢ wall thickening (+/– calcification)
➢ abnormal contour
• Urethra
➢ anatomy
➢ filling defects
➢ obstructive processes (strictures, valves)
Urachal Anomalies
• patent urachus
• umbilical-urachal sinus
Urachal carcinoma
• vesico-urachal diverticulum
• urachal cyst
Genitourinary Radiology 649 Imaging of the Urinary Bladder and Urethra
Filling Defects: (may be mobile) Figure 3-15-3
• clot
➢ often smooth
• stones
➢ shadowing on U/S, midline on supine radiograph
➢ occasionally radiolucent (or obscured) post-contrast
➢ history of infection (and/or)
➢ evidence for bladder outlet obstruction
❖ trabeculation
❖ hydroureter
❖ prostate impression
• fungus ball
➢ laminated, gas-containing
Malakoplakia
• most common in females with recurrent infection
• mimics infiltrating carcinoma
➢ cysto/bx to diagnose
• Michaelis-Gutman bodies
Tuberculosis
Schistosomiasis
• calcification in 50%
• calcification is rare in transitional / urothelial carcinoma
• Schistosomiasis is a risk factor for squamous cell ca of the bladder
Emphysematous cystitis
• urinary tract combined with uncontrolled diabetes mellitus
• gas may be intraluminal* as well as intramural
➢ linear, lucent streaks
• non-surgical condition
• treatment: antibiotics and insulin
• * if gas is only intraluminal, consider fistula
Abnormal contour
• smooth narrowing:
➢ pelvic lipomatosis
➢ pelvic hematoma
➢ (irregular narrowing = lymphoma, other mass?)
• focal outpouching (diverticula):
➢ bladder outlet obstruction
➢ stones/tumors/bleeding
➢ reflux/ureteral obstruction
❖ (especially in children)
Urethra: Anatomy
• posterior:
➢ prostatic
➢ membranous
• anterior:
➢ bulbous
➢ penile
Condyloma acuminata
1. Beer A, Saar B, Rummeny EJ. Tumors of the urinary bladder: technique, current use, and
perspectives of MR and CT cystography. Abdom Imaging 2003; 28:868.
2. Hahn WY, Israel GM, Lee VS. MRI of female urethral and periurethral disorders. Am J
Roentgenol 2004; 182:677-82.
3. Pavlica P, Menchi I, Barozzi L. New imaging of the anterior male urethra. Abdom Imaging 2003;
28:180.
Yu J-S, Kim KW, Lee H-J, Lee Y-J, et al. Urachal remnant diseases: spectrum of CT and US findings.
RadioGraphics 2001; 21: 451.
Outline
• Clinical and imaging characteristics of common non neoplastic ovarian and
adnexal pathology
• Role of CT / MR
• Gestational trophoblastic disease
Figure 3-16-1
Follicular cyst of left ovary with resolution one month later. a. initial
transabdominal ultrasound. b. initial transvaginal ultrasound. Echoes
are artefactual. c. Follow up.
MR of normal ovaries. a. T1-w image: left ovary (arrow) is isointense to muscle. On T2-w (b
and c) images the right and left ovaries (arrows) contain multiple high signal follicles
Corpora Lutea
Symptomatic functional a. Sagittal and b. coronal T2-w MRI showing a right sided follicular
cysts cyst (arrow) with surrounding ovarian parenchyma
• Internal hemorrhage
• Rupture
➢ May rupture and bleed into peritoneal cavity with peritoneal
Figure 3-16-4
signs and hypotension
➢ Or rupture with simple free fluid
Figure 3-16-6
Hyperstimulation Cysts
• Bilateral enlarged ovaries
• Multiple large cysts
• May bleed, rupture or torse
• OHSS associated with ascites, pleural
effusion, hemorrhage, DIC
Endometriosis
• Functioning ectopic endometrium
• Pelvic peritoneum, ovary, tube
Endometriosis Acute pain and pelvic guarding. Bleeding from left corpus
• Symptoms luteum cyst * into peritoneal cavity. U= uterus
➢ Dysmenorrhea
➢ Dyspareunia
➢ Pelvic pain
• Cyclic pain with menses
• Associated with infertility
➢ Prevalence 25%
Endometriosis:
MR Technique
• Axial T1-w SE Ground glass appearance of endometriotic cyst. a. Transabdominal
• *Axial fat-suppressed T1-w SE to and b. transvaginal ultrasound. Note homogeneous internal echoes
distinguish fat from blood* and posterior acoustic enhancement
• Axial/sagittal/coronal T2-w FSE
• Dynamic enhanced T1-w (optional)
Endometrioma: MR
• Less specific signs
➢ Multiple homogeneous hyperintense lesions on
T1-w and T2-w
➢ Low signal hemosiderin ring
➢ Enhancement of cyst wall/peritoneum Homogeneous endometriomas (*) with mural
reflectors (arrows)
Endometrioma
Rectus Endometriosis
Diffuse Endometriosis
• More common Figure 3-16-12
• Associated with fibrosis and adhesions
• Laparoscopy is gold standard allows
staging and treatment
• MR may be useful for inaccessible
sites or for evaluation of response to
medical treatment
High T1 signal ovarian endometrioma with no suppression on
fat sat. Low signal “shading” on FSE T2
Ovarian Torsion - US
• Gray scale non specific, depends on cause
➢ Most suggestive: ipsilateral enlarged hypoechoic ovary (+/-
peripheral follicles)
➢ Mass e.g. teratoma, functional cyst
➢ Hemorrhagic infarction
➢ Associated thickened fallopian tube
Figure 3-16-15
Torsion of Cystadenoma*
Figure 3-16-18
Hydrosalpinx/Pyosalpinx
Hydrosalpinx
Acute Salpingitis
Figure 3-16-21
Figure 3-16-23
Figure 3-16-24
Paraovarian Cysts
• Simple unilocular adnexal cyst
• Separate from ovary
• Lack of change with time
• Rarely bilateral or multiple or complex
Benign Mole
Classic “complete” mole Partial mole
➢ 80% Triploid
➢ 46 XX 69 XXY 80%
➢ Complete molar change 69 XXX
➢ No fetal tissue Hydropic placenta
➢ Nuclear DNA paternal 0.5% malignant change
➢ 10% malignant change
Partial Mole
• Triploid fetus
➢ IUGR, anomalies
• Hydropic placenta
• Spontaneous abortion
Malignant GTD
• Invasive mole
➢ Locally invasive, non metastatic, <10%
➢ Vesicular chorionic villi with myometrial invasion
• Choriocarcinoma Figure 3-14-28
➢ 5%, hematogenous metastases to lungs, brain, liver, etc.
➢ May not necessary follow a gestation
➢ No villous structure
Figure 3-16-27
References
1. Albayram F, Hamper UM. Ovarian and adnexal torsion: spectrum of sonographic findings with pathologic
correlation. J Ultrasound Med 2001;20:1083-1089.
2. Bennett GL, Slywotzky CM, Giovanniello G. Gynecologic causes of acute pelvic pain: spectrum of CT findings.
Radiographics 2002;22:785-801.
3. Christensen JT, Boldsen JL, Westergaard JG. Functional ovarian cysts in premenopausal and gynecologically
healthy women. Contraception 2002;66:153-157.
4. Descargues G, Tinlot-Mauger F, Gravier A, Lemoine JP, Marpeau L. Adnexal torsion: a report on forty-five cases.
Eur J Obstet Gynecol Reprod Biol 2001;98:91-96.
5. Green CL, Angtuaco TL, Shah HR, Parmley TH. Gestational trophoblastic disease: a spectrum of radiologic
diagnosis. Radiographics 1996;16:1371-1384.
6. Hertzberg BS, Kliewer MA, Paulson EK. Ovarian cyst rupture causing hemoperitoneum: imaging features and the
potential for misdiagnosis. Abdom Imaging 1999;24:304-308.
7. Jain KA. Imaging of peritoneal inclusion cysts. AJR Am J Roentgenol 2000;174:1559-1563.
8. Lee EJ, Kwon HC, Joo HJ, Suh JH, Fleischer AC. Diagnosis of ovarian torsion with color Doppler sonography:
depiction of twisted vascular pedicle. J Ultrasound Med 1998;17:83-89.
9. Levine D, Gosink BB, Wolf SI, Feldesman MR, Pretorius DH. Simple adnexal cysts: the natural history in
postmenopausal women. Radiology 1992;184:653-659.
10. Okai T, Kobayashi K, Ryo E, Kagawa H, Kozuma S, Taketani Y. Transvaginal sonographic appearance of
hemorrhagic functional ovarian cysts and their spontaneous regression. Int J Gynaecol Obstet 1994;44:47-52.
11. Pache TD, Wladimiroff JW, Hop WC, Fauser BC. How to discriminate between normal and polycystic ovaries:
transvaginal US study. Radiology 1992;183:421-423.
12. Patel MD, Feldstein VA, Chen DC, Lipson SD, Filly RA. Endometriomas: diagnostic performance of US.
Radiology 1999;210:739-745.
13. Rha SE, Byun JY, Jung SE, et al. CT and MR imaging features of adnexal torsion. Radiographics 2002;22:283-
294.
14. Sam JW, Jacobs JE, Birnbaum BA. Spectrum of CT findings in acute pyogenic pelvic inflammatory disease.
Radiographics 2002;22:1327-1334.
15. Siegelman ES, Outwater EK. Tissue characterization in the female pelvis by means of MR imaging. Radiology
1999;212:5-18.
16. Sohaey R, Gardner TL, Woodward PJ, Peterson CM. Sonographic diagnosis of peritoneal inclusion cysts. J
Ultrasound Med 1995;14:913-917.
17. Sugimura K, Okizuka H, Imaoka I, et al. Pelvic endometriosis: detection and diagnosis with chemical shift MR
imaging. Radiology 1993;188:435-438.
18. Togashi K, Nishimura K, Kimura I, et al. Endometrial cysts: diagnosis with MR imaging. Radiology 1991;180:73-
78.
19. Wagner BJ, Woodward PJ, Dickey GE. From the archives of the AFIP. Gestational trophoblastic disease:
radiologic-pathologic correlation. Radiographics 1996;16:131-148.
20. Woodward PJ, Sohaey R, Mezzetti TP, Jr. Endometriosis: radiologic-pathologic correlation. Radiographics
2001;21:193-216; questionnaire 288-194.
Transplantation
• Higher success rates with better anti rejection therapy, patient selection and
surgical techniques
• Rejection remains major cause of graft loss
• Immunosuppression predisposes to infection and neoplasm
• Symptoms and signs of infection subtle
• High index of suspicion
Types of Transplants
• Renal
• Pancreas
• Liver
Post-transplantation Imaging
• Ultrasound -- primary modality
➢ Parenchymal echotexture
➢ Blood supply
➢ Fluid collections
➢ Specific complications
➢ Guidance for interventional procedures
Post-transplantation Imaging
• CT
➢ Collections
➢ Infection
➢ Surgical Complications
➢ Neoplasm
➢ Guidance for procedures
Post-transplantation Imaging
• MRI and MRA
➢ Parenchyma
➢ Vascular complications
➢ Masses
➢ Rejection?
Post-transplantation Imaging
• Other
➢ Scintigraphy
➢ Cystography
➢ Cholangiography
➢ Arteriography and intervention
Renal Transplants
• CRT: Cadaveric renal transplant
• LRT: Living related renal transplant
• LNRT: Living non-related renal transplant
• Dual: “En bloc” pediatric or two adult
• SPK: Simultaneous pancreas-kidney
Resistive Index
RI= (PSV–EDV)
PSV
Complications
• Perinephric fluid collections (50%)
• Rejection – acute and chronic
• Obstruction (1–10%)
• Vascular Complications (10%)
• Acute tubular necrosis (DGF)
• Cyclosporine toxicity
• PTLD (1%)
• Torsion
Abscess
Hydronephrosis
• Early: edema of UVJ
• Late:
Compression by fluid
collections
➢ Denervation (non
obstructive)
➢ Full bladder (repeat with
empty bladder)
➢ Ureteric ischemia,
surgical technique Cystogram showing extra luminal contrast (arrow) from ureteral leak.(Left)
(kinks) Renogram showing collection of radioactivity (arrow) inferomedial to
➢ Rejection transplant and non visualization of bladder (Right)
➢ Intraluminal clot or
calculi
Figure 3-17-5
Ureteral Stricture [Figure 3-17-5]
Echoes Within
Collecting System
• Hemonephrosis
➢ Low level echoes
➢ Move with patient
➢ Hematuria
➢ Post biopsy: look for
AVF
➢ Urinary infection
Hemonephrosis
[Figure 3-17-6]
a. Hydronephrosis with clot in collecting system. b. Clot in bladder. c. CT showing high density
blood in left transplant ureter (arrow) and d. clot in bladder (arrow) as well as Foley catheter
Nephrocalcinosis
Gas/Stent
Rejection
• Non specific elevation of creatinine
• Fever, white count, pain over transplant
• Decreased urine outpout
• Acute (> 5 days) reversible with treament
• Chronic (months to years) irreversible
Acute Rejection
[Figure 3-17-7]
Thick Urothelium
[Figure 3-17-8]
Acute Rejection
[Figure 3-17-9] Circumferentially thickened renal pelvis (arrow) in acute rejection
• Vascular rejection results in
increased resistance with increase in resistive index
• Correlation highly variable
• Threshold? 0.7 or 0.9 Figure 3-17-9
Acute rejection
• BIOPSY - only reliable method to
determine cause of renal dysfunction
Chronic Rejection
• Small allograft
• Echogenic from fibrosis
• Fatty replacement
• Calcification High resistance arterial waveforms with reversal of diastolic
• Decreased blood flow flow in main renal artery and absence of diastolic flow in
interlobar arteries
Tardus Parvus
Arteriovenous Fistula
[Figure 3-17-12]
Arteriovenous Fistula
Embolization [Figure 3-17-13]
Pseudoaneurysms
[Figure 3-17-14]
• Gray scale
➢ Simple or complex cyst
• Doppler
➢ Yin yang swirling disorganized flow
➢ To and fro (neck)
• May rupture a. Color; b. Power Doppler of perivascular thrill.
c. duplex of artery and d. of draining arterialized vein
Renal Vein Stenosis
• Perivascular fibrosis
• Compression by fluid collections
• Doppler Figure 3-17-13
➢ Aliasing
➢ Velocity increase (x3–4)
Pancreas Transplants
• SPK: Simultaneous pancreas-kidney
• PAK: Pancreas after kidney
• PTA: Pancreas transplant alone
Pancreatic Transplantation:
Surgical Technique Selective renal arteriography. a. abnormal distal arterial branch
• Endocrine Drainage (Venous) with early venous filling (arrow). b. Prompt filling of renal and
➢ Systemic (iliac vein) iliac veins. c. Post embolization, the av fistula is no longer
➢ Portal vein visualized
• Exocrine Drainage
➢ Bladder
➢ Enteric
• Arterial supply from common iliac artery Figure 3-17-14
SPK
• Systemic bladder drainage
• Portal enteric drainage
Pancreatic Transplant
Complications
• Rejection Acute and Chronic
• Surgical complications a. Gray scale; b. color and c. duplex Doppler of
➢ Infection pseudoaneurysm.
➢ Anastomotic Leak Note to and fro flow in neck of pseudoaneurysm (arrow)
• Vascular thrombosis Arterial / Venous
• Pancreatitis
Pancreas Transplant CT
[Figure 3-17-16]
Pancreatic Transplant MR
Peripancreatic Collections
• 2-10%
• Hematoma, seroma, anastomotic leak,
abscess
• Nonspecific appearance
• Aspiration needed for diagnosis
Pancreatic Thrombosis
[Figure 3-17-18]
Liver Transplantation
• Established or fulminant liver failure
(hepatitis C, PBC, PSC, alcolhol,
cryptogenic cirrhosis, etc.)
• Cadaveric
• Living or cadaveric split liver (right lobe)
Reformatted coronal CT showing pancreas transplant * and
Liver Transplantation vessels (arrows)
• Gray scale evaluation includes
➢ Fluid collections
➢ Free fluid (ascites or bile) Figure 3-17-17
➢ Biliary dilatation – choledochojejunostomy or
choledocholedochostomy
➢ Parenchyma
Liver transplantation
• Doppler evaluation includes
➢ MPV, LPV, RPV
➢ CHA, LHA, RHA
➢ HV x 3
➢ IVC above and below anastomosis
MRA
• Normal
• Hepatic artery thrombosis
Cavernous Transformation
Biliary Tree
Collections
Lymphadenopathy
Summary
• Ultrasound with color and duplex Doppler is an ideal first line modality for
renal, pancreas and liver transplants
• Sensitive for vascular complications, fluid collections and hydronephrosis
• Biopsy needed for diagnosis of rejection
• CT for infection, fluid collections, procedures, malignancy
• MR for evaluation of vascular and parenchymal abnormalities
References
Goals
• Review normal nephrographic physiology
• Present 6 abnormal patterns with the respective differential diagnosis
Normal - Nephrographic
- Physiology
Normal Pyelogram
[Figures 3-18-1 and 3-18-2]
• Symmetric
• 3 minute film
• Delayed side is the diseased side
No Blood Out
Figure 3-18-6
Figure 3-18-8
Autonephrectmy from
renal tuberculosis. Top,
KUB shows multiple ill- Figure 3-18-9
defined calcifications in
the left kidney. Bottom,
IVP shows no function
Figure 3-18-11
Figure 3-18-13
Figure 3-18-14
Pyelonephritis
• Rarely produces a unilateral hyperdense nephrogram (unless
there is tubular or pelvic obstruction with pus)
ATN
• Tubular damage and obstruction
• Decrease blood flow
• “Acute vasomotor nephropathy”
Renogram
• ATN
• Bilateral ureteral obsruction
• Bilateral renal artery stenosis Acute tubular necrosis. Axial CT
(contrast 3 days ago): There are
persistent bilateral nephrograms with
delayed pyelograms
#6 Striated Nephrogram
[Figure 3-18-21]
• ARPCK
• Acute Pyelo
• Obstruction
• RVT
• Contusion
• Hypotension
• Tubular Obst
• Normal
References
1. Davidson AJ, Hartman DS, Choyke PL, Wagner BJ. Davidson’s Radiology of the Kidney & Genitourinary Tract 3rd
Edition, W.B. Saunders Philadelphia 1999.
Learning Objective
• To use radiological imaging for the characterization and management of the
problematic renal mass
Cell Cycle
• Proliferation
• Programmed death (Apoptosis)
Neoplasia
• Results from disequilibrium of proliferation and cell death
Carcinoma In Situ
• Confined by basement membrane
• Stops expanding after reaching diffusion limit of the nearest vessel
• “No” metastatic potential
• Very, very common
Carcinoma In Situ
• Most human tumors exist as in situ lesions
➢ 0.2– 2 mm
• Renal CIS is found in 22% of autopsies
Angiogenic Phenotype
• Ability to recruit host blood supply
• Penetrate basement membrane
• May enlarge to become macroscopic
Vascular Invasion
• Tumor shedding and vascular invasion may occur relatively early
• In animal models, tumors shed 3-6 million cells per Gram per 24 hours
• Most cells which are shed do not progress to viable metastases
Metastasis
• Very imprecise at knowing which, where and when RCC will metastasize
• Mets require activation of genes
• Each metastasis must become angiogenic to grow
Pathology / Radiology
Management Options
• Excise
• Ablation
• Follow
• Biopsy
• Nephrectomy
• Ignore
Always Consider
• Pretest probability Enhanced CT scans of 2 different patients both of
• Patient’s ability to tolerate uncertainty which have a lesion which is too small to
• Your ability to tolerate uncertainty characterize. Left, renal cell carcinoma; right,
renal cyst
How Should The TSTC Mass Be Managed?
• There is no large, prospective, pathologically proven series which indicates
correct management
Caveats
• The portion of the cystic mass which is most worrisome should be used in
deciding appropriate management.
• In cases with discordant imaging findings utilizing different radiological
examinations, the lesion should be managed based upon the most aggressive
imaging findings
Guidelines
• Ignore
• Excise
• Follow
Calcification
• Ignore
➢ “Small” amount
➢ Smooth
➢ Septal
➢ Milk of calcium
➢ No enhancement
Figure 3-19-5
Hyperdense/High Signal
• Ignore
➢ Sharp margin
➢ < 3 cm
➢ Not completely intrarenal
➢ Homogeneous or hematocrit
➢ No enhancement
➢ US: cyst or cystic
Significant Enhancement
• CT
➢ <10 H.U.=Beam hardening
➢ 10-15 H.U.=Indeterminate
➢ >15 H.U.=Vascularity
Hyperdense/High Signal
• Excise
➢ Poorly defined
➢ Heterogeneous
➢ Enhancement
➢ US: solid
• Follow
➢ Totally intrarenal
➢ > 3 cm
Septation
• Ignore
➢ Thin (< 1 mm)
➢ Smooth
➢ May calcify
➢ No enhancement
• Excise
➢ Thick, irregular
➢ Nodular
➢ Enhancement
• Follow
➢ Only slightly “greater than hairline”
ML-RCC
MLCN ML-RCC
• Female Male
• No Blood Blood
• Pelvic Herniation Venous Invasion
• Usually Benign Always Malignant
Enhancement
• Excise
➢ All enhancing masses
Wall Thickening
• Excise
➢ All noninfected masses with wall thickening
Figure 3-19-10
Figure 3-19-13
Figure 3-19-14
Figure 3-19-15
Minimally enhancing
hyperdense papillary renal cell
carcinoma. Top, unenhanced
CT scan: the mass measures
Hyperdense cyst which should be followed. Left, unenhanced
29 HU. Center, enhanced CT
CT: the 6 cm mass is homogeneous and measures 68 HU.
scan, nephrographic phase:
Center, enhanced CT, the mass remains homogeneous and
the mass enhanced 13.5 HU to
does not enhance. Right, ultrasound: the mass is cystic with a
42.5 Bottom, enhanced CT,
thin septation. Because the mass is greater than 3cm it should
pyelogram: the mass de-
be followed
enhances to 36 HU
Figure 3-19-18
Figure 3-19-19
2 different multiloculated
masses. Top: multilocular
cystic nephroma. Bottom:
multiloculated renal cell
carcinoma
Figure 3-19-22
References
1. Hartman DS, Choyke PL, Hartman MS.A practical approach to cystic renal masses.RadioGraphics 2004;24: S101-
S115.
Fetal Alpha-fetoprotein
• Glycoprotein produced by fetal liver, GI tract, and yolk sac
• Excreted through the urinary tract into the amniotic fluid
• Peaks at 14–16 wks
• Small amounts leak into maternal circulation
Case 1
Case 2
Elevated MSAFP
• Incorrect dates
• Twins
• Fetal death
• Open neural tube defect
• Abdominal wall defect
• Subchorionic hemorrhage
Placental hemorrhages
Elevated MSAFP
• Can perform amniocetesis and measure direct AFP and ACE
• Acetylcholinesterase (ACE) – neural tissue specific
Elevated MSAFP
• Inc AFP, inc ACE – ONTD
• Inc AFP, nl ACE – abdominal wall defect
• Nl AFP, nl ACE – prior bleed
Decreased MSAFP
• Trisomy 21,18
• Combine with human chorionic gonadotropin (hCG) and estriol (uE3) for
increased specificity – triple screen
Renal Calcifications
• Dystrophic calcification
• Nephrocalcinosis
➢ cortical
➢ medullary
• Nephrolithiasis
Dystrophic Calcification
• Calcification of abnormal tissue
• DDx
➢ tumor
➢ inflammatory mass (TB)
➢ hematoma
➢ cysts
66 yo with hematuria
Renal Tuberculosis
• Hematogenous spread
• Bacilli lodge in
corticomedullary jct.
• Progress along nephron
into pelvo-calyceal
system
• 75% of active TB only in
one kidney
Symptoms
• Asymptomatic
• Frequency
• Hematuria
• “Sterile” pyuria
Papillary necrosis
Granuloma formation
Radiologic Findings
• Infundibular stenosis
• Amputated calyx
• Parenchymal scarring
• Tuberculomas
Calcifications
• Present in 30–50%
• Variable appearance
➢ punctate – healed granulomas
➢ amorphous – granulomatous masses
➢ extensive reniform – autonephrectomy (putty kidney)
• Ureter and bladder may also be involved
Diffuse renal calcification
45 yo woman from Mexico with pyuria
Medullary Nephrocalcinosis
• Metastatic calcification – calcification in normal tissue
• Triangular deposition conforming to pyramids
• Renal function usually not impaired
• Often associated with nephrolithiasis
Medullary Nephrocalcinosis
• Hypercalcemic states
➢ hyperparathyroidism, paraneoplastic, sarcoidosis, milk-alkali syndrome,
hyper-vitaminosis D
• Medullary sponge kidney (renal tubular ectasia)
➢ may be unilateral or focal
Medullary Nephrocalcinosis
• Renal tubular acidosis – Type I (distal)
➢ distal tubule can not secrete hydrogen ion, urine becomes alkaline
➢ symmetric
• Oxalosis
➢ primary (children) -severe may also see cortical calcification
➢ secondary – distal small bowel resection
Cortical Nephrocalcinosis
• Egg-shell calcification
• Generally small kidneys
• Renal function usually impaired
Cortical Nephrocalcinosis
• Chronic glomerulonephritis
• Acute cortical necrosis
➢ pregnancy, sepsis, trauma, nephrotoxins (ethylene glycol)
• Chronic transplant rejection
• Alport’s syndrome
➢ nephritis, nerve deafness, hematuria, ocular abnormalities
I1
Bilomas (liver transplantation) 672 Calcifications (benign - breast) 225
Bladder Neoplasms 649 Fibroadenoma 226
Blastomycosis 104 Loa Loa 227
Pathology 105 Lobular 226
Radiologic Manifestations 105 Secretory 227
Bleeding - Gastrointestinal 468 Skin 226
Boerhaave’s Syndrome 403 Sutural 226
Bowel Disease (Idiopathic Inflammatory) 382 Vascular 227
Bowel Ischemia 487 Cancer (Male Breast) 261
Brachytherapy (Prostate Cancer) 622 Carcinoid
Breast 229 Atypical 193
Angiosarcoma 236 Typical 192
Congenital Anomalies 230 Duodenal, Jejunal, Ileal 358
Fibroadenoma 231 Gastric 341
Fibrosarcoma 236 Thymic 154
Invasive Ductal Cancer 233 Syndrome 358
Invasive Ductal Carcinoma 234 Carcinoma - Adrenal 646
Invasive Lobular Cancer 235 Carcinoma (Male Breast) 262
Lobular Neoplasia 232 Invasive Ductal Carcinoma 262
Mastitis 230 Lymphoma (Male Breast) 263
Medullary Carcinoma 234 Metastasis (Male Breast) 262
Normal Anatomy 229 Papillary Carcinoma 262
Paget’s Disease 234 Carcinoma (Scirrhous - Stomach) 334
Papilloma 232 Carcinoma Colon, Rectum (see Colorectal Carcinoma) 361
Phyllodes Tumor 231 Carcinosarcoma 197
Pregnancy Changes 230 Cardia (Carcinoma) 334
Sarcoma 236 Carney’s Triad 200
Spindle Cell Sarcoma 236 Caroli Disease 304
Tubular Carcinoma 235 Castleman Disease 151, 346
Breast (Male) 257 Cavitary pneumonia 190
Breast (Young Women) 246 Cavitation 190
Angiosarcoma 254 Cecal Volvulus 400
Benign Lesions 247 Cervix Carcinoma 559
Diabetic Mastopathy 251 Chest Wall 216
Fibroadenoma 247 Neoplasms 218
Granular Cell Tumor 249 Chiari II 604
Granulomatous Mastitis 252 Cholangiocarcinoma (intrahepatic) 279
Hamartoma 250 Cholangitis 309
Invasive Ductal Carcinoma 252 Acute Pyogenic 309
Juvenile Hypertrophy 251 Recurrent Pyogenic 309
Juvenile Papillomatosis 250 Cholecystitis 438, 441
Lactating Adenoma 250 Choledocholithiasis 442
Lymphoma 254 Cholelithiasis 438
Medullary Carcinoma 253 Cholescintigraphy 439
Phyllodes High Grade 254 Chondroma 201
Phyllodes Tumor 249 Chorionic Sac 594
Pseudoangiomatous Stromal Hyperplasia (PASH) 251 Choroid Plexus Cysts 605
Sarcoma 253 Chronic Idiopathic Intestinal Pseudo-obstruction 476
Secretory Carcinoma 253 Chronic Liver Disease 293
Bronchial Adenoma 192 Budd-Chiari Syndrome 298
Bronchial Carcinoid 194 Cirrhosis 293
Bronchiectasis 190 Hemochromatosis 300
Bronchiolitis Obliterans 80 Hemosiderosis 300
Bronchioloalveolar Carcinoma 117 Hepatocellular Carcinoma 295
Bronchocentric Granulomatosis 71 Nonalcoholic Steatohepatitis 297
Bronchogenic Cyst 159 Primary Biliary Cirrhosis 296
Brunner Gland 354 Steatosis 296
Hamartoma 354 Chronic Pancreatitis 460, 465
Hyperplasia 354 Chronic Thromboembolic Disease 133
Budd-Chiari Syndrome 298 Churg-Strauss Syndrome 67
Burkitt Lymphoma 348 Cirrhosis 293
CA-125 638 CNS Malformations (Fetal) 602
I2
Coccidioidomycosis 106 Diffuse Alveolar Damage 79
Coccidioidoma 107 Diffuse Lung Disease 3
Pathology 106 AIP 4
Radiologic Manifestations 106 Asbestosis 3
Colitis Asthma 3
Ischemic 398 Bronchiectasis 6
Colon (Inflammatory Disease) 391 Bronchoalveolar cell carcinoma 4
Cecal Diverticulitis 397 Constrictive bronchiolitis 3
Diverticular Hemorrhage 397 Cor Pulmonale 11
Diverticulitis 395 DAD 4
Diverticulitis vs. Carcinoma 396 DIP 4
Giant Sigmoid Diverticulum 397 Edema 6
Ischemic Colitis 398 Emphysema 3
Colonic Lymphoma 350 Granuloma 7
Colonic Polyposis 519 Hypersensitivity pneumonitis 3
Colorectal Carcinoma 361 LAM 3
Adenoma 363 LCH 4
Complications 366 Löfgren syndrome 12
EUS 368 Lymphoma 4
Inflammatory Bowel Disease 366 NSIP 4
Lymphatic Spread 369 Organizing Pneumonia (BOOP) 4
Multiple 365 Sarcoidosis 3, 6, 7
Obstructing 366 Differential Diagnosis 10
Rectal Adenocarcinoma: Lymphatic Drainage 369 Mycetoma 12
Screening 362 Diffuse Panbronchiolitis 36
Synchronous 365 Diverticulitis 396
Villous Adenoma 363 Cecal 397
Community-acquired Pneumonia 179 Colovesical Fistula 396
Congenital CNS Malformations 602 CT 397
Congenital Diaphragmatic Hernia 608 Differential Diagnosis 396
Constrictive Bronchiolitis 36 Pericolic Abscess 396
Cor Pulmonale 133 Ductal Carcinoma in Situ 238
Corpus Callosum - Agenesis 605 Biopsy 243
Cowden’s Syndrome 525 Calcification 240
Crohn disease 382, 386 Classification 239
Gastric 410 Ductal Plate 303
Cronkite-Canada syndrome 526 Duodenal Carcinoid 357
Cryotherapy (Prostate Cancer) 622 Duodenitis 455
Cryptorchidism 588 Echinococcosis 188
Cyst - Bile Duct (Hepatic) 272 Echinococcus granulosus 188, 286
Cyst (Breast) 223 Echinococcus multilocularis 286
Pneumocystography 223 Ectopic pregnancy 598
Thickened Skin Pattern (breast) 224 Eisenmenger Physiology 133
Cyst (Bronchogenic) 159 Emphysema 27
Cyst (thymic) 161 Emphysematous Cholecystitis 441
Cystadenoma (Biliary) 272 Emphysematous Cystitis 651
Cystic Abdominal/Pelvic Collections 611 Encephalocele 605
Cystic Adenomatoid Malformation 608 Endometrial Carcinoma 558
Cystic Disease of the Kidney 614 FIGO – Staging 559
Cystic Fibrosis (P. aeruginosa) 185 Endometrioma 656
Cystic Hygroma 607 Endometriosis 655, 656
Cystic Kidney Disease - Acquired 618 Endorectal Coil MRI 622
Cystic Lymphangioma (Male Breast) 258 Enteric Cyst 374
Cystic Nephroma 686 Enteritis - Chronic Radiation 497
Cystitis 650, 651 Enterography (MR - Crohn Disease) 389
Cysts (Congenital - Mediastinum) 160 Epidermal Inclusion Cyst (Male Breast) 260
Cytomegalovirus 78 Epidermoid Cyst(Testis) 588
Cytomegalovirus Pneumonia 78 Epididymal Masses 590
Dandy-Walker Malformation 604 Adenomatoid Tumor 590
Daughter cysts (E. granulosus) 287 Lipoma (Paratesticular) 592
Delayed Pyelogram 677, 678 Papillary Cystadenoma 590
Diabetic mastopathy 258 Polyorchidism 592
I3
Epididymis 586, 636 Gastritis 470
Epididymitis 591 Lower GI 469
Epiploic Appendagitis 430 Nuclear Scintigraphy 469
Epithelial Inclusion Cysts 661 Risk of Rebleeding 470
Esophageal Rupture (Causes) 403 Upper GI 469
Esophageal Varices 470 Gastrosplenic ligament 531
Esophagus - Inflammatory Diseases 444 Germ Cell Neoplasms 155 (Chest)
Barrett’s Esophagus 445 Germ Cell Tumors (Retroperitoneum) 583
Candida Esophagitis 446 Gestation 596
CMV Esophagitis 447 Gestational Sac 594
Drug-Induced Esophagitis 448 Gestational Trophoblastic Disease 661
Herpes Esophagitis 446 GIST (Gastrointestinal Stromal Tumors) 338
HIV Esophagitis 447 Glucagonoma 328
Intramural Pseudodiverticulosis 448 Goiter (mediastinal) 161
Reflux Esophagitis 444 Graft-vs-Host Disease 79
Esophagus - Malignant Tumors 452 Granular Cell Tumor (Male Breast) 260
Adenocarcinoma 453 Granuloma (lung) 205
Early Squamous Cell Carcinoma 453 Granulomatous Mastitis 261
Spindle Cell Carcinoma 454 Gut Hemangioma 471
Squamous Cell Carcinoma 452 Gynecomastia 257, 258
Esophagus Tumors 450 H.influenzae 178
Duplication Cyst 452 H.Pylori 459
Leiomyoma 450 Hamartoma 199
Leiomyomatosis 451 Hamartoma (Breast) 222
Squamous Papilloma 450 Hemangioma 268
Extralobar Sequestration 608 Hemangioma (Gut) 471
Extramedullary hematopoiesis 164 Hemangioma (Mediastinum) 163
Extrarenal Cysts 615 Hemochromatosis 300
Fetal Anomalies 607 Hereditary 300
Fibrolamellar Carcinoma 278 Secondary 301
Fibrous Pseudotumor 592 Hemosiderosis 300
Foramen Of Winslow Hernia 404 Hepatic Artery Thrombosis (liver transplantation) 671
Fournier Gangrene 591 Hepatic Cyst (Complex) - Differential Diagnosis 417
Galactocele 223 Hepatic Mass with a Scar - Differential Diagnosis 418
Gallbladder and Biliary Neoplasms 313 Hepatic Neoplasms 267
Gallbladder Empyema 442 Hepatic Portal Venous Gas 402
Gallbladder Wall Thickening 440 Hepatocellular Adenomatosis (see Benign Hepatic
Gallstone 438 Neoplasms) 271
Ganglion Cell Tumors 581 Hepatocellular Carcinoma 275
Ganglioneuroblastoma 158 Hereditary GI Polyposis Syndromes 524
Ganglioneuroma 158, 581 Herniations 164
Gangrenous Cholecystitis 441 Hiatus Hernia 164
Gastric Lymphoma 335 Morgagni 164
Gastric Malignancies 332 Herpes viruses (respiratory) 182
Carcinoid 340 Heterotopic Pregnancy 599
Carcinoma of the Cardia 334 Histoplasmosis 100
Gastric Adenocarcinoma 332 Acute Radiology 101
Gastrointestinal Stromal Tumors (GIST) 338 Chronic 102
Kaposi Sarcoma 341 Disseminated 102
Lymphoma 335 Fibrosing Mediastinitis 104
Mesenchymal Neoplasm 338 Histoplasmoma 103
Metastases 341 Mediastinal granuloma 103
Mucosa-Associated Lymphoid Tissue 335 Pathology 101
Scirrhous Carcinoma 334 Hodgkin Disease - Mediastinum 150
Gastric Ulcer Investigation 457 Holoprosencephaly 603
Gastric Volvulus 405 Hydranencephaly 602
Bezoar (Gastric) 407 Hydrocele 590
Zollinger-Ellison Syndrome 408 Hydrocephalus 603
Gastritis 455 Hydronephrosis 610
Gastrointestinal Bleeding 468 Hydronephrosis (post transplantation) 666
Angiography 470 Hydrosalpinx 658
Endoscopy 469 Hypoplastic Left Heart 608
I4
Idiopathic Inflammatory Bowel Disease 382 Cigarette smoking 111
Immunocompromised Host (Hepatic Infections) 289 Clinical Presentation 111
Candidiasis 289 Paraneoplastic Syndromes 111
Hepatosplenic Candidiasis 290 Lymphangioleiomyomatosis 38
Pneumocystis jiroveci 291 Lymphangioma
Infiltrating Colloid Carcinoma 323 Mediastinum 162
Inflammatory Carcinoma (breast) 225 Lymphangioma
Inflammatory Myofibroblastic Tumors 379 Retroperitoneum 582
Inflammatory Pseudotumor (lung) 202 Mesentery
Influenzae 178 Differential Diagnosis 374
Influenzae A 181 Lymphangitic Carcinomatosis 143
Inguinal Hernia 634 Imaging Features 143
Iniencephaly 607 Lymphocele (post kidney transplantation) 666
Interstitial Pneumonia 182 Lymphoma 150
Interstitial Pneumonias 14 Lymphoma
Acute Interstitial Pneumonia (AIP) 14 Burkitt) 348
Cryptogenic Organizing Pneumonia (COP) 14 Lymphoma
Desquamative Interstitial Pneumonia (DIP) 14 Primary Gastric 336
Idiopathic Pulmonary Fibrosis (IPF) 14 Lymphoma
NonSpecific Interstitial Pneumonia (NSIP) 14 Testicular 588
Respiratory Bronchiolitis-Interstitial Lung Disease (RB- Lymphomatoid Granulomatosis 70
ILD) 14 Epstein-Barr Virus 70
Usual Interstitial Pneumonia (UIP) 14 M. pneumoniae 180
Interstitial Pregnancy 599 Malabsorption 505
Intracranial Aneurysms 615 Malakoplakia 650
Intraductal Papillary Mucinous Neoplasm 324 Male Breast 257
Intrahepatic Portal Venous Air 492 Cancer 261
Intravenous Talcosis 134 Malignant Fibrous Histiocytoma 582
Ischemia Mimic (Mesenteric) 500 Malignant Germ Cell Neoplasms (Non-Seminomatous) 156
Jejunal and Ileal Carcinoid 357 Malignant Hepatic Neoplasms 275
Juvenile Laryngeal Papillomatosis 201 Angiosarcoma 280
Juvenile Polyposis: Syndrome 525 Epithelioid Hemangioendothelioma 280
K. pneumoniae 178, 183 Fibrolamellar Carcinoma 278
Kaposi Sarcoma (Gastric) 341 Hepatocellular Carcinoma 275
Kidney Intrahepatic Cholangiocarcinoma 279
Cystic Diseases 614 Malignant Neoplasia (Chest)149
Neoplasms 561 Malignant Peripheral Nerve Sheath Tumor 158
Transplants 664 Mallory-Weiss Tear 471
Trauma 576 MALT 335
KIT 338 Masaoka (Thymoma: Staging) 154
Krukenberg Metastasis 335 Mastitis 224
L. pneumophila 183 Mastitis (Granulomatous - Male Breast) 261
Langerhans Cell Histiocytosis 29 Mature Teratoma 155
Large Cell Carcinoma 114 Meckel Diverticulum (complications) 422
Legionella 178 Diverticulitis 424
Leiomyoma 258, 261 Diverticulitis with a Stone 425
Leiomyosarcoma (retroperitoneum) 582 Hemorrhage 424
Limb-Body-Wall Defect 610 Heterotopic Gastric Mucosa 423
Lipoma 258 Heterotopic Pancreatic Mucosa 423
Lipoma (breast) 222 Inverted 425
Lipomatous Tumors (Liver) Meckel’s Diverticulum 473
Angiomyolipoma 273 Mediastinal
Myelolipoma 273 Compartments 148
Liposarcoma (breast) 222 Fibrosis 135, 151
Liposarcoma (retroperitoneum) 583 Goiter 161
Liver Disease (chronic) 293 Masses 148
Liver Mass with Fat - Differential Diagnosis 420 Mediastinitis 165
Liver Neoplasms 267, 275 Mediastinum 148
Liver Transplantation 670 Medullary Carcinoma (Kidney) 565
Complications 671 Menetrier Disease 409
Liver Transplants 664 Meningocele (Thoracic) 158
Lung Cancer 111, 149 Mesenchymal Neoplasm of the Stomach 338
I5
Mesenteric Adenitis 430 Necrotizing Sarcoid Granulomatosis 69
Mesenteric Cyst 372 Neoplasms (Germ Cell) 155
Mesenteric Fibromatosis (Desmoid Tumor) 346, 376 Neoplasms (Neurogenic) 157
Mesenteric Ischemia 487 Nephrocalcinosis 694
Mesenteric Ischemia - Etiologies 495 Nephrogram 674
Embolus 495 Nephroma (Multilocular Cystic) 569
Thrombosis 497 Nerve Sheath Tumor 158 (Chest)
Mesenteric Masses (Differential Diagnosis) 346 Nerve sheath Tumors (Retroperitoneum) 581
Mesenteric Masses and Cysts 372 Neural Tube Defects 605
Benign Multicystic Mesothelioma 375 Neuroblastoma (Mediastinal) 158
Diffuse Peritoneal Malignant Mesothelioma 375 Neuroendocrine Tumors (pancreas) 328
Enteric Cyst and Mesothelial Cyst 374 Neurofibroma 157
Inflammatory Myofibroblastic Tumors (Inflammatory Neurofibromatosis (NF1) 158
Pseudotumor) 379 Neurogenic Neoplasms 157
Lymphangioma 373 Neurogenic Tumors (Retroperitoneum) 580
Nonpancreatic Pseudocyst 374 NF-1 (GI Neoplasms) 359
Sclerosing Mesenteritis 378 Nocardia 178
Mesothelioma Nodes (NHL - Gastrointestinal) 345
Malignant 215 Nodular Lymphoid Hyperplasia Colon 527
Mesenteric 374 Non Hodgkin Lymphoma (abdominal) 344
Benign Multicystic 375 Adenopathy 345
Cystic Malignant 375 AIDS-Related Lymphoma 349
Diffuse Malignant 375 Burkitt Lymphoma 348
Scrotal 593 Differential Diagnosis 346
Metastases (pleural) 216 Enteropathy-Type T-cell Lymphoma 349
Metastases (pulmonary) 138 Gastrointestinal Lymphoma 346
Calcification 142 Mantle Cell Lymphoma 348
Cannonball 140 Small Intestine 347
Cavitation 141 Small Intestine: Differential Diagnosis 349
Endobronchial 144 Non Hodgkin lymphoma - Mediastinum 150
Lymphangitic Carcinomatosis 143 Non-Hereditary GI Polyposes 524
Micronodular 141 Non-Neoplastic Lymphadenopathy - Mediastinum 151
Parenchymal Nodules 139 Non-Seminomatous Malignant Germ Cell Neoplasms 156
Pathogenesis of Hematogenous Metastases 139 Nosocomial Pneumonia 185
Pleural 144 Nosocomial Pneumonia and Aspiration 186
Solitary 142 Ogilvie Syndrome 401
Tumor Embolism 143 Oligohydramnios 609
Metastases Breast Young Women 254 Omental Infarction 431
Microcystic Adenoma 327 Oncocytoma 569
Microscopic Polyangiitis 67 Orchitis 591
Mole 661 Organ Transplantation 75
Benign Hydatidiform 661 CMV 76
Choriocarcinoma 662 Fungal Infections 77
Complete 662 Graft-vs-Host 76
Partial 662 Pneumocystis carinii 76
Morgagni (Herniation) 164 Ovarian Cyst 611
Mounier-Kuhn Syndrome 32 Ovarian Cysts 653
MR Enterography 389 Corpus Luteum 654
MRSA 186 Follicular 653
Mucinous Cystadenoma/Cystadenocarcinoma (Appendiceal) Functional 653
428 Hemorrhagic 654, 655
Mucinous Cystic Neoplasm 326 Hyperstimulation 655
Mucinous Noncystic Adenocarcinoma 324 Rupture 655
Mucoepidermoid Carcinoma 196 Theca Lutein 655
Multilocular Cystic Nephroma 686 Ovarian Neoplasms 637
Multiple Lymphomatous Polyposis (Mantle Cell Lymphoma) Epithelial Ovarian Neoplasms: Endometrioid 639
348 Epithelial Ovarian Neoplasms: Mucinous 639
Myasthenia Gravis (Thymoma and) 152 Epithelial Ovarian Neoplasms: Serous 638
Mycoplasma 178 Epithelial Ovarian Tumors: Clear Cell 639
Myelolipoma 647 Epithelial Tumors: Classification 637
Myofibroblastoma (Male Breast) 257, 260 Epithelial Tumors: Terminology 638
N. Asteroides 188 Mature Cystic Teratoma 640
I6
Ovarian Germ Cell Neoplasms 640 Malignant 213
Ovarian Malignant Germ Cell Tumors 641 Pleural Neoplasms 213
Sex-cord stromal tumors 641 Localized Fibrous Tumor 213
Ovarian Torsion 657 Mesothelioma 215
Ovary Pneumatocele 190
non neoplastic disorders 653 Pneumatosis Intestinalis 493
polycystic 660 Pneumocystis Jiroveci 78
Masses 637 Pneumocystis Jiroveci Pneumonia 78
Pancoast Tumor 113 Pneumonia 178
Pancreas 412 Pneumoperitoneum 403
Annular 412 Pneumothorax 211
Divisum 413 Polycystic Kidney Disease (Autosomal Recessive) 616
Intraductal Papillary Mucinous Neoplasm 415 Polycystic Liver Disease 306
Pancreatitis, Chronic 414 Polycystic Ovary Syndrome 660
Pancreas (Neoplasms) 321 Polyhydramnios 609
Adenocarcinoma 321 Polymastia 221
Intraductal Papillary Mucinous Neoplasm 324 Polyposis - Familial 519
Islet Cell Tumors 328 Polysplenia 534
Metastatic 329 Polythelia 221
Microcystic Adenoma 327 Post Transplant Lymphoproliferative Disorder 672
Mucinous Cystic Neoplasm 326 Post Transplant Malignancy 673
Mucinous Noncystic Adenocarcinoma 323 Posterior Urethral Valves 611
Oligocystic Adenoma 328 Post-transplantation Imaging 664
Solid and Pseudopapillary Epithelial Neoplasm 325 Post-transplantation Lymphoproliferative Disorder (GI) 349
Pancreas Transplants 664, 669 Pregnancy 598
Complications 669 Primary Ciliary Dyskinesia 32
Rejection 670 Prostate Cancer 620
Vascular Thrombosis 670 Grading 620
Pancreatic Adenocarcinoma 321 Screening 620
Resectability 323 Prostate Specific Antigen 620
Pancreatic Duct 411 Pseudoaneurysms (kidney transplantation) 669
Pancreatitis 460 Pseudocyst (Nonpancreatic) 374
Papilloma 201 Pseudocyst (Pancreatitis) 462
Papilloma (Male Breast) 257 Pseudogynecomastia 257, 259
Papillomatosis (Biliary) 319 Pseudopapillary Epithelial Neoplasm (Solid and) 325
Paraganglioma 159 Pulmonary Blastoma 198
Paraganglioma (Extra-adrenal pheochromocytoma) 581 Pulmonary Circulation 131
Paragonimiasis westermani 189 Idiopathic 132
Paraovarian Cysts 661 Pulmonary Embolism 82
Parathyroid Adenoma 162 Arterial Blood Gases 85
Pelvic Inflammatory Disease 659 Chest X-Ray 84
Pelvic MRI 553 Clinical Science Probability 85
Peptic Ulcer Disease 455 Combined Pulmonary CTA and Venography 89
Peribronchial abscesses 188 Common Radiographic Abnormalities 84
Perinephric Fluid Collections 665 CT Angiography 86, 87
Peritoneal Inclusion Cysts 523, 659 CT Findings 84
Peritoneal Lymphoma (Primary) 350 Diagnostic Algorithm 89
Persistent Bilateral Nephrogram 679 Pitfalls 88
Peutz Jeghers 525 Small Emboli 86
Pheochromocytoma 647 Ventilation/Perfusion Scanning 85
Pleural Disease 204 Pulmonary Gangrene 190
Bacterial Pneumonia 208 Pulmonary Hypertension 131
Empyema 208 Pulmonary Lymphoid Disorders 55
Pleural Effusion 208 B-Cell Lymphoma 58
Pleural Effusion: Asbestos Exposure 210 Follicular bronchitis 55
Pleural Effusion: Subpulmonic 209 Follicular Hyperplasia 55
Pleural Effusion: Tuberculosis 209 Lymphoid Interstitial Pneumonia LIP 56
Pleural Fibrosis 211 Lymphomatoid Granulomatosis 59
Pneumothorax 211 Nodular Lymphoid Hyperplasia 57
Pulmonary Ligament 207 Posttransplantation Lymphoproliferative Disease 60
Round Atelectasis 210 Pseudolymphoma 57
Pleural Effusion 213 Pulmonary Lymphoid System 54
I7
BALT 54 Cholangiocarcinoma 308
Bronchus Associated Lymphoid Tissue 54 Sclerosing Mesenteritis 378
Pulmonary Thromboendarterectomy 134 Scrotal Anatomy 630
Pulmonary Venous Hypertension 135 Scrotal Calculi 590
Pyelogram 674 Scrotum 585
Pyelonephritis 678 Seminoma 156
Pyogenic Hepatic Abscess 284 Sequestration 608
Pyosalpinx 659 Serous Inclusion Cysts 661
Radioactive Ablation (Prostate Cancer) 622 Serum Alpha-Fetoprotein (Elevated Maternal) 691
Rejection (kidney transplants) 667 Severe Acute Respiratory Syndrome 182
Renal Anomalies 610 Shock Bowel 500
Renal Artery (kidney transplantation) 668 Shwachman - Diamond Syndrome 513
Renal Calcifications 693 Sigmoid Volvulus 401
Dystrophic 693 Silicosis 46
Medullary 694 Adenopathy 47
Renal Cancer in ACKD 619 Alveolar Proteinosis 48
Renal Cell Carcinoma 563 Calcification 47
Renal Injuries 576 Conglomeration 48
Renal Masses 681 Scar emphysema 48
Carcinoma In Situ 681 Small Bowel Bleeding 472
follow up interval 683 Small Bowel Lymphoma 347
Multilocular Cystic Nephroma 686 Small Bowel Obstruction 475
Small renal mass 682 Small Cell Lung Cancer 113
Renal Neoplasms 561 Small Intestinal Benign Neoplasms 353
Angiomyolipoma 570 Adenoma 355
Infiltrating Renal Cell 564 Brunner Gland Hamartoma 354
Juxtaglomerular Cell Tumor 570 Brunner Gland Hyperplasia 354
Medullary Carcinoma 565 Differential Diagnosis: Duodenal Polyp 354
Metastases 569 Periampullary Adenocarcinoma 355
Multilocular Cystic Nephroma 569 Periampullary Duodenal Mass 355
Oncocytoma 569 Tubulovillous Adenoma 355
Renal Cell Carcinoma 563 Small Intestine 347
Renal Lymphoma 568 Adjacent Mesenteric Disease 348
Robson Staging 565 Cavitary Mass 348
Spontaneous Renal Hemorrhage 564 Mural Infiltration 347
Squamous Cell Carcinoma 568 Small Intestine Malignant Neoplasms
TNM Staging 565 Adenocarcinoma 355
Transitional Cell Carcinoma 567 Carcinoid 357
Tuberous Sclerosis 570 Carcinoid Syndrome 358
Uroepithelial Neoplasms 567 Differential Diagnosis 356, 359
Venous extension 562 Metastatic Disease 359
Renal Transplants 664 Small Intestine NHL - Differential Diagnosis 349
Renal Vein Thrombosis (kidney transplantation) 668 Smoking Related ILD 16
Respiratory Bronchiolitis 29 Macrophages 16
Respiratory Viruses 181 RB 16
Retroperitoneal Fibrosis 580 Respiratory bronchiolitis 16
Retroperitoneal Masses 611 Spermatic cord 586
Retroperitoneal Masses (Fat containing) 584 Spleen 531
Retroperitoneum 579 Splenorenal ligament 531
Ruvalcaba-Myhre-Smith 526 Splenosis 533
S. pneumoniae 178, 179 Sprue 505
S.aureus 184 Squamous Cell Carcinoma 111
Saber Trachea 28 Steatosis 296
Sacrococcygeal Teratoma 612 Stomach Malignancies 332
Salpingitis 659 Stone Urinary 624
Sandwich Sign (NHL) 345 Striated Nephrogram 679
SARS 182 Strongyloides stercoralis 189
Scar Carcinoma 116 Strongyloidiasis 188
Schistosomasis (Bilharziasis) 288 Swyer James Syndrome 38, 182
Schistosomiasis (Urinary) 651 Sympathetic Ganglia Tumors 159
Schwannoma 157 Tamoxifen 558
Sclerosing Cholangitis (primary) 307 T-cell Lymphoma (Enteropathy-Type T-cell Lymphoma) 349
I8
Teratoma (Mature) 155 Urinary Tract Trauma 573
Teratoma (Retroperitoneum) 583 Uroepithelial Neoplasms 567
Testicular Carcinoma (Risk Factors) 588 Urothelial carcinoma 649
Testicular Cysts 589 Usual Interstitial Pneumonia: Histology 15
Testicular Ischemia 635 Fibroblast foci 15
Testicular Masses (Bilateral) 589 Uterine Disorders 551
Testicular Neoplasms 586 Arcuate 555
Germ Cell Neoplasms 587 Bicornuate 554
Non Seminomatous Germ Cell Tumor 587 Diethylstilbestrol: DES – Related 556
Seminoma 587 Mullerian Duct Anomalies 554
Testicular Torsion 630 Septate 555
Testis 586 Unicornuate / Didelphys 554
Testis (torsion) 632 Uterine Masses - Benign 556
Thymic Carcinoid 154 Abnormal Uterine Bleeding 557
Thymic Cyst 161 Adenomyosis 557
Thymic Hyperplasia 161 Endometrial Hyperplasia 558
Thymolipoma 154 Endometrial Polyps 558
Thymoma 152 Leiomyoma 556
Torsion (Ovary) 657 Postmenopausal Bleeding 558
Torsion (Testicle) 591 VACTERL Syndrome 610
Transplants (Solid Organs) 664 Varicella Pneumonia 182
Transverse Colon Volvulus 401 Varices (Esophageal) 164
Trauma (Urinary Tract) (see Urinary Tract Trauma) 573 Varicocele 592
Trisomy 18 606 Ventilator-associated Pneumonia 186
Trisomy 21 600 Viruses - Respiratory 181
TRUS 621 Von Hippel Lindau 617
Tuberculosis 93 Water Lily Sign (E. granulosus) 287
Clinical features 95, 96 Wegener’s Granulomatosis 63
Hemoptysis 98 halo sign 66
Lymphatic gradient 95 Williams-Campbell 31
M. tuberculosis 93 Yolk sac 596
Mycetoma 98 Zollinger-Ellison Syndrome 328
Mycobacteria 93
Pathogenesis 94
Radiologic features 95, 96
Rassmussen (pulmonary artery) aneurysm 98
Tuberculoma 97
Tuberculosis (renal) 693
Tuberculosis (scrotal) 591
Tuberous Sclerosis 39, 616
Renal 570
Tubular Ectasia (Testis) 589
Twins 596
Dizygotic 596
Monozygotic 597
Ulcerative Colitis 382, 384
CT Features 384
Imaging Features 384
Toxic Megacolon 385
Ulcers - Duodenal 458
Ulcers - Gastric 456
Benign 456
Equivocal 457
Malignant 457
UPJ disruption 578
Urachal Anomalies 649
Ureteral Injury 575
Urethra 649, 652
Urethral Trauma 573
Urethrography 652
Urinary Bladder 649
Urinary Stone Disease 624
I9
Radiologic
Pathology
Fifth Edition
VOLUME 2
Musculoskeletal
Radiologic Pathology Correlation
2006
Editors
2007
Ellen M. Chung, LTC, MC, USA
Chief, Pediatric Radiology
Jeffrey R. Galvin, MD
Chief, Chest Radiology
Kelly K. Koeller, MD
Chief, Neuroradiology
Mark D. Murphey, MD
Six Week Course Director
Chief, Musculoskeletal Radiology
All rights reserved. No part of this publication may be reproduced or transmitted in any form
or by any means: electronic, mechanical, photocopy, recording, or any other information
storage and retrieval system without written permission of the publisher.
Great care has been taken to guarantee the accuracy of the information contained in this
volume. However, neither the American Registry of Pathology, Armed Forces Institute of
Pathology, nor the editors and contributors can be held responsible for errors or for any
consequences arising from the use of the information contained herein.
The opinions and assertions contained herein are the private views of the authors and are
not to be construed as official nor as representing the views of the Departments of the Army,
Air Force, Navy, or Defense.
987654321
ISBN 1-933477-00-8
Preface
The Armed Forces Institute of Pathology’s Radiologic Pathologic Correlation
course presented by the Department of Radiologic Pathology enters its 59th year
of educating radiology residents worldwide. For the fifth year, our staff and visiting
lecturers have contributed their lecture material and images to compile Radiologic
Pathology 2006 – 2007, continuing the tradition of presenting richly illustrated
material that teaches the pathologic basis of disease to improve our understanding
of the imaging appearance of disease. We hope the efforts of our authors and
editors have once again accomplished our goal of bringing the outstanding and
unique Radiologic Pathologic Correlation course to your fingertips.
Acknowledgements
iii
Faculty – VOLUME 2
Musculoskeletal Radiology
Mark E. Schweitzer, MD
Mark D. Murphey, MD Professor of Radiology and Orthopedic Surgery
Chief, Musculoskeletal Radiology Chief of Radiology - Hospital for Joint Diseases
Department of Radiologic Pathology Director, Musculoskeletal Radiology
Armed Forces Institute of Pathology New York University
Washington, DC New York, NY
Mark W. Anderson, MD
Associate Professor of Radiology and Orthopedic Surgery
Division Head, Division of Musculoskeletal Radiology
University of Virginia Health System
Charlottesville, VA
Donald J. Flemming, CAPT, MC, USN
G. Victor Rohrer Professor of Radiology Education
Associate Professor of Radiology
Penn State Hershey Medical Center
Hershey, PA
Mark J. Kransdorf, MD
Professor of Radiology
Mayo Clinic College of Medicine
Rochester, MN
and
Consultant, Musculoskeletal Radiology
Department of Radiology
Mayo Clinic
Jacksonville, FL
William B. Morrison, MD
Associate Professor of Radiology
Director, Division of Musculoskeletal
and General Diagnostic Radiology
Thomas Jefferson University Hospital
Philadelphia, PA
Michael Mulligan, MD
Associate Professor of Diagnostic Radiology
University of Maryland School of Medicine
Baltimore, MD
Thomas L. Pope, MD
Clinical Professor of Radiology/Orthopedics
Medical University of South Carolina
Charleston, SC
and
Former Distinguished Scientist
Department of Radiologic Pathology
Armed Forces Institute of Pathology
Washington, DC
Charles S. Resnik, MD
Professor of Diagnostic Radiology
Director, Section of Musculoskeletal Radiology
Director, Residency Program
University of Maryland School of Medicine
Baltimore, MD
Timothy Sanders, MD
Assistant Professor of Radiology
Department of Radiology
Uniformed Services University of the Health Sciences
Bethesda, MD
iv
Musculoskeletal Radiology
Mark D. Murphey, MD
Radiologic Assessment of Joint Replacement and Imaging of Bone Grafts . . . . . . . . . . . . . . . . . . . . . . . . .699
Musculoskeletal Manifestations of Chronic Renal Insufficiency . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .711
Fundamental Concepts of Musculoskeletal Neoplasm: Radiographs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .720
Fundamental Concepts of Musculoskeletal Neoplasm: CT and MR . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .733
Osteoid Lesions of Bone . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .743
Cartilaginous Lesions of Bone . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .757
Fibrous Lesions of the Musculoskeletal System . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .771
Alphabet Soup and Cystic Lesions of Bone . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .784
Juxtaarticular Soft Tissue Masses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .792
Musculoskeletal Angiomatous Lesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .805
Paget Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .812
Musculoskeletal Infection I . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .820
Musculoskeletal Infection II . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .829
Imaging of Cervical Spine Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .839
Christopher J. Fielding, COL, DC, USA
Radiographic Differential Diagnosis of the Jaws . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .849
Mark W. Anderson, MD
MRI of the Knee: Part 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .858
MRI of the Knee: Part 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .865
MRI of the Wrist . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .872
MRI of the Ankle and Foot . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .879
Mark J. Kransdorf, MD
Osseous Lesions: Unknown Histogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .887
Soft Tissue Lipomatous Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .893
Metabolic Bone Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .900
Osteonecrosis and Related Conditions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .906
Donald J. Flemming, CAPT, MC, USN
Approach to the Inflammatory Arthropathies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .912
MRI of the Rotator Cuff . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .925
Timothy Sanders, MD
MR Arthrography of Glenohumeral Instability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .932
Imaging of Upper Extremity Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .941
Charles S. Resnik, MD
Crystal Deposition Diseases and Neuropathic Osteoarthropathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .949
Mark Schweitzer, MD / William Morrison, MD
MRI of the Elbow . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .955
Michael Mulligan, MD
Skeletal Metastases, Myeloma, Lymphoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .961
Thomas Lee Pope, MD
Imaging of Hematologic Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .968
Generalized Musculoskeletal Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .976
Osseous Musculoskeletal Stress Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .987
Pelvis and Lower Extremity Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .995
Mark D. Murphey, MD
Musculoskeletal Seminar I . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1005
Musculoskeletal Seminar II . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1009
Musculoskeletal Seminar III . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1013
Musculoskeletal Seminar IV . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1018
Musculoskeletal Seminar V . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1025
v
Musculoskeletal Radiology
697
698
Radiologic Assessment of Joint Replacement and Bone Grafts
Mark D. Murphey, MD
Metallic Components
• Cobalt-chromium-molybdenum alloy
• Cobalt-chromium-tungsten alloy
• Titanium-aluminum-vanadium alloy
Loosening and/or Infection Aseptic loosening of both acetabular and femoral components
• Most common complication historically of a total hip arthroplasty with bone cement (arrows), and
• Difficult to differentiate cement-metal lucency (arrowheads) that progresses over
• 4–13% hip replacement several years (right image). Cement fracture (open arrow) and
• 7–10% knee arthroplasty lateral migration of the femoral stem (curved arrow) are also
apparent
Radiographic Signs: Loosening-Infection Cemented Arthroplasty [Figure 4-1-1]
• Cement-bone lucency or cement metal lucency >2mm
• Progressive widening of interfaces post-op
• Component migration
• Fracture of metal or cement
• Periosteal reaction Figure 4-1-2
• Smooth endosteal scalloping with cement lucency
• Air in soft tissues or joint
Bone Scintigraphy
• Normal increased activity post-op (6–9 months)
• Increased activity subsequently suspicious for
loosening/infection
• Nonspecific
• Overall accuracy 50%-70%
Figure 4-1-10
Small particle disease as a cause for
loosening of femoral and acetabular
components of a total hip replacement
with multiple largely intracortical areas of
radiolucency (arrowheads)
Abnormal Alignment
Predisposing to Subluxation Dislocated noncemented total hip replacement, both femoral
[Figure 4-1-10] (arrowhead) and acetabular components (arrows), with
increased inclination of the acetabular component as a
• Varus position of knee is unacceptable
predisposition to this complication
• Acetabular angle > 50/55 degrees – AP view
• Acetabular anteversion < 0 degrees or > 30 degrees lateral view
• Exceeding extremes of motion
• Interposed material
• Greater trochanteric separation Figure 4-1-11
• Joint effusion
• Loss of soft tissue support or imbalance (knee)
Brooker Classification
Heterotopic Bone
• After hip replacement
➢ Class I: Small islands of bone
➢ Class II: Bone projection from acetabulum or femur with >1 cm
between osseous surfaces
➢ Class III: <1cm between opposing bridge surfaces
➢ Class IV: Osseous ankylosis bridging joint
Cement Extrusion
• Usually clinically insignificant
• Vein or lymphatic
• Rarely nerve, vascular, bowel or bladder injury
References
Joint Replacement
1. Bauer TW, Schils J. The pathology of total joint arthroplasty. I. Mechanisms of implant fixation. Skeletal Radiol.
1999 Aug;28(8):423-32. Review.
2. Keogh CF, Munk PL, Gee R, Chan LP, Marchinkow LO. Imaging of the painful hip arthroplasty. AJR Am J
Roentgenol. 2003 Jan;180(1):115-20.
3. Manaster BJ. From the RSNA refresher courses. Total hip arthroplasty: radiographic evaluation. Radiographics.
1996 May;16(3):645-60. Review.
4. Oswald SG, Van Nostrand D, Savory CG, Callaghan JJ. Three-phase bone scan and indium white blood cell
scintigraphy following porous coated hip arthroplasty: a prospective study of the prosthetic tip. J Nucl Med. 1989
Aug;30(8):1321-31.
Imaging Modalities
• Radiographs
• Conventional Tomography
• Scintigraphy
• Computed Tomography (CT)
• Magnetic Resonance Imaging (MRI)
Normal Bone Graft: Repair/Incorporation CT of normal iliac bone graft donor site with outer shell of bone
[Figures 4-1-18 and 4-1-19] retrieved (arrowheads) and no violation of the SI joint (arrow)
• Cancellous autograft
• Cortical autograft
• Vascularized autograft Figure 4-1-17
• Allograft
Figure 4-1-18
necrotic
osteoclastic
Vessels
Artery Peroneal Posterior Intercostal Deep circumflex-iliac
or Superficial
circumflex iliac
Vein 2 Venae Comitnantes 1 Intercostal 1 Vena comitante
Autograft Limitations
• Insufficient volume
• Postoperative morbidity risk
• Inability to mold for function
Allograft
• Particulate
• Intercalary
• Osteoarticular
Osteoarticular Allograft
• Osteochondral shell
• Half-joint
• Whole joint
Osteoarticular Allograft
• Low ratio bone: cartilage requires less pretreatment
• Cartilage immuno-privileged tissue
• Success depends on osseous component
Fracture
• Linear lucency through graft
• Callus
• Stress views helpful
Fracture
• Autograft
➢ Not infrequent
➢ Often after healing with stress (6–8 months)
➢ More common in longer grafts
• Vascularized Autograft
➢ Decreased incidence 3.5% due to improved strength
• Allograft
➢ 16.5% most at weak points
➢ Affected by pretreatment method
Xenograft
• Supply-demand limitations of other graft
• Calf and ox-bone
• Treated to prevent rejection
• Used as spacer prevents soft tissue ingrowth
• Other graft material in combination
Porous Ceramics
• Goniopora-cancellous bone
• Porites-cortical bone
• Approved human studies 1982
• Initially weak mechanically
• Strength increases after incorporation
• More dense than native bone
• Lucent peripheral band obliterated with ingrowth
• Complications: Fractures, Implant failure, Infection
Hyperparathyroidism (HPT)
• Primary
• Secondary
• Tertiary
Renal Osteodystrophy
• Secondary hyperparathyroidism
• Osteosclerosis
• Osteoporosis
• Osteomalacia
• Soft tissue and vascular calcification
Figure 4-2-4
Cortical Resorption
[Figure 4-2-4]
• Caused by osteoclastic activity within haversian canal Intracortical resorption with areas of intracortical
• Radiographs-intracortical tunneling with increased lucent tunneling (arrows) resulting from hyperparathyroidism
striations in cortex on radiography and matched histologic macrosection
• Nonspecific finding showing resorption along preexisting Haversian canals
(arrowheads)
Endosteal Resorption
[Figure 4-2-5] Figure 4-2-5
• Causes scalloping of endosteum- hands
• Osteopenia with loss of trabecular sharpness
• Calvarium – “salt and pepper” appearance with loss of distinction of
tables
Subchondral Resorption
[Figures 4-2-6 to 4-2-8]
• Common in appendicular and axial skeleton
• Often in hands-single DIP joint (4th or 5th) also MCP and
PIP joints
• More recently polyarticular involvement 40% of patients on
long-term hemodialysis IP and first CMC joints with
symmetry
• Simulates erosions, often progress, 50% symptomatic
• Other frequent sites-distal clavicle, AC joint (20%), SI joint,
SC joint, symphysis pubis, posterior patella Brown tumor (*), diffuse sclerosis and subchondral
• Pathologically-collapsed cortical bone and overlying resorption (arrows) about the SI joints are seen on this
cartilage CT of the pelvis in a patient with chronic renal failure
• Initiate an osteogenic synovitis
• Accentuated by mechanical stress, joint incongruity and
intraarticular debris
Subligamentous/Subtendinous Resorption
[Figure 4-2-9]
• Patients usually asymptomatic
• Radiographs-smooth and scalloped or irregular
• Common sites Figure 4-2-9
➢ Inferior calcaneus
➢ Greater and lesser trochanters
➢ Anterior inferior iliac spine
➢ Humeral greater tuberosity
➢ Ischial tuberosity
➢ Elbow
Osteosclerosis
[Figure 4-2-11] Brown tumor of hyperparathyroidism involving the tibia
• Cause unknown with pathologic fracture (arrows) on radiography and
• 9%–34% coronal macrosection. Cyst formation (*) is seen on
• Predilection for axial skeleton the macrosection
• “Rugger Jersey” spine
• Other sites-pelvis, ribs and clavicles Figure 4-2-11
• Metaphyses and epiphyses can be involved
• After renal transplant osteosclerosis may regress but more common to
further increase
Osteopenia
• Accumulated effect of osteomalacia, bone resorption and osteoporosis
• Contributory factors-acidosis, poor nutrition, azotemia, steroids,
hyperparathyroidism, and reduced vitamin D
• After renal transplant osteopenia may worsen or bone mineral content
may increase
• Predisposed to fractures (5%–25%): vertebral body, pubic rami and ribs
• Fracture healing-normal but delayed
Osteomalacia
• Decreased active form of vitamin D
• Renal tissue hydroxylates vitamin D to active form
• Additional factors-hypocalcemia, inhibitors to calcification in uremia,
aluminum toxicity, hepatic dysfunction
Periarticular Calcification
[Figures 4-2-14 and 4-2-15]
• Asymptomatic or pain and joint limitation
• Prevalence
➢ 7% after 1 year hemodialysis
➢ 55% after more than 4 years hemodialysis
• Often regresses with treatment
• Often multifocal and symmetric
• Dense and cloudlike on radiographs
• Hydroxyapatite - chalky paste-like material
• Can extend into tenosynovial tissue and joints
• Sites - phalangeal joints, wrists, elbows, shoulders,
hips, knees, ankles
Figure 4-2-15
Visceral Calcification
• Usually not apparent on radiographs
• May detect on bone scintigraphy (poor looking bone scan)
• Sites - heart, lungs, stomach, kidneys
• Prevalence - 79%
• In myocardial tissue important, can cause conduction defects and death
Aluminum Toxicity
• Prevalence 1%–30% (rare today)
• Results in osteomalacia previously responsible for most osseous abnormalities
in patients on long-term hemodialysis
• Unknown mechanism
• Clinically - low PTH, serum aluminum > 100ng/mL
• Cause - ingestion of aluminum salts in phosphate - binding antacids to control
hyperphosphatemia
• Cannot excrete alumina
• Toxic effects
➢ Cerebral (Encephalopathy)
➢ Osseous system
Amyloidosis
• Musculoskeletal Involvement
➢ Carpal tunnel syndrome
➢ Osseous and intraarticular deposition Osteomalacia due to aluminum toxicity in a renal failure patient
➢ Destructive spondyloarthropathy with radiograph showing multiple nontraumatic fractures
(arrows) and acetabulae protrusio (curved arrows)
Destructive Spondyloarthropathy
• Described 1984 by Kuntz and colleagues
• Usually in patients on long-term hemodialysis
(2–19 years)
• Prevalence - 15%; symptoms - pain
• Cervical and lumbar spine
• Multiple levels >50% of patients Amyloid deposition in the hip joint of a renal failure patient on
hemodialysis on coronal T1 and T2-weighted MR images
• Rapid progression 33%; simulates infection
showing low signal intensity material in the joint (*) with
• Initial postulated etiology - crystal and noncrystal extrinsic bone erosion (arrow)
deposition, neuropathic and hyperparathyroidism
• Amyloid now considered offending agent Figure 4-2-19
Destructive Spondyloarthropathy: Radiographic
Findings
[Figure 4-2-19]
• Discovertebral erosions with sclerosis
• Vertebral body compression
• Disk space narrowing with Schmorl nodes
• Lack of osteophytes
• Facet involvement with subluxation
References
1. Camacho CR, Talegon Melendez A, Valenzuela A, Gonzalez Guirao MA, Gomez Benitez S, Gil L, palma Alvarez A,
Mateos Aguilar J. Radiological findings of amyloid arthropathy in long-term haemodialysis. European Radiology.
1992; 2:305-309.
2. Leone A, Sundaram M, Cerase A, Magnavita N, Tazza L, Marano P.. Destructive spondyloarthropathy of the cervical
spine in long-term hemodialyzed patients: a five-year clinical radiological prospective study. Skeletal Radiol. 2001
Aug;30(8):431-41.
3. Murphey MD, Sartoris DJ, Quale JL, Pathria MN, Martin NL. Musculoskeletal manifestations of chronic renal
insufficiency. Radiographics. 1993 Mar;13(2):357-79.
4. Slavotinek JP, Coates PT, McDonald SP, Disney AP, Sage MR.. Shoulder appearances at MR imaging in long-term
dialysis recipients. Radiology. 2000 Nov;217(2):539-43.
Skeletal Components
(Derived from Embryonal Mesenchyme)
• Bone and cartilage progenitor cells
• Periosteal cells
• Hematopoietic cells
• Lipocytes
• Nerve and Schwann cells
• Fibroblasts
• Osteoclasts and Osteoclast-like cells
• Endothelial cells
• Perithelial cells
• Notochordal cells (rests) HISTOGENIC CLASSIFICATION
• Histiocytic cells OSTEOID BONE TUMORS
• Epithelial cells (rests)
BENIGN MALIGNANT
ENOSTOSIS OSTEOSARCOMA
OSTEOID OSTEOMA
OSTEOMA
OSTEOBLASTOMA
HISTOGENIC CLASSIFICATION
CARTILAGE BONE TUMORS
BENIGN MALIGNANT
CHONDROBLASTOMA CHONDROSARCOMA
CHONDROMYXOID FIBROMA
ENCHONDROMA
JUXTACORTICAL CHONDROMA
OSTEOCHONDROMA
HISTOGENIC CLASSIFICATION
MARROW BONE TUMORS
BENIGN MALIGNANT
LIPOMA LIPOSARCOMA
LYMPHOMA
MYELOMA/PLASMACYTOMA
BENIGN MALIGNANT
HISTOGENIC CLASSIFICATION
HISTIOCYTIC TUMORS
BENIGN MALIGNANT
HISTOGENIC CLASSIFICATION
NOTOCHORD BONE TUMORS
BENIGN MALIGNANT
HISTOGENIC CLASSIFICATION
VASCULAR TUMORS
HEMANGIOMA HEMANGIOPERICYTOMA
LYMPHANGIOMA
HISTOGENIC CLASSIFICATION
BENIGN MALIGNANT
EWING SARCOMA
ADAMANTINOMA
15
5
Figure 4-3-5
Figure 4-3-8
Figure 4-3-9
Biologic Activity
Margin Growth Rate
Geographic IA Slow
Geographic IB Slow to Intermediate
Geographic IC Intermediate
Motheaten Intermediate
Permeative Fast
1A Margin
[Figure 4-3-12]
• Geographic
• Well-Defined
• Sclerosis
Geographic 1A
Geographic 1A: Differential Diagnosis
[Figure 4-3-13] Figure 4-3-13
• Bone cyst
• Brodie abscess [Figure 4-3-14]
• Cartilage lesions
➢ Chondroblastoma
➢ Chondromyxoid Fibroma
➢ Enchondroma
• Fibroxanthoma
• Fibrous Dysplasia
Figure 4-3-16
Geographic 1B
Figure 4-3-17
1C Margin
[Figure 4-3-17]
• Geographic Geographic 1C
• Ill-Defined
Figure 4-3-18
Geographic IC: Differential Diagnosis
• Chondrosarcoma
• Enchondroma (Active)
• MFH/Fibrosarcoma [Figure 4-3-18]
• Giant Cell Tumor
• Osteosarcoma
• Metastasis/Myeloma
Tumor Margin
• Motheaten [Figure 4-3-19]
• Permeative[Figures 4-3-20 and 4-3-21]
Fibrosarcoma
Motheaten Permeative
Figure 4-3-22
Figure 4-3-23
Figure 4-3-24
Invisible Margin
[Figure 4-3-25: Lymphoma]
Figure 4-3-25
Lymphoma (same patient) with extensive marrow replacement (*) on T1 weighted MR, not seen on
radiograph images.
Figure 4-3-26
Figure 4-3-27
Figure 4-3-28
Figure 4-3-29
(a) (b)
(c) (d)
Figure 4-3-30
(a) (b)
(c) (d)
Langerhans cell histiocytosis with areas of calvarial lysis in the Multiple myeloma on lateral skull radiograph
frontal and occipital areas (arrows) with multiple areas of bone lysis
References
1. "General Considerations". In: Bone Tumors, ed Dorfman HD, Czerniak B, Mosby: St.
Louis 1998. p. 1-33.
2. Ghelman B. Radiology of bone tumors. Orthop Clin North Am. 1989 Jul;20(3):287-
312. Review.
3. Lodwick GS, Wilson AJ, Farrell C, Virtama P, Dittrich F. Determining growth rates of
focal lesions of bone from radiographs. Radiology. 1980 Mar;134(3):577-83.
4. Madewell JE, Ragsdale BD, Sweet DE. Radiologic and pathologic analysis of solitary
bone lesions. Part I: internal margins. Radiol Clin North Am. 1981 Dec;19(4):715-48.
5. Ragsdale BD, Madewell JE, Sweet DE. Radiologic and pathologic analysis of solitary
bone lesions. Part II: periosteal reactions. Radiol Clin North Am. 1981 Dec;19(4):749-
83.
6. Sweet DE, Madewell JE, Ragsdale BD. Radiologic and pathologic analysis of solitary
bone lesions. Part III: matrix patterns. Radiol Clin North Am. 1981 Dec;19(4):785-
814.
Figure 4-5-1
T1 T2
Lipoma (coronal T1 and T2-weighted images) isointense to fat
on all pulse sequences (*) with single thin septation (arrows)
Figure 4-5-3
II
III
Soft Tissue
High grade histo: IIA High grade histo: IIB Stage III
BONE BONE
Figure 4-5-7
Figure 4-5-10
Figure 4-5-11
Figure 4-5-13
Figure 4-5-14
CT Indications
• Cannot perform MRI
• Matrix producing neoplasm not adequately evaluated on radiographs
• Unusual location
➢ Ribs, sternoclavicular region, scapula
➢ Abdominal/chest wall
➢ Fibula
Figure 4-5-19
Figure 4-5-21
References
1. Berquist TH. Magnetic resonance imaging of musculoskeletal neoplasms. Clin Orthop Relat Res. 1989
Jul;(244):101-18. Review.
2. Sundaram M, McGuire MH. Computed tomography or magnetic resonance for evaluating the solitary tumor or
tumor-like lesion of bone? Skeletal Radiol. 1988;17(6):393-401.
3. Enneking WF. A system of staging musculoskeletal neoplasms. Clin Orthop Relat Res. 1986 Mar;(204):9-24.
4. Enneking WF, Spanier SS, Goodman MA. A system for the surgical staging of musculoskeletal sarcoma. Clin
Orthop Relat Res. 1980 Nov-Dec;(153):106-20.
5. Stacy SG, Mahal RS, Peabody TD. Staging of Bone Tumors: A Review with Illustrative Examples. Am. J.
Roentgenol., Apr 2006; 186: 967 - 976.
6. Murphy WA Jr. Imaging bone tumors in the 1990s. Cancer. 1991 Feb 15; 67(4 Suppl):1169-76. Review.
Osteopathia Striata: Radiology [Figures 4-5-5 to 4-5-7] Mixture of osteopoikilosis (circular areas of
• Linear bands of sclerosis from metaphysis in long bones sclerosis-arrow) and osteopathia striata (linear
• Fan-like bands of sclerosis in flat bones (iliac) areas of sclerosis-arrowhead)
➢ Could simulate heavy metal poisoning
• Sometimes associated with osteopoikilosis Figure 4-5-6
• Bone scan-normal
Melorheostosis: Pathology
• Thickened and enlarged cortical Figure 4-5-7
bone
• Haversian canals normal with
irregular arrangement
• Marrow space may show
increased cellularity
• Soft tissue may contain mass of
fibrous tissue with or without Mixture of osteopoikilosis (arrowhead)
and osteopathia striata (arrow) showing
ossification low signal intensity on MRI
Melorheostosis
involving foot
with increased
uptake on bone
Melorheostosis with mineralized
scan (same
inguinal soft tissue mass
patient as
(arrowhead)
previous two
images)
Figure 4-5-11
Osteoma: Clinical
Characteristics
• A benign, slow growing tumor, composed of osteoid tissue
• Found in cranial vault, sinuses, mandible and (rarely) long bones
• Represent protruding mass of dense periosteal intramembranous bone
on surface of host bone
• Signs/symptoms depend on size/location
• Sinus lesions may lead to sinusitis, headache, or can grow into cranial
vault
• Orbital lesion may cause exophthalmos, displacement of globe, diplopia
• 0.42% patients with sinus radiographs
Osteoma: Pathology
• Nodules of dense osseous tissue Calvarial osteoma (*)
• Differences from bone island:
➢ Often a mix of woven & lamellar bone Figure 4-5-12
➢ May/may not contain haversian system
➢ Arises from cortex rather than intramedullary
➢ Do not blend with trabecular bone
➢ Most frequent in the skull
• In craniofacial area often in spectrum of fibrosseous
lesions
Figure 4-5-17
Figure 4-5-19
Osteoblastoma
• Rare benign osteoid producing tumor characterized by osteoid and woven
bone production
• Synonyms include: giant osteoid osteoma and osteogenic fibroma Subtle intraarticular osteoid osteoma
• About 1.0% of excised primary osseous tumors (arrow) with central calcification
causing effusion and hip joint widening
• Osteosarcoma 20x more common, osteoid osteoma 4x more frequent simulating septic arthritis on CT and
MR. The CT shows typical nidus with
central calcification (arrow) that is
difficult to perceive on the MR
Osteoblastoma: Pathology
• Micro: large number of osteoblasts producing trabeculae, osteoid or
bone
• Virtually indistinguishable from osteoid osteoma on high-power
histologic examination
• At times minor microscopic differences from osteoid osteoma but may
rely on radiology
Osteoid Osteoma/Osteoblastoma
Differential Diagnosis: Spine
• Osteoblastoma
➢ Size > 1.5–2.0cm
➢ Growth and soft tissue mass
➢ Matrix - multifocal - noncentral
➢ Scoliosis and classic symptoms absent
• Pedicle sclerosis - lymphoma, mets, spondylolysis, congenital CT of C3 osteoblastoma with extensive
absence/ hypoplasia posterior elements, malaligned apophyseal joints, mineralization
unusual infection
Aggressive Osteoblastoma:
Clinical and Radiologic Characteristics
[Figure 4-5-25]
• Older patients average 33 years of age
• Similar locations
• Larger more aggressive on radiologic examination
with soft tissue mass Aggressive osteoblastoma with large soft tissue mass (arrow)
• Local recurrence rate up to 50% and multilevel involvement
• Usually no metastases
Osteosarcoma: Definitions
• A mesenchymal malignancy that differentiates to produce osteoid
• “...If only 1% of a tumor manifests osteoid and/or bone production by
malignant cells, it is by general convention an osteosarcoma”
• “No matter how meager the osseous component”
• Only true for intraosseous neoplasm
Mirra “Bone Tumors”. Lee & Febiger 1989
Osteosarcoma: Pathology-General
• Osteoid and/or immature bone production by tumor cells
• Malignant stromal cells graded on their degree of anaplasia I-IV
Osteosarcoma Telangiectatic
• Tumor largely composed of cystic cavities containing
necrosis and hemorrhage ( > 90%)
• ABC like – misdiagnosed on radiographs
• Distribution similar to other intramedullary
osteosarcomas
➢ Femur, tibia, humerus
➢ Metaphyseal (90%), diaphyseal (10%)
Juxtacortical Osteosarcoma
• Parosteal (65%)
• Periosteal (25%)
• High grade surface (10%)
• Prognosis varies with grade and extent
Intramedullary osteosarcoma with skip metastases (*) on
coronal STIR MR image and gross specimen with distal
primary lesion (arrow) and intervening normal marrow (M)
Telangiectatic osteosarcoma of
scapula with thick peripheral
mineralization (arrow) Telangiectatic osteosarcoma of scapula with thick enhancing
nodular wall containing calcification (arrowheads) and central
hemorrhage/necrosis (*) on CT
Figure 4-5-33
Figure 4-5-32
Figure 4-5-.37
Low-grade intramedullary
osteosarcoma simulating fibrous
dyplasia on radiograph and CT.
Note soft tissue mass medially (*)
Figure 4-5-44
Figure 4-5-45
References
1. Greenspan A, Stadalnik RC.. Bone island: scintigraphic findings and their clinical application. Can Assoc Radiol J. 1995
Oct;46(5):368-79.
2. Judkiewicz AM, Murphey MD, Resnik CS, Newberg AH, Temple HT, Smith WS. Advanced imaging of melorheostosis
with emphasis on MRI. Skeletal Radiol. 2001 Aug;30(8):447-53.
3. Klein MH, Shankman S. Osteoid osteoma: radiologic and pathologic correlation.
Skeletal Radiol. 1992;21(1):23-31. Review.
4. Kroon HM, Schurmans J. Osteoblastoma: clinical and radiologic findings in 98 new cases. Radiology. 1990
Jun;175(3):783-90.
5. Murphey MD, Robbin MR, McRae GA, Flemming DJ, Temple HT, Kransdorf MJ. The many faces of osteosarcoma.
Radiographics. 1997 Sep-Oct;17(5):1205-31.
6. Sundaram M, Falbo S, McDonald D, Janney C. Surface osteomas of the appendicular skeleton. AJR Am J Roentgenol.
1996 Dec;167(6):1529-33.
Osteochondroma
• The most common benign neoplasm of bone that
leads to biopsy
Osteochondroma: Pathology
• Medullary and cortical continuity with underlying
bone
• Hyaline cartilage cap
• Cartilage cap involutes after growth (skeletal
maturity)
• Only benign skeletal neoplasm associated with
radiation
• Can be induced by implanting epiphyseal tissue
• Traumatic osteochondroma
Gross specimen and macrosection of resected Axial T1-weighted MR images show cortical and marrow
osteochondroma with thin bluish cartilage cap (*) correlating ((arrowheads) continuity and thick cartilage cap (*) (15 year old
with the imaging (same patient as 4-6-5) boy; same patient as previous radiographs)
Enchondroma: Types
• Solitary enchondroma
• Multiple enchondromatosis
• Ollier disease
• Maffucci syndrome
Enchondroma: Clinical Data HME with typical pelvic and proximal femoral deformity. Bone
• 3%–5% all biopsied primary bone lesions; 1% all scan shows a left pelvic lesion to reveal more intense
bone tumors radionuclide uptake(*) and this area demonstartes a very thick
hyaline cartilage cap (>3 cm) and soft tissue mass with
• No sex predilection chondroid mineralization (rings and arcs) on radiograph, CT
• Peak incidence 3rd decade (10–30 years old) and T1/T2 weighted MR images (arrows) resulting from
• Hands and feet (40%–65%), long tubular bones malignant transformation to chondrosarcoma. This is also
(25%) shown on the gross specimen
• Phalanges and metacarpals most common locations
• May be incidental finding or present with pathologic fracture
Enchondroma: Pathology
• Rests of hyaline cartilage
• Hyaline cartilage often with myxoid areas
• Variable amorphous calcification and enchondral ossification
• May cause expansile remodeling and cortical thinning
Figure 4-6-18
Figure 4-6-19
Juxtacortical Chondroma
• Arise adjacent to cortex beneath periosteum
• Metaphyseal
• Proximal humerus (50%), femur and tibia also
hands and feet (25%)
• < 30 years old, M > F (2:1)
• Often more cellular than enchondroma
Chondroblastoma: Location
• Epiphysis/apophysis only 40%
• Epiphysis and metaphysis 55%
• Metaphysis only 4%
Chondroblastoma: Location
• Proximal femur 23%
➢ Head and neck 16%
➢ Trochanter 7%
• Distal femur 20%
• Proximal tibia 17%
• Proximal humerus 17%
• Hands and feet 10%
Chondroblastoma: Imaging
[Figures 4-6-24 to 4-6-28]
• Geographic lytic lesion IA / IB
• Eccentric > central; rarely expansile
• Calcified chondroid matrix 30% - 50%
• Periosteal reaction 30% - 50%
➢ Adjacent diaphysis/metaphysis Chondroblastoma of greater trochanter (apophysis =
• CT/MRI-fluid/fluid levels epiphyseal equivalent) on coronal T2-weighted MR image
• MRI – not typical chondroid characteristics with typical low signal intensity lesion (arrow)
➢ BEWARE!! - low/intermediate T2W ( 95%) and surrounding edema (*)
➢ Extensive surrounding edema
➢ Joint effusion (30% - 50%)
Figure 4-6-27
Chondroblastoma: Treatment
• Curettage and cryosurgery or en bloc resection
and bone graft
• Radiofrequency ablation
• Local recurrence 5%-10%
• Malignant chondroblastoma very rare
Figure 4-6-28
Chondroblastoma with ABC component in the patella
presenting as a pathologic fracture. Radiograph and sagitally
sectioned gross specimen and macrosection show the lytic
expansile lesion with fracture, largely composed of cystic areas
(*) and small solid component of chondroblastoma inferiorly
(arrow)
Intramedullary Chondrosarcoma:
Clinical Data
• Symptoms — pain (95%-99%) and mass (82%)
• Male > Female (3:2)
• Average age 40–45 years; metaphysis
• Location — femur (25%), pelvis (30%), shoulder
(15%), ribs/sternum (10%), vertebrae (7%),
scapula (5%)
• 8%-17% all biopsied primary bone tumors Low grade chondrosarcoma of the humerus with typical
features on multiple imaging modalities. Radiograph shows
typical ring and arc mineralization of a chondroid lesion (white
Intramedullary Chondrosarcoma: Imaging arrows) with deep endosteal scallop (black arrow).
[Figures 4-6-29 to 4-6-37] Bone scan reveals marked increased radionuclide uptake
• Geographic IA -IC to permeative
➢ Often predominantly sclerotic
• Deep endosteal scalloping
Figure 4-6-30
• Cortical thickening/periosteal reaction
• Expansile remodeling
• Soft tissue mass (20% - 76%)
• Chondroid matrix (78% by X-ray; 94% by CT)
• CT/conventional tomography if matrix subtle
• MRI - similar to muscle T1W images
➢ Lobulated high intensity T2W images
➢ Matrix calcification low intensity
➢ Peripheral/Septal contrast enhancement
Figure 4-6-32
Intramedullary
chondrosarcoma of femur with
chondroid mineralization
superiorly (arrow) and deep
area of scalloping laterally
(arrowhead)
Acetabular intramedullary
Figure 4-6-35 chondrosarcoma shows subtle bone
destruction (arrow) and matrix
mineralization in this
complex area of anatomy
Figure 4-6-36
Figure 4-6-37
Coronal T2-weighted MR image of acetabular intramedullary
chondrosarcoma shows large high signal intensity mass (*)
(same patient as previous CT)
Figure 4-6-41
Extraskeletal Chondrosarcoma:
Mesenchymal Type
• Young patients 23 – 44 years
• 20%–30% soft tissue
• Location – meninges and thigh
• High grade malignancy
• Mesenchymal cells with islands of cartilage
• Large soft tissue masses – may have chondroid Mesenchymal chondrosarcoma showing very aggressive bone
matrix calcification destruction with large soft tissue mass and chondroid matrix
• Metastases – lymph node, lung mineralization (arrows) on radiograph and CT
Figure 4-6-43
Mesenchymal Chondrosarcoma: Pathology
• Undifferentiated mesenchymal cells
• Multifocal islands of malignant cartilage
• Hemangiopericytoma like areas
• Aggressive high grade lesions
• Poor prognosis
Dedifferentiated Chondrosarcoma:
Pathology
• Low grade chondrosarcoma
• Small foci higher grade chondrosarcoma
• Spindle cell component
• MFH/ fibrosarcoma, osteosarcoma,
rhabdomyosarcoma, GCT
• Collision of two tumors
Dedifferentiated chondrosarcoma with radiographs showing
typical chondroid mineralization (rings and arcs-arrows). There
Dedifferentiated Chondrosarcoma: Imaging is anterior cortical destruction with a small soft tissue mass
[Figures 4-6-46 and 4-6-47] (arrowheads)
• Radiology emulates pathology: beware the dual
characteristic
➢ One region chondrosarcoma
➢ Second area aggressive bone destruction
• Cortical permeation and soft tissue mass (70%)
• Biopsy of anaplastic region – confusing
• Dedifferentiated component compared to chondroid component Figure 4-6-47
➢ Different intrinsic characteristics
➢ Different contrast enhancement (diffuse)
Radiologic Differential of
Chondrosarcomatous Lesions
• Aggressive chondroid lesion with soft tissue mass
➢ Higher grade conventional chondrosarcoma
➢ Dedifferentiated chondrosarcoma
➢ Mesenchymal chondrosarcoma
• Large fluid component bone or soft tissue
➢ Myxoid chondrosarcoma
• Change in appearance or foci of more aggressive
nature
➢ Dedifferentiated chondrosarcoma
Dedifferentiated chondrosarcoma with post contrast fat
suppressed T1-weighted MR image showing typical peripheral
Low-Grade Chondroid Lesion: and septal enhancement in the cartilaginous portion of the
Differential Diagnosis lesion (arrows) and diffuse enhancement in the dedifferentiated
• Enchondroma anterior soft tissue component (*) correlating with the sagitally
• Low-grade chondrosarcoma sectioned gross specimen
• Bone infarct
1. Bloem JL, Mulder JD. Radiol. 1985;14(1):1-9. Chondroblastoma: a clinical and radiological study of 104 cases.
Skeletal Radiol. 1985;14(1):1-9.
2. Murphey MD, Choi JJ, Kransdorf MJ, Flemming DJ, Gannon FH. Imaging of osteochondroma: variants and
complications with radiologic-pathologic correlation. Radiographics. 2000 Sep-Oct;20(5):1407-34. Review.
3. Murphey MD, Flemming DJ, Boyea SR, Bojescul JA, Sweet DE, Temple HT. Enchondroma versus chondrosarcoma
in the appendicular skeleton: differentiating features. Radiographics. 1998 Sep-Oct;18(5):1213-37; quiz 1244-5.
4. Murphey MD, Walker EA, Wilson AJ, Kransdorf MJ, Temple HT, Gannon FH. From the archives of the AFIP:
imaging of primary chondrosarcoma: radiologic-pathologic correlation. Radiographics. 2003 Sep-Oct;23(5):1245-
78. Review.
5. Robinson P, White LM, Sundaram M, Kandel R, Wunder J, McDonald DJ, Janney C, Bell RS. Periosteal chondroid
tumors: radiologic evaluation with pathologic correlation. AJR Am J Roentgenol. 2001 Nov;177(5):1183-8.
6. Wilson AJ, Kyriakos M, Ackerman LV. Chondromyxoid fibroma: radiographic appearance in 38 cases and in a review
of the literature. Radiology. 1991 May;179(2):513-8. Review. Erratum in: Radiology 1991 Aug;180(2):586.
Fibroxanthoma: Pathology
• Whorls/bundles of fibrous tissue
• Variable cellularity
• Giant cells
• Foam or xanthoma cells
• Areas hemorrhage/hemosiderin
Figure 4-7-4
Nonossifying
fibroma/fibroxanthoma in the
fibula with medullary location
(arrow) as is typical for lesions
in this location
Figure 4-7-6
Figure 4-7-7
Fibroxanthoma: Natural History
[Figures 4-7-6 and 4-7-7]
• Often heal with residual sclerosis start from diaphyseal
side
• May persist or grow
• Pathologic fracture – greater likelihood in lesions > 3
cm and with >50% bone width involved and weight
bearing bones
Figure 4-7-12
Figure 4-7-13
Figure 4-7-17a
Figure 4-7-17b
Osteofibrous Dysplasia:
Clinical Characteristics
• Unusual lesions – 0.2% of biopsied primary bone Monostotic fibrous dysplasia of the proximal femur with
tumors malignant transformation to MFH on radiograph and gross
• Patients <10 years age; rare after 16 years specimen. Note ground glass appearance distally (*) and more
• Tibia alone (75% - 80%) or also fibula (12%); fibula aggressive bone destruction proximal with extension through
lesser trochanter proximally (arrows)
only (7%), both tibiae (3%), rarely radius/ulna
Adamantinoma:
Radiology and Prognosis [Figures 4-7-21 to 4-7-24]
• MRI
➢ Very heterogeneous high intensity T2W
➢ Vascularity with prominent enhancement
• Locally aggressive
• 10 year survival: 10% - 65%
• 15% patients die with metastases
Osteofibrous Dysplasia:
Relationship to Adamantinoma
• Differentiation - patient age
➢ Multiple recurrence
➢ MRI heterogeneous, intense enhancement
• Epithelial nests; both can be keratin positive
• Several cases reported of foci of adamantinoma in osteofibrous
dysplasia and progression to adamantinoma
Adamantinoma of the tibia on radiograph with
mixed lytic and sclerotic lesion centered in the
cortex and an elongated lesion
Cortical Desmoid [Figures 4-7-26 and 4-7-27 overleaf] Desmoplastic fibroma of the iliac bone with prominent
• Avulsive cortical injury (chronic) multilocular appearance caused by internal trabeculation
• Posteromedial distal femur metaphysis
• Stress related at attachment
➢ Adductor magnus
➢ Medial head gastrocnemius
• Pathology simulates aggressive lesion
• Children 1st decade (35%)
• More frequent in boys, often bilateral
• Surface irregularity/lucency
• CT – looks like NOF – no soft tissue mass
• MRI – may see surrounding inflammation
Fibromatosis: Types
• Extra-abdominal desmoid (deep)
Figure 4-7-28
• Aggressive infantile fibromatosis (deep)
• Juvenile aponeurotic fibroma (sup.)
• Infantile dermal/digital fibromatosis (sup.)
• Adult palmar and plantar (sup.)
• Infantile myofibromatosis (both)
Fibromatosis: Pathology
• Gross - glistening white, variable cellularity
• Spindle shaped fibrous cells
• Abundant collagen, can see mitoses
• Infiltrative growth common
• No malignant potential Post-contrast axial T1-weighted MR image showing
extraabdominal desmoid (fibromatosis) with an enhancing
Fibromatosis: Radiology paraspinal mass (*) and ill-defined margins
• Soft tissue mass, unusual to calcify
• Can erode adjacent bone
• CT-soft tissue mass – may show attenuation greater than muscle
• MRI Figure 4-7-29
➢ T1W image – low / intermediate signal
➢ T2W image – variable signal
➢ Fascial tail sign
➢ Low signal bands
• Enhance with contrast
Fibromatosis:
Juvenile Aponeurotic Fibroma Aggressive infantile fibromatosis on sagittal T1-weighted MR
image with large mass eroding bone (*) which ultimately led to
• Children/adolescents; M>F amputation following multiple recurrences.Note low intensity
• Hands (77%), feet (13%) – palms and soles bands (arrowheads)
• Painless slowly growing mass
• Calcification and local recurrence (50%) common
• Attached to tendon/aponeurosis Figure 4-7-31
Infantile Myofibromatosis
• Discovered at birth or within weeks
• Solitary form (good prognosis)
Multifocal (poor prognosis) – soft tissue, muscle,
viscera
• Bone lesions common but involute
Osseous MFH with radiograph showing solitary geographic
• Lesions grow in perinatal period lytic lesion with wide zone of transition (arrows)
• Myoblastic and fibroblastic lesion
Fibrosarcoma: Pathology
• Malignant collagen producing spindle cells
• “Herringbone” pattern – lower grade lesions (I-II)
• Higher grade (III-IV) lesions – more anaplasia
• No matrix or malignant giant cells
Soft tissue MFH with mass replacing vastus lateralis muscle (*) on
axial T1-weighted MR image [left]; with high signal intensity mass (*)
on axial T2-weighted MR image [right]
Largely hemorrhagic (*) soft tissue MFH in Sagittal T1-weighted MR images before and after contrast
the anterior thigh on CT with the only solid show enhancement of the solid component (arrowheads) of the
component adjacent to the anteromedial MFH and nonenhancing hemorrhagic areas (*)
femur (arrowhead)
Figure 4-7-42
Fibrosarcoma and MFH:
Therapy and Prognosis
• Treatment - wide local resection/amputation
• Local recurrence common (50%)
follow up imaging
• Metastasis (40%) common
hematogenous - lung, lymph nodes, liver and
bone
Dermatofibrosarcoma Protuberans
(DFSP): Clinical Features
• 6% all soft tissue tissue sarcomas
• Third to fifth decades of life
• Reddish brown to bluish superficial nodule
• May be multiple
• Most common to affect trunk (50%) Soft tissue MFH with soft tissue mass (*) causing extrinsic
➢ Remainder head/neck, upper/lower extremities erosion of adjacent femur (arrowheads)
T1
1. Fitzpatrick KA, Taljanovic MS, Speer DP, Graham AR, Jacobson JA, Barnes GR, Hunter TB. Imaging findings of
fibrous dysplasia with histopathologic and intraoperative correlation. AJR Am J Roentgenol. 2004 Jun;182(6):1389-
98. No abstract available.
2. Jee WH, Choe BY, Kang HS, Suh KJ, Suh JS, Ryu KN, Lee YS, Ok IY, Kim JM, Choi KH, Shinn KS. Nonossifying
fibroma: characteristics at MR imaging with pathologic correlation. Radiology. 1998 Oct;209(1):197-202.
3. Jee WH, Choi KH, Choe BY, Park JM, Shinn KS. Fibrous dysplasia: MR imaging characteristics with radiopathologic
correlation. AJR Am J Roentgenol. 1996 Dec;167(6):1523-7.
4. Murphey MD, Gross TM, Rosenthal HG. Musculoskeletal malignant fibrous histiocytoma: radiologic-pathologic
correlation. RadioGraphics 1994; 14:807-826.
5. Ritschl P, Karnel F, Hajek P. Fibrous metaphyseal defects--determination of their origin and natural history using a
radiomorphological study. Skeletal Radiol. 1988;17(1):8-15.
6. Robbin MR, Murphey MD, Temple HT, Kransdorf MJ, Choi JJ. Imaging of Musculoskeletal Fibromatosis.
RadioGraphics 2001; 21:585-600.
7. Torreggiani WC, Al-Ismail K, Munk PL, Nicolaou S, O'Connell JX, Knowling MA. Dermatofibrosarcoma protuberans:
MR imaging features. AJR Am J Roentgenol. 2002 Apr;178(4):989-93.
8. Van der Woude HJ, Hazelbag HM, Bloem JL, Taminiau AH, Hogendoorn PC. MRI of adamantinoma of long bones
in correlation with histopathology. AJR Am J Roentgenol. 2004 Dec;183(6):1737-44.
Giant Cell Tumor: Radiology [Figures 4-8-1 to 4-8-10] CT of giant cell tumor shows no mineralized
• Solitary eccentric geographic lytic lesion extending into matrix (*) (same patient as previous
subchondral bone radiograph)
• Center of lesion-metaepiphysis
• Margin IB (80%-85%), IC (10%-20%), IA (1%-2% but up to 20% by CT)
• No mineralized matrix
Figure 4-8-4
Giant cell tumor of distal femur shows well defined geographic (1B
margin-arrow)) lysis extending to subchondral bone. Bone scan
reveals marked increased uptake in femur. Bone scan reveals
marked increased uptake in the femoral GCT but also in the
adjacent tibia and patella. The increased uptake in the tibia and
patella are due to hyperemia and disuse, not tumor involvement
Figure 4-8-5
Figure 4-8-6
Sagittally sectioned gross specimen and macrosection
show identical findings as on the previous images of this
benign giant cell tumor including extension to subchondral
bone (arrows) and anterior soft tissue component (*)
Figure 4-8-8
Figure 4-8-7
Aneurysmal bone cyst (primary) with more prominent expansile Aneurysmal bone cyst (primary) with “donut” sign (increased
remodeling of bone posteriorly (more aggressive appearance- uptake peripherally and photopenia centrally) on bone
arrow) versus rim of sclerosis in other areas (indolent scintigraphy (same patient as previous radiographs)
appearance-arrowheads)
Figure 4-8-18
Figure 4-8-17
T2
Subchondral Cyst
• Other terms - geodes and synovial cyst; no true epithelial or
synovial lining
• Middle to older aged patients
• Around joints and associated with other arthritic changes
• Etiology - synovial fluid intrusion vs. osseous contusion
• Can be large/solitary, articular damage subtle simulating neoplasm
(GCT)
Intraosseous Ganglion [Figures 4-8-23 and 4-8-24] Epidermoid inclusion cyst with well-
• Uncommon lesion; middle aged adults defined terminal phalangeal lytic lesion
• Pain increases with activity (arrows)
• Periarticular, eccentric, geographic IA-B lytic lesion
Figure 4-8-23
• Tibia (medial malleolus), femur, about wrist (>65%
of lesions)
• Pathology - same as soft tissue ganglion
Figure 4-8-25
1. Kransdorf MJ, Sweet DE. Aneurysmal bone cyst: concept, controversy, clinical presentation, and imaging. AJR Am
J Roentgenol. 1995 Mar;164(3):573-80. Review.
2. Martinez V, Sissons HA. Aneurysmal bone cyst. A review of 123 cases including primary lesions and those secondary
to other bone pathology. Cancer. 1988 Jun 1;61(11):2291-304.
3. Murphey MD, Nomikos GC, Flemming DJ, Gannon FH, Temple HT, Kransdorf MJ. From the archives of AFIP.
Imaging of giant cell tumor and giant cell reparative granuloma of bone: radiologic-pathologic correlation.
Radiographics. 2001 Sep-Oct; 21(5):1283-309. Review.
4. Parman LM, Murphey MD. Alphabet Soup: Cystic Lesions of Bone. Seminars in Musculoskeletal Radiology 2000;
4(1):89-101.
Tumoral calcinosis about the elbow extensor surface. Tumoral calcinosis about the hip
Contralateral elbow revealed identical findings (not with calcium fluid levels (arrowheads) on CT
shown)
Figure 4-9-6
P V N S: Pathology
• Etiology unknown - inflammatory/neoplasm/trauma
• Variable degree of villous/nodular synovial proliferation and pigmentation
(hemosiderin) and inflammation components
• Giant cells, fibrous tissue, xanthoma cells
GCT-TS: Radiology
• Second most common mass hand/wrist
• Lobulated soft tissue mass < 2 cm
• More common volar surface
• Osseous erosion uncommon 10%–15%
Same patient as previous MR image with intermediate signal PVNS of the hip (diffuse type) with radiograph showing
intensity in the giant cell tumor of tendon sheath (*) of the erosions on both sides of the joint (arrows) and maintained
thumb on axial T2-weighted MR joint space
Figure 4-9-10
Figure 4-9-14
Myxoma: Pathology
• Ovoid/globular whitish
appearance Intraarticular ganglion (*) in the knee on sagittal
• Contain gelatinous T2-weighted MR image with septations and
material Intraarticular ganglion in the knee on CT marked high signal intensity (same patient as
• Unusual to have cystic with low attenuation and multiple previous CT)
spaces septations (*)
• No fibrous capsule, but edema and muscle atrophy surround mass
Synovial Lipoma
• Two types Lipoma arborescens with villonodular fronds of
➢ Localized form fatty tissue (arrows) extending into the knee joint
➢ Diffuse form - lipoma arborescens on sagittal T1-weighted MR image
Figure 4-9-29
Figure 4-9-30
Figure 4-9-31
Figure 4-9-34
Figure 4-9-41
References
1. Al-Nakshabandi NA, Ryan AG, Choudur H, Torreggiani W, Nicoloau S, Munk PL, Al-Ismail K. Pigmented villonodular
synovitis. Clin Radiol. 2004 May;59(5):414-20. Review.
2. Kransdorf MJ, Meis JM, Jelinek JS. Myositis ossificans: MR appearance with radiologic-pathologic correlation.
AJR Am J Roentgenol. 1991 Dec;157(6):1243-8.
3. Martinez S, Vogler JB 3rd, Harrelson JM, Lyles KW. Imaging of tumoral calcinosis: new observations. Radiology. 1990
Jan;174(1):215-22.
4. Murphey MD, Choi JJ, Kransdorf MJ, Flemming DJ, Gannon FH. Imaging of osteochondroma: variants and
complications with radiologic-pathologic correlation. Radiographics. 2000 Sep-Oct;20(5):1407-34. Review.
5. Murphey MD, McRae GA, Fanburg-Smith JC, Temple HT, Levine AM, Aboulafia AJ. Imaging of Soft Tissue Myxoma
with Emphasis on CT and MRI and Comparison of Radiologic and Pathologic. Radiology 2002; 225:215-224.
6. Ortega R, Fessell DP, Jacobson JA, Lin J, Van Holsbeeck MT, Hayes CW. Sonography of ankle Ganglia with
pathologic correlation in 10 pediatric and adult patients. AJR Am J Roentgenol. 2002 Jun;178(6):1445-9.
7. Robinson P, White LM, Kandel R, Bell RS, Wunder JS. Primary synovial osteochondromatosis of the hip: extracapsular
patterns of spread. Skeletal Radiol. 2004 Apr;33(4):210-5. Epub 2004 Feb 18.
8. Steinbach LS, Johnston JO, Tepper EF, Honda GD, Martel W. Tumoral calcinosis: radiologic-pathologic correlation.
Skeletal Radiol. 1995 Nov;24(8):573-8.
9. Tschirch FT, Schmid MR, Pfirrmann CW, Romero J, Hodler J, Zanetti M. Prevalence and size of meniscal cysts,
ganglionic cysts, synovial cysts of the popliteal space, fluid-filled bursae, and other fluid collections in asymptomatic
knees on MR imaging. AJR Am J Roentgenol. 2003 May;180(5):1431-6.
10. Valenzuela RF, Kim EE, Seo JG, Patel S, Yasko AW. A revisit of MRI analysis for synovial sarcoma. Clin Imaging.
2000 Jul-Aug;24(4):231-5.
Angiomatous Lesions
• Hemangioma
• Lymphangioma
• Glomus Tumor
• Angiomatosis and associated syndromes
• Hemangioendothelioma
• Hemangiopericytoma
• Angiosarcoma
Hemangioma: Pathology
• Subtype based on predominant vascular
component – but usually mixed tumor
• Capillary – most common – first years of life –
skin, subcutaneous, vertebrae (low flow)
• Cavernous – childhood – larger and deeper
(low flow)
• Arteriovenous – deep or superficial – persistent
fetal capillary bed (high flow)
• Venous – adults – deep involvement –
retroperitoneum, mesentery or extremities Vertebral hemangiomas with thickened vertical trabeculae
(low flow) (arrows-corduroy appearance) on radiograph and coronally
• Epithelioid – dermis/subcutis sectioned gross specimen (different patients)
S.T. Hemangioma Radiology: Calvarial hemangioma with spoke wheel pattern of trabecular
S.T. Changes [Figure 4-10-6] thickening (arrows) on radiograph, CT and vascular
• Calcification – curvilinear or amorphous, phlebolith channels/spaces on gross specimen (arrowheads)
(30%-50% of lesions)
• Angiography – irregular enlarged feeding arteries, Figure 4-10-5
contrast pooling, arteriovenous shunting
• Venous lesions seen only with venography
Figure 4-10-6
Figure 4-10-7
Figure 4-10-12
Lymphangioma:
Clinical Characteristics
• Rare lesion in bone, usually S.T.
• Often present at birth (50% – 65%)
• 90% apparent by age 2 years
• Head, neck, axilla – 75% of cases
• Soft fluctuant mass
Lymphangioma of the neck on CT with a
Lymphangioma: Pathology homogeneously low attenuation mass (*)
• Sequestrated noncommunicating lymphoid tissue
• Large multiloculated cystic spaces
• Lined by lymphatic endothelium
• Filled with proteinaceous material Figure 4-10-14
Angiomatosis
• Multifocal or diffuse infiltration of bone by hemangiomatous or Lymphangioma of the neck in an infant on
lymphangiomatous lesions with or without soft tissue coronal T1-weighted MR image with
involvement heterogeneous mass (arrow) showing both
high and low signal intensity areas extending
Angiomatosis: Clinical Characteristics along the chest wall (arrowhead)
• Young patients – first 3 decades
• M > F (2:1)
• Osseous involvement only – benign course
• Visceral involvement – poor prognosis Figure 4-10-15
• No malignant potential
Angiomatosis: Pathology
• Capillary or cavernous hemangioma’s
• Lymphangioma’s – lymphatic backflow
• Mixed vascular lesion difficult to distinguish
Angiomatous Syndromes
• Maffucci syndrome
• Osler – Weber – Rendu
• Klippel – Trenaunay – Weber
• Massive osteolysis of Gorham
• Associated osteomalacia and thrombocytopenia
Maffucci Syndrome
Angiomatosis (lymphangiomatosis) with extensive infiltration of
• Multiple enchondromata the entire lower extremity causing elephantiasis on coronal T1-
• Cavernous soft tissue hemangiomata weighted MR image and clinical photograph
• Often hands/feet, unilateral predominance
• Malignant potential both lesions and viscera
Klippel-Trenaunay-Weber
[Figure 4-10-17]
• Nonhereditary, lower extremity
• Unilateral cutaneous capillary
hemangioma
• Varicose veins and local gigantism Klippel-Trenaunay-Weber syndrome on clinical photograph and coronal T1-
• Can have arteriovenous component weighted and T2-weighted MR images showing classic triad of
hemihypertrophy,varicose veins and extensive predominantly slow flow
Massive Osteolysis of Gorham: angiomatous lesion (arrowheads). Smaller high flow component is also seen on
“Vanishing Bone Disease” T2-weighted image (arrows)
[Figure 4-10-18]
• Patients < age 40 years
• History trauma 50% Figure 4-10-18
• Upper extremity favored, may extend across joint
• Progressive bone resorption and fragmentation
(simulate neuropathic)
• Pathology - proliferating vascular channels
Hemangioendothelioma (HE)
• Intermediate – benign or malignant
• Composed of vascular endothelial cells
• Often in young patients
• Bone or soft tissue
• Locally aggressive, unusual to metastasize
Hemangiopericytoma (HPC)
• Intermediate – benign or malignant
• Tumor of cells around vessels – pericytes
• Tumor of middle-aged adults
• Sites – soft tissue of thigh, pelvis and retroperitoneum
• Rare in bone
Angiosarcoma (ASC)
• Malignant; M > F (2:1)
• Composed of hemangiosarcoma or lymphangiosarcoma cellular
elements
• Location: skin, muscular, viscera, bone
• Associated with lymphedema post-mastectomy (Stewart-Treve
syndrome) Malignant hemangioendothelioma of bone with
multifocal lytic lesions (arrowheads) in the tibia
and fibula on radiograph and osseous
Osseous HE, HPC, ASC: Skeletal Location replacement by hemorrhagic tissue (*) on
• Hemangioendothelioma: skull, vertebrae, lower extremity photograph of coronally sectioned gross
• Hemangiopericytoma (rare): pelvis, proximal long bones, specimen
vertebrae, mandible
• Angiosarcoma: long tubular bone lower extremity
Hemangiopericytoma in of the thigh showing high flow vessels (arrows) in the soft tissue mass (*) and
feeding the lesion on both axial T1-weighted and coronal T2-weighted MR images. Photograph of the
sectioned gross specimen also shows the soft tissue mass (*) and the high flow vessels (arrowheads)
Cannot distinguish HE, HPC or ASC from other soft tissue masses
if prominent serpentine vessels are not recognized
Summary:
Musculoskeletal Angiomatous Lesions
• Osseous – Multifocal bone lysis – Honeycomb appearance
• Look for serpentine vascular pattern – MRI
• Overgrowth of fat – MRI
• Multiple associated syndromes and angiomatosis
• Higher grade lesions – HE, HPC, ASC
➢ Larger aggressive lesions
➢ Infiltrative characteristics
References
1. Baudrez V, Galant C, Vande Berg BC. Benign vertebral hemangioma: MR-histological correlation. Skeletal Radiol.
2001 Aug;30(8):442-6.
2. Coldwell DM, Baron RL, Charnsangavej C. Angiosarcoma. Diagnosis and clinical course. Acta Radiol. 1989 Nov-
Dec;30(6):627-31.
3. Fayad L, Hazirolan T, Bluemke D, Mitchell S. Vascular malformations in the extremities: emphasis on MR imaging
features that guide treatment options. Skeletal Radiol 2006; 35:127-137.
4. Laredo JD, Assouline E, Gelbert F, Wybier M, Merland JJ, Tubiana JM. Vertebral hemangiomas: fat content as a sign
of aggressiveness. Radiology. 1990 Nov;177(2):467-72.
5. Lorigan JG, David CL, Evans HL, Wallace S. The clinical and radiologic manifestations of hemangiopericytoma.
AJR Am J Roentgenol. 1989 Aug;153(2):345-9.
6. Murphey MD, Fairbairn KJ, Parman LM, Baxter KG, Parsa MB, Smith WS. From the archives of the AFIP.
Musculoskeletal angiomatous lesions: radiologic-pathologic correlation. Radiographics. 1995 Jul;15(4):893-917.
Paget Disease: Clinical Presentation Marrow replacement by fibrovascular tissue (*) in active Paget
• Pain disease (left image) versus fat (F) in marrow with inactive
disease (right image)
• Osseous bowing and enlargement
• Neurologic symptoms Figure 4-11-2
• High output congestive failure
• Lab
➢ Serum alkaline phosphatase (blastic phase)
➢ Urinary and blood hydroxyproline (lytic phase)
Figure 4-11-4
Figure 4-11-5
Lytic phase of Paget disease with sharp margins and subchondral extension
Figure 4-11-8
Figure 4-11-9
Coronal T1-weighted (noncontrast) and axial T1-weighted (after contrast) MR Axial T2-weighted MR image shows
images show speckled marrow pattern with enhancement in more active Paget speckled pattern of increased intensity (*)
disease (noncomplicated) (*) and more intense enhancement of the intracortical in more active Paget disease
component that is most active (noncomplicated-same patient as previous
MRI and radiograph)
Paget Disease: Complications Figure 4-11-17
• Osseous deformity
• Fractures
• Neurologic symptoms
• Arthropathy
• Neoplasm
Paget Disease:
Differential Diagnosis
• Diffuse sclerosis – chronic renal
failure (CRF), myelofibrosis,
metastasis, lymphoma, sickle cell
anemia
• Trabecular thickening – hemangioma,
chronic infection, osteomalacia,
fluorosis
• Polyostotic lesions – CRF
(hyperparathyroidism), Langerhans
Paget disease with malignant transformation to osteosarcoma in the humeral
cell histiocytosis, unusual infection, midshaft where there is mass-like marrow replacement (*) and soft tissue
metastasis, fibrous dysplasia, extension (arrows) on radiograph and multiple sagittal T1-weighted MR
lymphoma, Gaucher, mastocytosis images, CT and gross specimen
Figure 4-11-23
Paget Disease: Treatment
• Calcitonin – inhibits resorption
• Biphoshonates – inhibits bone
resorption and production
• Mithramycin – cytotoxic antibiotic
• Often relieve pain
Paget Disease:
Radiology Post-Treatment
• Often subtle or no change
• Occasionally improved radiographs
• Watch for fractures: may increase
with diphosphonates
• Bone scans best treatment indicator
Hereditary Hyperphosphatasia:
Juvenile Paget Disease
• Described 1956: Bakwin/Elger Paget disease with benign giant cell tumor of the clavicle associated with
• Autosomal recessive pathologic fracture showing cortical thickening (arrows) and destructive lesion
(*) on CT scans, gross specimen radiograph and gross specimen
• Disorder of infants/children
• Elevated alkaline and acid phosphatase, uric acid
Figure 4-11-24
Juvenile Paget Disease: Radiographic Findings
[Figure 4-11-24]
• Generalized cortical thickening
• All bones including skull involved
• Osteopenia and bowing
• Epiphyses may be spared
• Patients severely deformed
References
1. Boutin RD, Spitz DJ, Newman JS, Lenchik L, Steinbach LS.. "Complications in Paget disease at MR imaging."
Radiology. 1998 Dec;209(3):641-51.
2. Cooper C, Dennison E, Schafheutle K, Kellingray S, Guyer P, Barker D.. "Epidemiology of Paget's disease of bone."
Bone. 1999 May;24(5 Suppl):3S-5S.
3. Moore TE, Kathol MH, el-Khoury GY, Walker CW, Gendall PW, Whitten CG.. "Unusual radiological features in
Paget's disease of bone." Skeletal Radiol. 1994 May;23(4):257-60.
4. Smith SE, Murphey MD, Motamedi K, Mulligan ME, Resnik CS, Gannon FH.. "From the archives of the AFIP.
Radiologic spectrum of Paget disease of bone and its complications with pathologic correlation." Radiographics.
2002 Sep-Oct;22(5):1191-216.
5. Vande Berg BC, Malghem J, Lecouvet FE, Maldague B.. "Magnetic resonance appearance of uncomplicated Paget's
disease of bone." Semin Musculoskelet Radiol. 2001;5(1):69-77.
6. Vellenga CJ, Bijvoet OL, Pauwels EK.. "Bone scintigraphy and radiology in Paget's disease of bone: a review." Am
J Physiol Imaging. 1988;3(3):154-68.
Figure 4-12-2
Progression of osteomyelitis through the cortex into the subperiosteal space (*)
Osteomyelitis: Organisms
• Staph aureus (80% - 90% of pyogenic cases)
• H. flu, strep (shoulder, trauma from delivery)
• Gram negatives, uncommon except enterics (25% of infections)
• Pseudomonas – penetrating trauma/IVDA
• Salmonella – sickle cell
• Blood cultures positive 50%
Figure 4-12-5
Pictorial
representation of
infection
deposition sites
in an infant long
bone
Figure 4-12-6
Figure 4-12-7
Figure 4-12-8
There is marrow replacement on the T1-weighted MR image with focal rim enhancing subperiosteal abscess (arrowheads) posteriorly
showing high signal on T2-weighting (*)
Figure 4-12-19
Osteomyelitis/Septic Arthritis
Contiguous Spread: Source
• Soft tissue infection
➢ Trauma
➢ Human/animal bites
➢ Puncture wounds
➢ Ulcers
➢ Surgery
Osteomyelitis/Septic Arthritis
Contiguous Spread: Radiographs
• Soft tissue swelling/air
• Periosteal reaction Chronic osteomyelitis of the ulna
• Cortical destruction into marrow with diffuse sclerosis on
• Joint space loss radiograph
Osteomyelitis/Septic Arthritis
Contiguous Spread: Other Sites [Figure 4-12-21]
• Foot – pathways: medial, intermediate, lateral
➢ Puncture: pseudomonas
➢ Diabetes: multiple organisms
➢ Aerobic/anaerobic
Diabetic patient with ulcer lateral to fifth MTP joint and
• Pelvis – decubitus ulcers (paraplegics)
radiograph shows underlying destruction of distal fifth
➢ Ischial tuberosity chronic osteomyelitis metatarsal head and proximal phalanx resulting from
• Post-operative: ring sequestra osteomyelitis and pyarthrosis. Amputation specimen shows
similar findings
Osteomyelitis: Diabetes Mellitus Figure 4-12-22
• Bone destruction/periosteal reaction
• Bone scan – normal – no osteomyelitis
• WBC scan – good predictive value
• MRI – marrow replacement geographic area T1 and
increased signal STIR, post gado
➢ Normal on T1 or subtle/subcortical only; then
probably marrow reaction not osteomyelitis
(Collins et al AJR 185:2005)
➢ Focal fluid collections
Osteomyelitis vs Neuropathic
Diabetes Mellitus
• Factors favoring infection: Sinus tract (84%/0%); ST
replacement (68%/32%); Fluid collection
(95%/48%); Extensive marrow abnormality
(41%/12%)
• Factors favoring neuropathic: Thin rim enhancement Chronic osteomyelitis with sinus tract and secondary
of effusion (68%/21%); Presence of subchondral epidermoid carcinoma. Aggressive bone destruction is seen
cysts (76%/2%); Intraarticular bodies (53%/12%) distally and medially corresponding to malignancy (arrow
and *) as sinus tract enters bone
Ahmadi et al, Radiology 238; 622-631, 2006
Figure 4-12-24
Septic Arthritis: Pathology [Figure 4-12-23]
• Synovial inflammation /hyperemia/fluid production
• Fibrin deposits inhibit cartilage nutrition
• Attract WBC’s release enzymes (collagenase)
• Pannus formation
• Cartilage destruction/bone erosion
Septic Arthritis:
Complications/Sequelae [Figure 4-12-26]
• Avascular necrosis Septic arthritis in the right hip of a young child with joint widening
• Slipped epiphysis indicating a joint effusion on radiography
• Growth disturbance
• Osteomyelitis Figure 4-12-26
• Secondary osteoarthritis
• Synovial cyst, tendon/capsule injury
Cellulitis
• Acute inflammatory process of deep subcutaneous tissues
• Location
➢ Extremities, thorax, abdomen, neck
• Organisms
➢ Streptococci, staphylococci, H. influenza
Invertebral Discitis:
Clinical Characteristics
• Hematogenous – children (1–16 years)
➢ Disc vascularized
• Symptoms – mild after primary infection
• Cultures negative (50%–90%); staph aureus
• Antibiotics given empirically
Brucellosis
• Malta fever – undulant fever
• WHO – 500,000 cases annually
• B. – abortis, melitensis, suis, canis
• Endemic Midwest USA, Saudi Arabia, South America, Spain, and Italy
• Ingested milk/meat – reticuloendothelial system (marrow)
Tuberculous Spondylodiscitis
• May result in neurologic symptoms
• Hematogenous – venous (Batson) plexus
• L1 most common: decreases above/below
• More than one level frequent
➢ Usually contiguous
➢ Separate foci: 1%–4%
Tuberculous Osteomyelitis
• Not common, usually with arthritis
• Often epiphyseal, any bone, joint
• Children metaphyseal cross plate
• Cystic variety – multifocal defined lytic foci
• Dactylitis – < age 5 (0.5%–14% cases)
➢ Multifocal (25%–35%)
➢ Spina (spike-like) ventosa (puffed full of air)
a b
Tuberculous spondylodiscitis:
a) Radiographs show myelographic block (arrowhead) with
endplate destruction, collapse, and disc involvement (arrow);
b) CT reveals large paraspinal mass (*);
c) Sagittal T1-weighted MR images show marrow replacement
and disc involvement at two levels (arrowheads) as well as
anterior paraspinal and posterior epidural masses (arrows) ;
d) Sagittal and axial post-contrast T1-weighted MR images
reveal rim enhancement about anterior paraspinal and
posterior epidural abscesses (arrows);
e) High signal intensity is seen on the axial and sagittal T2-
weighted MR images in the involved vertebrae, discs and
paraspinal abscesses (*)
c
e
d
Teardrop paraspinal calcification (*) in CT of the spine in a patient with tuberculous spondylodiscitis and
a tuberculous paraspinal abscess calcified paraspinal abscesses (arrows)
related to spondylodiscitis
Figure 4-13-8
Tuberculous Arthritis [Figure 4-13-8]
• Large joints (knee/hip); monoarticular
• Synovial thickening covered by fibrin
• Granulation tissue erodes cartilage bone
• Slow process/lack proteases
• Areas of cartilage contact spared
Figure 4-13-10
Pelvis radiographs over a
two month interval show
slow pancompartmental
loss of the right hip joint
resulting from tuberculous
arthritis
Figure 4-13-12
Figure 4-13-13
Spirochetes
• Syphilis
• Yaws
Actinomyces osteomyelitis in the mandible on radiograph
• Lyme disease
showing patchy areas of destruction and sclerosis (arrowheads)
• Tropical ulcer
• Bejel, rat bite, fever, leptospirosis
Yaws
• Treponema pertenue
• Africa, South America, South Pacific
• Very similar to syphilis – less nose changes, more phalanges (spares distally)
• Exostosis maxilla – goundou
Tropical Ulcer
• Central/East Africa
• Lower leg ulcer destroys muscle/tendon
• To bone focal osseous production tibia/fibula
• Multiple organisms including spirochetes
• Epidermoid carcinoma 25% (>10 years latency)
Candidiasis (Moniliasis)
• C. Albicans but many other species
• Patients on hyperal, antibiotics, intraarticular steroids
• Bone involvement rare (1%–2%)
• Monostotic/monoarticular – long bone, sternum, spine, knee
• Arthritis more often precedes osteomyelitis
Coccidioidomycosis
• C. Immitis – soil- inhalation
• SW USA, Mexico
• <1% disseminated; (10%–50% MSK changes)
• Metaphyseal, may be symmetric Aspergillus infection with pulmonary
• Joints – ankle, knee, also migratory arthritis and rib (arrowheads) involvement
Histoplasmosis
• H. Capsulatum – USA (Miss. River Valley)
• H. Dubosii – Africa – MSK changes 80% cases
• Soil – inhalation; most common fungal in USA
• Pelvis, skull, ribs, small tubular bones
• Arthritis – knee, ankle, wrist, hand
Mucormycosis
• Phymycetes – rhizopus, mucor, absidia
• Diabetes, uremia, burns
• Entry via sinuses
• Skull/face (maxillary/ethmoid sinuses)
• Bone destruction
Sporotrichosis
• Sporothrix schenckii Blastomycosis of the humerus with
extensive involvement demonstrating
• Saprophyte on vegetation
mixed lysis and sclerosis
• Inhalation/skin wound (rose thorn)
• Disseminated form 80% MSK changes
• Arthritis (monoarticular) common – knee (66%) hand wrist (52%) ankle, elbow
• Osteopenia often not prominent
• Osteomyelitis – due to arthritis
Figure 4-13-19
Figure 4-13-20
Sporotrichosis of
the knee with CT
(post-arthrogram)
and MR showing
enhancing
nonspecific
nodular synovial
thickening
(arrowheads) after
intravenous
contrast
Histoplasmosis with multifocal area of lysis, many of which
involve tuberosities and trochanteric regions ("lumps and
bumps" of bone)
Helminths/Worms
• Musculoskeletal changes usually soft tissue
calcification
• Loa loa - Africa – subcutaneous calcification (fine
lace-like or thicker bead-like)
• Filariasis – lymphatic obstruction (elephantiasis)
• Guinea worm (dracunculosis) – long calcification
female worm lower extremity hand – can cause
arthritis
• Cysticercosis – linear/oval rice grain calcification
along axis of muscle (up to 20–25 mm length)
Mycetoma (Madura foot) on radiographs, sagittal T1-and T2-
weighted MR images and gross specimen show extensive
Echinococcus: Musculoskeletal Changes multifocal destruction with sclerosis/fibrosis representing
[Figure 4-13-23] chronicity
• Echinococcus (E. multilocularis/granulosis)
• Bone disease: 0.5%–4% (E. granulosis) Figure 4-13-22
• Spine, long bone epiphysis,iIlium, skull, rib
• Multiloculated (bundle of grapes) lysis/expansion
• May be soft tissue loculated, cyst margins may
calcify
Sarcoid: Musculoskeletal
• Usually have chest changes (80%–90%)
• Muscle – myositis (50%–80% patients)
➢ MRI low signal central scar
• Subcutaneous soft tissue nodules (5%)
• Arthritis (10%–35%) – acute/chronic
➢ Hand, wrist, ankle, knee, elbow
Sarcoid - Musculoskeletal:
Osseous Changes [Figures 4-13-24 and 4-13-25]
• 1%–13% of patients; may be asymptomatic
• Lattice like lysis (hands)
• Punched out lytic lesions
• May appear aggressive
• Acroosteolysis, acrosclerosis (30%–50%)
• Areas of sclerosis Coronal STIR MR shows a focal fluid collection (*)
• Marrow replacement creating mottled appearance representing pyomyositis in an HIV patient
(MRI)
1. Erdman WA, Tamburro F, Jayson HT, Weatherall PT, Ferry KB, Peshock RM. Osteomyelitis: characteristics and
pitfalls of diagnosis with MR imaging. Radiology. 1991 Aug;180(2):533-9.
2. Jung NY, Jee WH, Ha KY, Park CK, Byun JY. Discrimination of tuberculous spondylitis from pyogenic spondylitis
on MRI. AJR Am J Roentgenol. 2004 Jun;182(6):1405-10.
3. Lawson JP, Rahn DW. Lyme disease and radiologic findings in Lyme arthritis. AJR Am J Roentgenol. 1992
May;158(5):1065-9. Review.
4. Palestro CJ, Kipper SL, Weiland FL, Love C, Tomas MB. Osteomyelitis: diagnosis with (99m)Tc-labeled
antigranulocyte antibodies compared with diagnosis with (111)In-labeled leukocytes--initial experience. Radiology.
2002 Jun; 223(3):758-64.
5. Sharif HS, Aideyan OA, Clark DC, Madkour MM, Aabed MY, Mattsson TA, al-Deeb SM, Moutaery KR. Brucellar
and tuberculous spondylitis: comparative imaging features. Radiology. 1989 May;171(2):419-25.
6. Sharma P. MR features of tuberculous osteomyelitis. Skeletal Radiol. 2003 May; 32(5):279-85. Epub 2003 Mar 25.
7. Unger E, Moldofsky P, Gatenby R, Hartz W, Broder G. Diagnosis of osteomyelitis by MR imaging. AJR Am J
Roentgenol. 1988 Mar;150(3):605-10.
Figure 4-14-9
Figure 4-14-10
Lateral radiograph of a bilateral facet dislocation
with anterolisthesis (arrow) at C4-5. Also on the
lateral film the inferior facets (IF) of the level
above is anterior to the superior facets (SF) of
the level below
Atlas Fractures
• Avulsion of anterior arch C1
➢ Rare stable injury
➢ Results from anterior atlantoaxial ligament
➢ Horizontal cleft in anterior arch (difficult on CT)
• Posterior C1 arch fracture
➢ Bilateral posterior fractures (no anterior
component)
➢ No anterior soft tissue swelling; stable
➢ Distinguish from normal congenital cleft
Laminar Fractures
• Lamina crushed on extension from above/below
• Often in older patients with spondylosis Pictoral representation of an extension injury
• Usually C5 to C7
• Difficult to detect on radiographs
• CT optimal
• Mechanically stable (Intact anterior column/facets)
• Neurologically unstable due to cord impingement by fragments
Hyperextension Fracture/Dislocation:
Pedicolaminar Fracture-Separation
• Combined hyperextension, compression and rotation
• Fractures of pillar, lamina, pedicles and spinous process opposite
side of translation Lateral radiograph of an extension fracture
• Vertebral body often mildly (3 – 6 mm) anteriorly displaced subluxation at C5-6 (arrow) in a patient with
• Spinous process not rotated ankylosing spondylitis (syndesmophytes-
arrowhead)
Hyperextension Fracture/Dislocation:
Pedicolaminar Fracture-Separation
Radiologic Characteristics
• Disc narrowing and vertebral rotation above injury
• Opposite facet may be widened/dislocated
• Commonly involve foramen transversarium
➢ Vertebral artery (MRA)
• Important to distinguish from flexion injury
Pillar Fracture
• Not common, 3% - 11% of cervical injuries (C6 – C7)
• Hyperextension and rotation
• Articular mass compressed on side of rotation
• Stable, radiculopathy common without cord damage
Traumatic Spondylolisithes:
“Hangman” Fracture (“Hangee” Fracture)
• Common 5% of all cervical spine injuries
• Hyperextension is probably transient modified by
flexion/compression/distraction Pictoral representation of an extension teardrop fracture
• Unstable injury
• Neurologic symptoms unusual unless distraction
➢ Large canal relative to cord at C2
Figure 4-14-17
➢ “Autodecompression” from bilateral
posterior fractures
Traumatic Spondylosithes:
Radiologic Characteristics
[Figures 4-14-18 and 4-14-19]
• Effendi classification
➢ I: Minimally displaced fracture
➢ II: More displacement, involves C2 -
3 disc (widening)
➢ III: Bilateral facet dislocation
• Oblique C2 pedicle fracture – lateral view
• Mild anterolisthesis, posteriorly displaced
spinolaminar line
• Associated injuries-anterior corner
fractures C2/C3
➢ C1/high thoracic fractures (10%)
➢ Vertebral artery injuries
Lateral radiograph and tomogram of an extension teardrop fracture with
Figure 4-14-18 avulsed fragment (arrow) from the attached anterior longitudinal ligament (ALL)
Figure 4-14-19
Jefferson Fracture:
Radiologic Characteristics
[Figure 4-14-21] Pictoral representation of a Jefferson fracture
• Open mouth view best
➢ Laterally displaced lateral masses
• Lateral radiograph may only show soft tissue swelling; look Figure 4-14-21
for posterior fractures
• CT optimal for bilateral fractures
➢ Jefferson variants
• Lateral mass displacement > 7 mm / predental space > 6
mm = ruptured transverse atlantal ligament
• Small nondisplaced fragment medial to articular mass –
intact ligament
Figure 4-14-22
Lateral radiograph, axial CT and sagittal CT of burst type fractures in different patients showing the comminuted fracture (circle),
retropulsed fragments (solid arrows) and fracture at the junction of the lamina and spinous process (open arrow)
Odontoid Fracture
• Most common of C2 fractures (41%)
• 11% - 13% of all cervical spine injuries
• Mechanism – flexion and or extension
• Other fractures (13%) – face, mandible,
posterior arch C1, extension teardrop,
hangman, atlantoaxial dissociation
• Anderson/D’Alonzo classification
Figure 4-14-25
Figure 4-14-26
References
1. Blackmore CC, Mann FA, Wilson AJ.. "Helical CT in the primary trauma evaluation of the cervical spine: an
evidence-based approach." Skeletal Radiol. 2000 Nov;29(11):632-9. Review.
2. Jarolimek AM, Coffey ECC, Sandler CM, West OC. "Imaging of uppercervical spine injuries -- Part III: C2
below the dens." Applied Eadiology. 2004 July; 9-21.
3. Murphey MD, Batnitzky S, Bramble JM. "Diagnostic imaging of spinal trauma." Radiol Clin North Am. 1989
Sep;27(5):855-72.
4. Stabler A, Eck J, Penning R, Milz SP, Bartl R, Resnick D, Reiser M.. "Cervical spine: postmortem assessment of
accident injuries--comparison of radiographic, MR imaging, anatomic, and pathologic findings." Radiology. 2001
Nov;221(2):340-6.
Generalities
• Dentists like plain films
• Act as radiologist
➢ Oral & Maxillofacial Surgery
➢ Oral & Maxillofacial Radiology
Primary Dentition
Eruption/Exfoliation
Tooth Numbering
Primary Tooth Numbering
Primary tooth “numbering”
Tooth Numbering
Imaging Techniques
• Intraoral
➢ Bitewing
➢ Periapical
➢ Occlusal
• Extraoral
➢ Panoramic
➢ AP, PA, lateral, oblique, Water’s, Townes
➢ CT, MRI, technetium scan
Bitewing
Radiographic Description
• Size : in centimeters
• Border: well circumscribed, poorly circumscribed, ill-
defined
• Shape: unilocular, multilocular, uniform, irregular
• Number: focal, multifocal
• “Color”: radiolucent, radiopaque, mixed;
➢ buzzwords: “ground glass”, “cotton wool”
• Location: exact location within the maxilla or
mandible; location in relation to adjacent structures
(periapical, interradicular, pericoronal, etc)
• Teeth
➢ Impaction, displacement, or resorption
• Periodontal supporting structures
➢ Periodontal ligament space enlargement or loss
Tooth numbering (adult)
of the lamina dura
Overview
• Radiolucent lesions
➢ Periapical
➢ Pericoronal
➢ Multilocular
• Radiopaque/mixed density lesions
➢ Periapical
➢ Interradicular
➢ Multifocal confluent
➢ Target lesion
• Osteosarcoma of the gnathic skeleton
Periapical cyst/periapical granuloma
Radiolucent Lesions: Periapical
• Periapical granuloma
• Periapical cyst
• Traumatic bone “cyst” Figure 4-15-2
• Nasopalatine duct cyst
• Early focal cemento-osseous dysplasia
Cemento-osseous Dysplasia
• Focal
➢ Single site
➢ 90% occur in F
➢ Whites > blacks
➢ Posterior mandible most common site
❖ Many occur in extraction sites
➢ Most lesions smaller than 1.5 cm in diameter
➢ Well defined
• RL ---> mixed density ---> RO
➢ Early lesions RL
➢ Calcification with maturation of lesion
Odontogenic Keratocyst
• Treated by thorough enucleation and curettage
• Occasionally, en bloc resection required
• Up to 1/3 will recur
• Long term radiographic follow-up requiredfollow-up quiredfo
• If multiple, evaluate for nevoid basal cell carcinoma syndrome
(Gorlin syndrome)
Figure 4-15-9
Ameloblastoma
• Treatment:
➢ Curettage or en bloc resection for mandibular lesions
➢ Resection for maxillary lesions
➢ Recurrence rate is high
➢ Unilocular ameloblastomas have a better prognosis with rare
recurrence and requiring only simple enucleation
➢ Rare malignant transformation has been reported
Condensing Osteitis
• Tx/prognosis
➢ Endodontic/ext
➢ 85% regress or resolve
➢ Bone scar
❖ Residual lesion
Focal sclerosing osteomyelitis (condensing
Radiopaque and Mixed Lesions: Interradicular osteitis)
• Ossifying fibroma
➢ Active ossifying fibroma
• Focal cemento-osseous dysplasia
• Osteoblastoma
• Adenomatoid odontogenic tumor
• Odontoma
Fibrous Dysplasia
• Occurs in children, teenagers and young adults of both sexes Figure 4-15-17
• Four main forms: monostotic, polyostotic, McCune-Albrights,
and craniofacial
➢ Craniofacial FD may involve multiple contiguous bones in
the midface and cranium
➢ McCune-Albright’s disease includes polyostotic FD, focal
skin hyperpigmentation (“café-au-lait spots”) and endocrine
disturbances (usually precocious puberty and/or
hyperthyroidism)
• Painless expansile process of osteoprogenitor tissue
• Slow growth with facial deformity
• More common in the maxilla Fibrous dysplasia (“ground glass”
appearance)
Lecture Outline
• Part 1
➢ Technique
➢ Menisci
• Articular cartilage
• Part 2
➢ Bones
➢ Stabilizers
➢ Miscellaneous
Technique
• Surface coil
• High resolution
• T1, T2, fat suppression
• Sagittal, coronal, axial planes
Menisci: Attachments
[Figures 4-16-5 and 4-16-6]
• Tibia
• Capsule Figure 4-16-6
• Ligaments
➢ Transverse
➢ Meniscofemoral Normal transverse intermeniscal ligament
❖ Humphrey
❖ Wrisberg
➢ Oblique menisco-
meniscal
Meniscus
• Microstructure
➢ Collagen bundles
❖ Circumferential
❖ Transverse (“tie fibers”)
➢ Resist longitudinal loading
❖ “hoop stresses”
Menisci: Pathology
• Degeneration
• Tear
➢ traumatic vs. degenerative
• 20% asymptomatic pts > 50 y.o. show MR evidence of tear
A. Diagram of a meniscus cut in cross-section
Surgical Considerations revealing an oblique undersurface tear.
• Primary goal B. Similar tear in the posterior horn of the
➢ Preserve as much meniscal tissue as possible medial meniscus on sagittal image
Figure 4-16-13
Radial tear involving the body of the lateral meniscus (arrow)
Figure 4-16-12
Meniscal Tears [Figure 4-16-12]
• Longitudinal
➢ Vertical
➢ Along axis of meniscus
➢ Bucket handle
❖ displaced fragment
❖ medial meniscus
❖ locking
➢ Peripheral
❖ potentially reparable
❖ outer 1/3 (red zone)
Longitudinal tear
Peripheral Tears [Figure 4-16-13]
• Outer 1/3 of meniscus
• Vascular region
➢ (red/red zone)
• Tend to heal A. Diagram of a peripheral tear.
➢ primary repair B. Peripheral tear involving the posterior horn
of the medial meniscus (arrow).
➢ conservative therapy
Coronal image corresponding to the dashed line Sagittal image corresponding to the dashed line shows the
demonstrates the displaced meniscal fragment of this bucket large bucket handle fragment within the notch creating the
handle tear (large arrow) and irregular, truncated body of the “double PCL” sign (P = PCL)
meniscus (thin arrow)
Menisci: Post-surgical
• Truncated, absent, “normal”
• Healed tear can look like new tear
• MR arthography
➢ 0.2 cc Gd + 20 cc saline
➢ T1W with fat-saturation
➢ Gd extending into tear
Menisci: Post-surgical
• Signs of new or recurrent tear?
➢ Fluid in tear
➢ Displaced fragment
➢ Tear in new area
References
1. Helms CA, Laorr A, Cannon WD, Jr. The absent bow tie sign in bucket-handle tears of the menisci in the knee.
AJR Am J Roentgenol 1998; 170:57-61.
Bones
• Femur, tibia, patella, fibula Spectrum of acute osseous injuries
• Cortical
➢ compact
➢ subchondral plate
• Cancellous
➢ trabecular Figure 4-17-2
Trabecular Bone
• 10 x load-bearing capacity of cortical bone
• Dissipates forces
• Support for subchondral plate
Bones: Injuries
• Acute
➢ Impaction (contusion, occult fracture)
➢ Avulsion
• Chronic
➢ Fatigue, insufficiency fracture
• Spontaneous osteonecrosis
• Osteochondritis dissecans
Figure 4-17-5
Acute Trauma: Fracture [Figure 4-17-6]
• Linear
➢ T1
❖ – signal intensity
➢ STIR
❖ + or – signal intensity
Figure 4-17-6
Figure 4-17-12
Figure 4-17-13
Normal MCL
Patellofemoral Joint
• Patellar subluxation
➢ Lateral
➢ Hypoplastic intercondylar notch
Patellofemoral Syndrome
• Anterior pain
• Patellar tilt / subluxation
• Impingement of infrapatellar fat
“Cystic” Structures
• Recesses
• Bursae
• Ganglia Patellar tendinits with thickening and
high grade partial tearing in its proximal
Normal Recesses fibers
• Suprapatellar “bursa”
• Infrapatellar cleft Figure 4-17-18
• Popliteus hiatus
• Gastrocnemius/ Semimembranosus
• Posterior recesses
Synovial Plica
• Embryologic remnants
• Infrapatellar
• Suprapatellar
• Medial
Loose Bodies
[Figure 4-17-20]
• Intercondylar notch Loose body in posterior joint recess (arrow)
• Baker’s cyst
• Popliteus sheath
• GRE (T2*)
References
1. Johnson DL, Urban WP, Jr., Caborn DN, Vanarthos WJ, Carlson CS. Articular cartilage changes seen with
magnetic resonance imaging-detected bone bruises associated with acute anterior cruciate ligament rupture. Am J
Sports Med 1998; 26:409-414.
Anatomy: Coronal
• Bones
• Intrinsic ligaments.
• TFCC
Anatomy: Axial
• Tendons
• Three levels
➢ Distal radioulnar joint
➢ Pisotriquetral joint
➢ Hamate
• Median nerve (Carpal tunnel)
• Ulnar nerve (Guyon’s canal)
Anatomy: Sagittal
• Carpal alignment
• Pisotriquetral joint
• Triangular fibrocartilage
Anatomy / Pathology
• Bones
• Intrinsic ligaments (SL, LTL)
• TFCC
• Tendons
• Nerves
• Masses
Bones: Normal
• Signal intensity
Alignment
➢ sagittal alignment
➢ ulnar variance
AVN Lunate
• Kienbock’s Disease Mid scaphoid fracture
Left: Coronal T1 - Right: Coronal STIR
• Repetitive trauma, fracture, ulna (-) variance
• End arteries Figure 4-18-4
• Central position
Figure 4-18-6
Intrinsic Ligaments
• Pitfalls
➢ Intermediate signal
➢ Attach to bone or articular cartilage
Carpal Stability
• Scaphoid <-> Lunate <-> Triquetrum
Figure 4-18-11
DISI deformity
SLAC wrist
Figure 4-18-14
Normal volar and dorsal radioulnar ligaments (arrows), and normal TFC
(open arrow).
Extensor Compartments
• 1st Abd. pollicis longus
Ext. pollicis brevis
• 2nd Ext. carpi radialis longus/brevis
• Lister’s Tubercle A. Artifactual intermediate signal in the flexor pollicis longus
tendon on gradient echo image.
• 3rd Ext. pollicis longus
B. Tendon appears normal on fat-saturated T2-weighted image
• 4th Ext. digitorum
Ext. indicis
• 5th Ext. digiti minimi Figure 4-18-18
• 6th Ext. carpi ulnaris
Tendon Pathology
• Tenosynovitis
➢ Surrounding fluid, +/- enlargement
➢ Stenosing (loculated, septations)
• Partial tear
➢ Enlarged / thinned / focal signal
• Complete tear
Bones
• Marrow Edema Fracture of the anterior process of the
calcaneus
• Differential Diagnosis
➢ Activity related
➢ Contusion/occult fracture Figure 4-19-2
➢ Osteonecrosis
➢ Osteomyelitis
➢ Tumor
• Interosseous ligament
• Anterior tibiofibular
• Posterior tibiofibular
• Talus = rectangular
Calcaneonavicular coalition
Figure 4-19-7
Figure 4-19-10
Plantar Fasciitis
• Inflammation
➢ Mechanical (pes cavus, etc.)
➢ Degenerative (age related) Normal plantar fascia
➢ Systemic disease (RA, seronegative)
• DDx:
Figure 4-19-14
➢ Calcaneal stress fx
➢ Tendinitis
➢ Heel pad trauma/inflammation
Tendons
• Change orientation
• Pulleys
➢ Osseous or soft tissue
• Magic angle effect
Figure 4-19-18
Figure 4-19-19
Figure 4-19-25
Ganglion cyst (G) displacing the neurovascular Split peroneus brevis tendon (arrow = intact
bundle (arrow) within the tarsal tunnel peroneus longus tendon)
References
1. Mintz DN, Tashjian GS, Connell DA, Deland JT, O'Malley M, Potter HG. Osteochondral lesions of the talus: a new
magnetic resonance grading system with arthroscopic correlation. Arthroscopy 2003; 19:353-359.
Learning Objectives
• Recognize the spectrum of imaging appearances of
these specific osseous lesions
• Identify differentiating features
Ewing Sarcoma
• Highly malignant primary bone sarcoma
• Ewing provided first comprehensive description in
1921, designating it “diffuse endothelioma” of bone Sheets of monotonous malignant "round cells“ with indistinct
• Later (1924) termed “endothelial myeloma” of bone, cytoplasmic margins. Areas of necrosis and hemorrhage are
frequent
and “Ewing Tumor” by Codman
• Origin controversial but likely derived from primitive
mesenchyme
Hair-on-end” periosteal reaction Ewing sarcoma with pathological fracture. Radiograph (left) and
bone scan (right)
Ewing sarcoma. Flat bone (rib). Large soft tissue Ewing sarcoma. Note permeative osteolysis with
mass obscure osseous origin evidence of associated mass
LCH: History
• 1940: Jaffe & Lichtenstein eosinophilic granuloma
• 1941: Farber, Green & Farber EG could be solitary or multiple
• 1953: Lichtenstein proposed the name histiocytosis X for the inflammatory
histiocytoses
LCH: Phases
• Solitary or multiple lesions localized to bone: Eosinophilic granuloma (> 5 y)
• Chronic disseminated histiocytosis: Hand-Schuller-Christian disease (1–5 y)
• Acute or subacute disseminated histiocytosis: Letterer-Siwe disease (<1 y)
• Supports the concept that this is a disorder of immune regulation
LCH: Phases
• LCH, localized to bone: limited to a single or a few bones
• LCH, chronic disseminated: multifocal bone lesions and es involvement of
lymph nodes, skin and abdominal viscera
• LCH, acute or subacute disseminated: disseminated multisystem involvement
Eosinophilic Granuloma:
Pathologic Features [Figures 4-20-13 and 4-20-14]
• Characterized by a collection of histiocytes
• Histiocytes are either oval, lobulated or reniform,
w/ clefts or indentations
• Eosinophils may be seen singly, in sheets,
clusters or not at all
• Birbeck bodies on EM
Hand-Schuller-Christian Disease:
LCH Chronic Disseminated
• Patients are young, usually less than 5 years
• Classic triad in 10%–15%, <50% have DI, exophthalmos about 25%
• Any bone may be involved, 90% have cranial involvement, 7% hand or foot
lesion(s)
• Hepatosplenomegaly and adenopathy
• Anemia, fever, neurologic complaints
• Fatal in about 15%, morbidity may be high
Summary
• Review the imaging appearances of Ewing sarcoma and the family of lesions
know as Langerhans cell histiocytosis
• Demonstrate how the radiologic images reflect the underlying pathophyiology
and appropriate differentiating features
References
Learning Objectives
• Recognize the spectrum of common lipomatous soft tissue masses
• Identify the radiologic appearance of the common fatty masses
• Identify imaging limitations and pitfalls
Outline:
• Fundamental definitions
• Incidence of soft tissue tumors
• Overview
• Common lipomatous tumors
• Liposarcoma
• Mimics
• Cases
Definitions
• Soft tissue is the nonepithelial extraskeletal tissue, excluding the RES, glia and
supporting tissue of parenchymal organs
• It is derived primarily from mesenchyme, and by convention is comprised of
skeletal muscle, fat, fibrous tissue and the serving vessels and nerves.
Incidence: Variations
• It is estimated that the relative frequency of benign to malignant tumors is
100:1
• US overall annual incidence: 1.4 per 100K
• Age specific incidence ≥ 80 years: 8.0 per 100k
Classification
• World Health Organization subdivides benign lipomatous tumors into 9 groups
• For imaging purposes, it is more useful to use the classification proposed by
Weiss and Goldblum
Weiss SW, Goldblum JR. Enzinger and Weiss’s Soft Tissue Tumors, 4th ed. St.
Louis; 2001
Figure 4-21-4
T1 T2
MR. Fibrolipoma
Figure 4-21-7
Figure 4-21-8
Intramuscular Lipoma
• Lipoma arising in skeletal muscle
• Most common member of subgroup of lipomatous tumors (fatty tumors arising
in intimate association with non-adipose tissue)
• Other entities in this category include: intermuscular lipoma, lipoma of tendon
sheath, and lipomatosis of nerve
Figure 4-21-10
Liposarcoma
• Malignant mesenchymal tumor
• Second most common soft tissue tumor after MFH
• Approximately 16%–18% all sarcomas
• Presents ages 40–60 years
• Exceedingly rare in children
• Usually extremities or retroperitoneum
• Extremity lesions present 5–10 yrs earlier
Lipomatosis. Clinical photo. MR different patient
Classification: World Health Organisation Figure 4-21-14
(WHO) (From low to high)
• Well differentiated
• Myxoid
• Pleomorphic
• Dedifferentiated
Classification:
World Health Organisation (WHO)
• Well differentiated ---> Dedifferentiated
• Myxoid ---> Round cell *
• Pleomorphic
* Round cell liposarcoma was previously a distinct
subtype, now considered the hypervascular variant
of myxoid liposarcoma
Liposarcoma:
Well-Differentiated [Figure 4-21-16] Lipomatosis trunk
• Predominantly fatty mass, usually more than 75% fat
• Irregularly thickened or nodular septa
Figure 4-21-15
• Presence of nodular/globular areas
• A small number of lipomas will have a similar
imaging appearance
Figure 4-21-16
A B
Mild lipomatosis right lower extremity
C
D
Well-differentiated
liposarcoma. Typical features.
Radiograph (a), CT (b),
MR T1 (c) and T2 (d).
Liposarcoma: Dedifferentiated
[Figures 4-21-18]
• Bimorphic lesion with:
➢ WD liposarcoma
➢ Juxtaposed high grade sarcoma (MFH)
• Most common dedifferentiated sarcoma
• May be a time-related phenomenon
• Imaging typically shows a well differentiated fatty
mass
Well-differentiated liposarcoma. Typical features
• Fatty mass associated with a focal dominant
nonadipose component
Figure 4-21-18
Liposarcoma: Higher Grade Lesions
[Figure 4-21-19]
• Only 50%-80% of the myxoid or pleomorphic types
show fat on imaging studies
• Fat usually minor component (<25%)
• Hypervascular myxoid (round cell) and pleomorphic
types are typically more heterogeneous
Figure 4-21-20
Liposarcoma: Mimics
• Hemorrhage
• Malignancies engulfing portion fat
• Muscle atrophy with fat replacement
• Myxoid tumors: intramuscular myxoma, ES myxoid chondrosarcoma, myxoid
MFH
• Neural tumors
Summary
• Fatty tumors are common
• There is a wide spectrum of lipomatous tumors
• Imaging of fatty tumors is frequently characteristic
References
1. Christopher et al. WHO Classification of tumors. Lyon, France: IARC Press; 2002
2. Kransdorf et al. Fat-containing masses of the extremities. RadioGraphics 1991;11:81
3. Peterson et al. Malignant fatty tumors. Skeletal Radiol 2003;32:493
4. Weiss & Goldblum. Enzinger and Weiss's Soft Tissue Tumors, 4th ed. St. Louis: CV Mosby; 2001
Learning Objectives
• Identify the pathophysiologic alterations that occur
in rickets and osteomalacia and scurvy
• Recognize the spectrum of radiological features of
these diseases
Osteomalacia
• Inadequate or delayed mineralization of mature
cortical or spongy bone
Pitt MJ. Rad Clin No Amer:1991;29:97
Osteoporosis
• Insufficient quantity of normal bone
Osteopenia
• Increased radiolucency of bone
Vitamin D: Prohormone
• D2 – Synthetic
• D3 – Natural
Normal bone formation (left); rachitic bone formation (right)
Vitamin D: Biochemistry
[Figure 4-22-1]
Figure 4-22-4
Vitamin D: 1, 25 Dihydroxyvitamin D
[Figures 4-22-2 to 4-22-4]
• Most active form of vitamin D
• Calcium/phosphorus homeostasis
• Maintenance bone mineralization
Osteoid seams
Figure 4-22-6
Figure 4-22-7
Craniotabes Overgrowth wrist cartilage (a) with corresponding clinical photo (b)
Figure 4-22-14
25-OH Vitamin D
• Liver disease
• Anticonvulsant therapy
Looser zones
Rachitic disease with fracture distal left femur Rachitic disease from nec
Figure 4-22-17
Renal Related
[Figures 4-22-17 to 4-22-19]
• 1, 25 Dihydroxyvit D
➢ Renal osteodystrophy
➢ Vitamin D dep rickets
➢ Tumor related
• Renal Tubular Disorders
➢ X-linked hypophosphatasia
➢ Familial vitamin D res rickets
➢ Fanconi syndromes
➢ Tumor related
➢ Ifosfamide
Figure 4-22-18
Figure 4-22-19
Scurvy: Pathophysiology
• Deficiency of dietary vitamin C
• Decrease cellular activity
• Decreased collagen and osteoid production
Figure 4-22-22
Figure 4-22-23
References
1. Holick. Vitamin D deficiency: what a pain it is. Mayo Clin Proc 2003;78:1457
2. Leggett et al. Scurvy. NEJM 2001;345:1818
3. Narchi et al. Symptomatic rickets in adolescence. Arch Dis Chil 2001;84:501
4. Pitt. Rickets and osteomalacia. In: Resnick. Diagnosis of bone and joint disorders, 4th ed. Philadelphia, W.B.
Saunders Company, 2002:1901
5. Sundaram et al. Oncogenic osteomalacia. Skeletal Radiol 2000; 29:117
Learning Objectives
• Identify the spectrum of radiological features of osteonecrosis
• Recognize various associated conditions
• Identify differentiating features
Outline
• Definitions
• Pathophysiology of osteonecrosis
• Infarct geometry
• Radiologic-pathologic correlation
• Associations
• Complications
• Related conditions
Definitions
• Osteonecrosis – ischemic death of cellular components of bone and marrow
• Aseptic necrosis – equivalent to ischemic necrosis and avascular necrosis
• Bone infarct – osteonecrosis involving the metaphysis or diaphysis
• Osteochondrosis – variety of conditions in which there is increased bone
density
Figure 4-23-1
Pathophysiology: Osteonecrosis
• Cellular changes from ischemic injury
➢ Interruption of intracellular enzymes
➢ Cessation intracellular metabolic activity
➢ Cell death
• Cellular sensitivity to anoxia
➢ Hematopoietic elements (6 hrs – 12 hrs)
➢ Bone cells (12 hrs – 48 hrs)
➢ Marrow fat cells (48 hrs – 5 days)
Osteonecrosis: Radiologic-Pathologic
Correlation
[Figures 4-23-2 and 4-23-3]
• Phase I: Cellular death initial response
• Phase II: Cell modulation
• Phase III: Emergence reactive interface
• Phase IV: Remodeling reactive interface
• Phase V: Crescent sign & collapse
Osteonecrosis: Causes
• Thrombophilia (increased tendency to develop
thrombosis)
• Hypofibrinolysis (reduced ability to lyse thrombi)
• Found in 76% of patients with osteonecrosis*
*Glueck et al. Osteonecrosis. AAOS 1997
Osteonecrosis: Causes [Figure 4-23-4] Radiograph and specimen radiograph showing osteonecrosis
• Increased size fat cell → compresses sinusoid with collapse and crescent sign
vascular bed → impedes blood flow
Figure 4-23-4
Figure 4-23-5
Figure 4-23-9
Figure 4-23-11
Figure 4-23-13
Complications: Osteonecrosis
[Figures 4-23-16]
• Cartilaginous abnormalities
• Intra-articular loose bodies
• Cyst formation
• Malignant transformation
Figure 4-23-16
Bilateral osteonecrosis
Osteochondritis Dissecans
[Figures 4-23-19 to 4-23-21]
• Fragmentation and possible separation of articular
surface
• Typically childhood to adolescent
• Variable symptoms
• Non-weight bearing surface
• Classic: lateral medial femoral condyle
• Probably traumatic in origin Spontaneous osteonecrosis medial femoral condyle.
Presentation (a) and at 5 months (b)
Figure 4-23-18
Figure 4-23-19
MR-Osteochondritis dissecans, classic location Osteochondritis dissecans, classic location, Radiograph (left)
and MR (right)
Scheuermann Disease
[Figures 4-23-23]
• Described in adolescent farm workers
• Common, seen in about 4%–8% population
• Presents second decade, M=F
• Variable clinical presentation
• Radiographs show end plate irregularity, narrowed
disc spaces, and Schmorl’s nodes involving three
or more vertebrae
References
1. Sweet et al. Osteonecrosis: pathogenesis. In: Resnick D, ed. Diagnosis of bone and joint disorders, 4th ed.
Philadelphia: WB Saunders, 2002
2. Iida et al. Correlation between bone marrow edema and collapse of the femoral head in steroid-induced
osteonecrosis. AJR 2000;174:735
3. Vande Berg et al. MR imaging of avascular necrosis and transient marrow edema of the femoral head.
RadioGraphics 1993;13:501
4. Glueck et al. Thromophilia, hypofibrinolysis, and osteonecrosis. Clin Orthop 1997;334:43
Radiographic Assessment
• Soft Tissue Swelling
• Soft Tissue Calcification
• Mineralization
• Joint Space Change AP radiograph with non specific fusiform soft tissue swelling
• Erosion surrounding the proximal interphalangeal joint of the ring finger.
• Bone Production Clinical photograph in a different patient with rheumatoid
• Subluxation arthritis and synovitis and fusiform soft tissue swelling involving
the proximal interphalangeal of the index and middle fingers
• Distribution
Mineralization
• Normal
• Juxta-articular AP radiograph of patient with psoriatic arthropathy and diffuse
• Diffuse swelling of the second toe producing a sausage appearance of
the digit. Clinical photograph in a different patient with psoriatic
arthropathy and sausage enlargement of the third and fourth
Juxtaarticular Osteoporosis [Figure 4-24-4] toes
Figure 4-24-3
Figure 4-24-4
Figure 4-24-6
Figure 4-24-8
Rheumatoid Arthritis
• Most common in females – 2–4:1
• Most common in the fourth and fifth decades
• Incidence – 0.2-0.4/1,000 in females
• Prevalence – 0.5% – 1.0%
• Probably heterogeneous disorder
Patient A has psoriatic arthritis with erosions and bone
production in the metatarsal phalangeal and interphalangeal
Rheumatoid Arthritis joints. Bone formation is present amongst the erosive changes
• Genetic influence – HLA-DR4 (DRB1 allele) producing a “whiskering” type appearance and the digits are
• Pregnancy – increased risk postpartum dense secondary to osteitis. Patient B has rheumatoid arthritis
with erosive disease in the metatarsal phalangeal joints but no
• Infectious agents ?
bone production
➢ Chlamydia
RA – Presentations
• Gradual onset, polyarthritis – typical
• Mono or pauciarticular – unusual
Figure 4-24-10
• Abrupt, acute polyarthritis – unusual
• Systemic disease
• Felty Syndrome
➢ RA
➢ Splenomegaly
➢ Leukopenia
RA – Diagnostic Criteria
• Morning stiffness -Three or more joints involved
• Arthritis of hand joints
• Symmetric arthritis
• Rheumatoid nodules
• Rheumatoid factor – 90% patients
➢ Positive CCP increases specificity
• Radiographic changes Classic manifestations of rheumatoid arthritis. Erosions and
• Four criteria to have diagnosis joint space narrowing are present in the proximal
interphalangeal, metacarpal phalangeal and wrist joints in a
bilateral and symmetric distribution
Rheumatoid Arthritis: Radiographic
Manifestations Figure 4-24-11
• Fusiform soft tissue swelling
• Diffuse or juxta-articular osteoporosis
• Uniform joint space narrowing
• Aggressive marginal erosions
• No bone production
• Synovial/subchondral cysts
• Bilateral symmetrical – distribution
PA view (A) of the wrist is shows subtle joint space narrowing in
RA – Hand and Wrist [Figures 4-24-10 and 4-24-11] the wrist in this patient with rheumatoid arthritis. The Norgaard
• “100%” of patients view (B) reveals erosive disease in the pisotriquetral joint the is
• MCP, PIP joint space loss/ erosions impossible to appreciate in the PA projection
• Pancarpal joint space loss/ erosions
➢ ulnar styloid/ pisotriquetral early
• Ulnar drift – carpus and digits
• Swan-Neck, Boutonniere deformities
• Ankylosis rare – limited to carpus
RA- Feet [Figure 4-24-13 ] Coronal T1 weighted MR of the wrist shows numerous erosions
• 80%–90% of patients depicted by intermediate signal replacing fat in subchondral
• May precede hand dz – 10%–20% bone that are difficult to appreciate on the PA radiograph (B)
• Forefoot – MTP disease predominates
• Midfoot – talocalcaneonavicular joint Figure 4-24-13
➢ May see osseous ankylosis
• Hindfoot – retrocalcaneal bursa
Figure 4-24-15
Spondyloarthropathy – Criteria
• Inflammatory spine pain or synovitis
and one or more of following
• Positive family hx
• Psoriasis/ IBD
• Urethritis/cervicitis/diarrhea – within 1 month
• Buttock pain
• Enthesopathy
• Sacroiliitis
HLA B27
• Normal population -USA ~0–8%
• Ankylosing spondylitis – >90%
• Reiter Disease – 63%–75%
• Psoriasis – not increased without arthritis
➢ with peripheral arthritis – 20%
➢ with axial arthritis – 50% Figure 4-24-16
• IBD with axial arthritis – 50%
Psoriatic Arthritis
• Peak ages – 20–40 years
• M:F – 1:1
➢ Spine and DIP – M>F
➢ Symmetric polyarthritis – F>M
• Arthritis in 5%–8% of patients with psoriasis
• Skin dz before arthritis in 75%
• Arthritis before skin dz in 10%
Psoriatic Arthritis:
Radiographic Manifestations
[Figures 4-24-16 and 4-24-17]
• Hand/Feet
➢ Distribution
❖ IP joints – asymmetric
❖ Ray distribution
❖ RA distribution
➢ Acroosteolysis
➢ Ankylosis – ~ 15%
➢ Calcaneal erosion – plantar bone proliferation
• Wrist – pancarpal
Psoriatic Arthritis:
Radiographic Manifestations
• SI Joints – 30%–50%
➢ Bilateral asymmetrical (symmetrical)
➢ Erosion (iliac > sacral) and repair
• Spine – 17%
➢ Large, bulky, lateral bone outgrowths
➢ Unilateral or bilateral, asymmetrical Typical fluffy inflammatory plantar calcaneal enthesophyte that
parallels the undersurface of the calcaneus in patient with
➢ Infrequent apophyseal involvement in lumbar reactive arthritis. The bone is dense and an erosion is present
spine in the posterior superior aspect of the calcaneus
Ankylosing Spondylitis
• Peak age of onset – 15–35 years
• M:F – 3–5:1
• Incidence ~ 6.6/100,000
• Strong association with HLA B27
Rare in blacks
• Predilection for axial involvement
AS-Extraskeletal Manifestations
• Uveitis
• Ascending aortitis/ aortic valve disease
• Cardiac conduction abnormalities
• Interstitial lung dz - upper lobes
Juvenile Chronic Arthritis Bulky paravertebral ossification in patients with DISH is usually
• JRA (seronegative) – 70% easily distinguished from the thin anterior syndesmophytes of
➢ Still Disease, pauci/monarticular, polyarticular ankylosing spondylitis that typically have no horizontal
component
• Juvenile-onset adult type RA – 10%
• Juvenile-onset ankylosing spondylitis
• Psoriatic arthritis
• Enteropathic arthritis
• Reactive/ Reiter arthritis
JRA: Polyarticular
• M:F = 1:1
• Symmetric arthritis
• Hands – MCP, PIP
• Wrists
• Knees/Ankles
• Feet – intertarsal, MTT, MTP, IP’s
• Cervical spine
Osteoarthritis: Definition
• American College of Rheumatology
“ a heterogeneous group of conditions that lead to
joint symptoms and signs which are associated with
defective integrity of articular cartilage, in addition to
related changes in the underlying bone at the joint
margins.”
Coronal SPGR image of the left hip in patient with JRA showing
marked irregularity in the articular cartilage
Polyarticular JRA of the hands. Generalized osteoporosis and Adult patient with JRA as a child. Note ballooned appearance of
joint space narrowing is present with striking lack of erosions the metacarpal heads right greater than left. Wrist involvement
was also aymmetric in this patient. Minimal erosions are seen
Osteoarthritis: Clinical
• Increasing prevalence with age over 40
• Pain, stiffness, and loss of range of motion
• Symptoms may regress or be cyclic
• Risk Factors
➢ Heredity – AD trait with Heberden nodes
➢ Obesity – risk factor for knee and possibly hand
❖ Not risk factor for hip
➢ Hypermobility – increases risk
➢ Occupation – increased risk in heavy manual labor
❖ No increased risk from recreational sports
➢ Diabetes – increases risk
➢ OA in one joint increases risk for other joints
➢ Osteoporosis – protective effect in hip OA
➢ Cigarette smoking – protective effect
Figure 4-24-33
Figure 4-24-34
Figure 4-24-35
Figure 4-24-38
Osteoarthritis - Knee:
Radiographic Manifestations
[Figures 4-24-38 and 4-24-39]
• May require weight-bearing views
• Medial compartment – 75%
Non weight bearing AP of the knee (A) shows osteoarthritis in
• Patellofemoral joint – 48% the medial compartment with subchondral sclerosis and
• Lateral compartment – 26% osteophyte formation but the joint space appears maintained.
• Pancompartmental AP weight bearing view of the knee (B) shows the expected
➢ Think deposition dz or prior inflammatory loss of joint space in the medial aspect of the knee
arthropathy
Figure 4-24-39
Osteoarthritis - Hip: Radiographic
Manifestations
• Superolateral migration
➢ 60%
➢ M>F
• Medial migration
➢ 25%
➢ F>M
• Axial migration
➢ Think deposition dz or prior inflammatory dz
References
1. Brower A: Arthritis in Black and White, 2nd ed. Philadelphia, Pa: WB Saunders; 1997: 252.
2. Resnick D ed. Diagnosis of bone and joint disorders, 4th Ed. Philadelphia: W.B.Saunders, 2002:
Shoulder Pain
• Rotator Cuff Disease
• Impingement
• Arthritis
• Adhesive Capsulitis
Figure 4-25-1
• Cervical Spine
• Referred Pain
• Instability
• Fracture
• Osteonecrosis
• Nerve Entrapment Syndromes
• Bursitis
Pulse Sequences
• Spin-echo
• Fast spin-echo (fat-sat)
➢ Sensitive for cuff tear
• STIR Axial gradient echo image (A) with typical planscan for coronal
• Gradient echo oblique images drawn perpendicular to the glenoid. Axial
• 3D volume gradient echo image through the supraspinatus at the superior
aspect of the shoulder in internal rotation (B) shows the plane
Imaging Planes of acquisition will cross the tendon obliquely. Axial gradient
echo image through the supraspinatus at the superior aspect of
• Axial the shoulder in external rotation (C) shows the plane of
➢ Assess subscapularis, biceps tendon acquisition will parallel the tendon
• Coronal obliques
➢ Parallel to supraspinatus tendon Figure 4-25-4
➢ Assess all tendons
• Sagittal oblique (FSE T2)
➢ 900 to coronals
➢ Assess all tendons
Sagittal oblique T2 weighted image at the level of the glenohumeral joint shows
the normal rotator cuff muscle anatomy
Normal Anatomy
• http://rad.usuhs.mil/rad/anatomy/shoulder/intro.html Figure 4-25-8
Rotator Cuff Tear
• Impingement
• Overuse
• Aging
• Chronic inflammatory disease
• Acute trauma
• Instability
Impingement Syndrome
• Clinical - not radiologic diagnosis
➢ Pain with abduction and external rotation
➢ Pain with elevation and internal rotation
(Neer impingement sign)
• Mechanical causes
➢ Acromial shape, position
➢ AC joint osteophyte
➢ Thick coracoacromial ligament
➢ Instability
Acromial Variation
• Shape
➢ Type I
➢ Type II
➢ Type III
• Lateral Downsloping
• Anterior Downsloping
• Os acromiale
Acromial Variation
• Increase in number increases risk of tear
• Type I - flat
• Type II – curved
• Type III – hooked With abduction, flexion and internal rotation,
the rotator cuff may impinge on the
• Assess on sagittal images
coracoacromial arch
Signal within Tendon: Long TE images Axial gradient echo image at the superior aspect of the humeral
• Mild degeneration – Low Magic angle head (A) shows the anterior aspect of infraspinatus tendon
• Severe degeneration – Intermediate Partial Tear overlapping (lateral) the posterior aspect of the supraspinatus
tendon (medial). Coronal T1 weighted image at the level of
• Tear – High
infra and supraspinatus tendon overlap shows normal high
signal within the junction of the two tendons
Tendon Overlap [Figure 4-25-11]
Partial Tears
• Twice as common as full thickness
Figure 4-25-12
• Intrasubstance – most common
• Bursal Surface – least common
➢ Poor response to conservative Rx
• Increased detection
➢ Contrast
➢ ABER
• Significant if >50% of tendon thickness
Coronal T2 weighted image through the supraspinatus tendon
Partial Undersurface [Figure 4-25-12] (left) shows a deep partial undersurface tear. Coronal T2
weighted image through the supraspinatus tendon of a different
patient (right) shows fluid signal interrupting the articular
surface of the supraspinatus tendon but the bursal surface is
intact indicating an undersurface tear. Both patients have SLAP
tears of the superior labrum
Figure 4-25-16
Sagittal T2 weighted image at the level of the lesser tuberosity
shows a focus of high signal in the subscapularis tendon
representing a partial undersurface tear. The tear is also seen
on the axial T1 weighted gradient echo image following indirect
arthrography (right) but is easier to see on the sagittal image
Calcific Tendonitis
• Rotator cuff most common site
• Primary or secondary disorder?
HADD in tendon
• Concretion – low T1 and T2
• Variable surrounding edema
• May erode cortex/ invade marrow
Figure 4-25-20
Coronal oblique T1 (left) and fat sat T2 (right) weighted images Axial T1 weighted gradient echo image (A)
through the pectoralis major muscle show hemorrhage shows marked enhancement in the anterior
associated with a myotendinous injury. The distal tendon is inferior capsule following IV contrast
intact administration indicating adhesive capsulitis in
the atraumatic setting
Radiologic Report
• Acromion-os acromiale
• Tendon – normal, tendinosis, tear
• Size and location of tear
➢ Massive>5cm
• Partial thickness tear
➢ > or < 50% thickness of tendon
• Retraction/Muscle atrophy
References
1. Zlatkin MB, Needell SD, Hoffman C. MRI of the Shoulder, 2nd Edition. Lippincott
Williams & Wilkins, Philadelphia, PA. 2003.
2. Steinbach LS, Peterfy CG, Tirman PFJ, Feller JF eds. Shoulder Magnetic Resonance
Imaging. Lippincott Williams & Wilkins, Philadelphia, PA. September 1998
Glenohumeral Joint
• Intrinsically Unstable joint
➢ Shallow glenoid fossa
➢ Large articular surface of the humeral head Figure 4-26-1
• Static Stabilizers
➢ Joint capsule
➢ Glenohumeral Ligaments
➢ Glenoid labrum
• Dynamic Stabilizers
➢ Rotator cuff
➢ Long Head of the Biceps Tendon
Classification
• TUBS
➢ Traumatic
➢ Unidirectional
➢ Bankart
➢ Surgery Superior glenohumeral ligament
• AMBRI
➢ Atraumatic
➢ Multidirectional Figure 4-26-2
➢ Bilateral
➢ Rehabilitation
➢ Inferior Capsular Shift
Multidirectional Instability
• AMBRI Patient
• Causes of Multidirectional Instability
➢ Hypermobility or Laxity
➢ Stretching or Overuse of Support Structures
• MR Imaging not usually Required
➢ MR Findings Nonspecific
➢ MR Useful if Direction Unknown to Rule Out Conventional
Causes
Normal Labrum
• Anterior and Posterior Labrum best seen in the Axial Plane
• LABRUM:
➢ Dark on all Pulse Sequences
➢ May be triangular, rounded, or blunted
Anterior Instability
• 95% of all dislocations
• Mechanism
➢ Fall on outstretched arm
➢ Abduction and external rotation
Bufford complex
Perthes Lesion
• Bankart variation (non-displaced)
• Labro-ligamentous disruption Osseous Bankart
• Medial scapular periosteum intact
• May resynovialize in place Figure 4-26-9
• Best detected on ABER view
Perthes Lesion
Figure 4-26-11
ALPSA lesion
Avulsion of Subscapularis
• Subscapularis muscle can avulse off of lesser
tuberosity
• Associated with dislocation of the biceps tendon
• Seen best in axial plane
Humeral Avulsion of the Glenohumeral Ligament (HAGL)
Lesion
Disruption of Subscapularis
• Disruption of subscapularis at musculotendinous junction
• Requires surgical repair
Figure 4-26-14
Hagl Lesion
• Humeral avulsion of the glenohumeral ligament
• Results from dislocation
• No age predilection
• MR findings: contrast extravasation from joint
capsule/ avulsion of subscapularis
Posterior Instability
• 2% - 4% of all traumatic dislocations
• 20% - 25% of shoulder instability cases in active duty military population
• Adduction with internal rotation
• Seizure, electrocution, weight lifting, swimming, lineman blocking
• “Reverse” Hill Sachs, Bankart
“SLAP” Tears
• The superior labrum, anterior-to-posterior lesion, can include
biceps tendon
• Mechanism
➢ Fall on outstretched arm
➢ Repetitive overhead activity (throwing, swimming)
• Symptoms: pain with overhead activity, catching, popping
sensation Posterior Superior Glenoid Impingement
Figure 4-26-20
SLAP Type III: Bucket-handle tear of the superior labrum Figure 4-26-21
Paralabral Cyst
• High association with labral tears and GH joint
instability Figure 4-26-22
• Superior labral cyst: SLAP tears
• Posterior labral cyst: posterior labral tears
• Labral tear may resynovialize
• Can result in shoulder pain and adjacent nerve
entrapment
• DDX: Intramuscular cysts of rotator cuff associated
with PT tear of the cuff tendon
Paralabral cysts
• Small inferior labral cyst
• Teres Minor normal
• 3 years later; persistent pain
• Paralabral cyst larger Left: Direct arthroscopic repair of Bankart lesion. Suture
• Axillary nerve entrapment anchors at the 3, 4, and 5 o’clock positions
• Atrophy Teres Minor Right: Sagittal MR image shows location of suture anchors
Direct Repairs
• Arthroscopic/ open (deltopectoral interval)
➢ Suture anchors 3-,4-,5-, o’clock position
• Capsulorapphy (open/ arthroscopic)
➢ Staple redundant capsule
➢ Done in conjunction with direct repair
➢ High failure rate if done as isolated procedure
• Osseous Bankart Recurrent displace Bankart lesion
Chondrolysis Shoulder:
Proposed Etiologies
• Damage from use of thermal probe for capsular
shrinkage
• Marcaine pump
• Unknown infectious agent Left: MR appearance of a proud suture anchor
• Bioabsorbable material Right: CT appearance of a proud suture anchor
• Mechanical trauma at time of arthroscopy
• Chemical trauma to the chondrocytes
• Event during arthroscopy that triggers an immune response and subsequent Figure 4-26-29
migration of inflammatory cells into the GH joint
Figure 4-26-30
Postoperative infection
1. Bankart ASB: Recurrent or habitual dislocation of the shoulder-joint. Br J Surg 26: 23-29, 1938
2. Beltran J, Rosenberg ZS, Chandnani VP, et al: Glenohumeral instability: Evaluation with MR arthrography.
Radiographics 17: 657-673, 1997
3. Chandnani VP, Gagliardi JA, Murnane TG, et al: Glenohumeral ligaments and shoulder capsular mechanism:
Evaluation with MR arthrography. Rad 196: 27-32, 1995
4. Cvitanic O, Tirman PFJ, Feller JF, et al: Using abduction and external rotation of the shoulder to increase the
sensitivity of MR arthrography in revealing tears of the anterior glenoid labrum. AJR 169 837-844, 1997
5. Kaplan PA, Bryans KC, Davick JP, et al: MR imaging of the normal shoulder: Variants and pitfalls. Rad 184: 519-
524, 1992
6. Linker CS, Helms CA, Fritz RC: Quadrilateral space syndrome: Findings at MR imaging. Rad 188: 675-676, 1993
7. Neviaser RJ, Neviaser TJ, Neviaser JS: Concurrent rupture of the rotator cuff and anterior dislocation of the
shoulder in the older patient. JBJS 70-A: 1308-1311, 1988
8. Neviaser TJ: The anterior labroligamentous periosteal sleeve avulsion lesion: A cause of anterior instability of the
shoulder. Arthroscopy 9: 17-21, 1993
9. Neviaser TJ: The GLAD lesion: Another cause of anterior shoulder pain. Arthroscopy 9: 22-23, 1993
10. Palmer WE, Brown JH, Rosenthal DI: Labral-Ligamentous complex of the shoulder: Evaluation with MR
arthrography. Rad 190: 645-651, 1994
11. Petersilge CA, Witte DH, Sewell BO, et al: Normal regional anatomy of the shoulder. MRI Clin North Am 5: 667-
681, 1997
12. Sanders TG, Tirman PFJ, Linares R: The Glenolabral articular disruption lesion: MR arthrography with
arthroscopic correlation. AJR 172: 171-175, 1999
13. Schweitzer ME: MR arthrography of the labral-ligamentous complex of the shoulder. Rad 190: 641-643, 1994
14. Synder SJ, Karzel RP, Pizzo WD, et al: SLAP lesions of the shoulder. Arthroscopy 6: 274-279, 1990
15. Tirman PFJ, Bost FW, Garvin GJ, et al: Posterosuperior glenoid impingement of the shoulder: Findings at MR
arthrography and MR arthrography with arthroscopic correlation. Rad 193: 431-436, 1994
16. Tirman PFJ, Feller JF, Jansen DL, et al: Association of glenoid labral cysts with labral tears and glenohumeral
instability: Radiographic findings and clinical significance. Rad 190: 653-658, 1994
17. Tirman PFJ, Feller JF, Palmer WE, et al: The Buford complex—A variation of normal shoulder anatomy: MR
arthrographic imaging features. AJR 166: 869-873, 1996
18. Tirman PFJ, Steinbach LS, Feller, FJ: Humeral avulsion of the anterior shoulder stabilizing structures after anterior
shoulder dislocation: demonstration by MRI and MR arthrography. Skeletal Radiol 25: 743-748, 1996
19. Wolf EM, Cheng JC, Dickson K: Humeral avulsion of glenohumeral ligaments as a cause of anterior shoulder
instability. Arthroscopy 11: 600-607, 1995
Sterno-clavicular Joint
• Dislocation most common injury
➢ Anterior more common than posterior
Grade II separation of AC Joint
• Best evaluated with limited CT scan
• Normal distal clavicle extends above manubrium- use symmetry as guide
• Plain film- 40º cephalic angulation
Clavicle Fractures
• Mechanism: indirect trauma- fall on outer prominence of shoulder
• Most common site of injury is middle third
• Healing may result in deformity (extensive callous)
• Distal third fracture must evaluate coracoacromial ligament integrity
Scapular Fractures
• CT- imaging modality of choice for evaluating scapula
Scapular Fractures
• Acromion process fractures
• Direct trauma
• Restore active range of motion; if severely comminuted- excise fragments
Anterior Dislocation
• Axillary view
• Scapular “Y” view
Posterior Instability
• 2% - 4% of all traumatic dislocations
• 20% - 25% of shoulder instability cases in active duty military
population
• Adduction with internal rotation
• Seizure, electrocution, weight lifting, swimming, lineman blocking
• “Reverse” Hill-Sachs, Bankart
“Trough” Sign
• Vertical line of dense cortical bone paralleling the medial cortex of the humerus
• Results from impaction fracture of the posterior Figure 4-27-7
medial aspect of humeral head
• “Reverse” Hills Sachs Fracture
Calcific Tendonitis
• HADD: periarticular calcifications: shoulder most Left: AP view of the shoulder demonstrating posterior
common dislocation of the humeral head
• Results from chronic repetitive micro-trauma Right: Axillary view demonstrating posterior dislocation of the
• Easily detected on x-ray; can be subtle on MR humeral head
imaging
Complications of Dislocation
• Brachial artery or nerve damage
• Post-traumatic ossification: stiffness- intra and periarticular
adhesions: forms in subperiosteal and capsular hematoma
Figure 4-27-11
Colles Fracture
• Most common fracture of distal radius in patient over 40 y.o.
• FOOSH injury with wrist in dorsiflexion
• Distal fragment displaced dorsally
Figure 4-27-15
Figure 4-27-16
Figure 4-27-17
Figure 4-27-21
Bennett Fracture
Boxer’s Fracture
• 4th or 5th MC
• Dorsal angulation
• Treatment open >35º angulation
References
Related Disorders
• Hemochromatosis
➢ Iron deposition
• Alkaptonuria
➢ Homogentisic acid
Gout
• Monosodium urate crystals
• Intra-articular, periarticular
• Acute inflammatory response
• Chronic granulomatous reaction
Gout: Secondary
• Hereditary diseases
• Myeloproliferative diseases
• Endocrine disorders
• Drug therapy
Gouty Arthritis
• Polyarticular
• Asymmetric
• 1st MTP joint (90%)
• Tarsometatarsal
• Carpometacarpal
• Olecranon bursitis
Differentiation of Pyrophosphate
Arthropathy from Degenerative Joint
Disease
• Unusual articular distribution
• Unusual intra-articular distribution
• Variable osteophyte formation
• Prominent subchondral cysts CPPD crystal deposition disease. A. Frontal radiograph of the
• Progressive destruction knee shows chondrocalcinosis including meniscal fibrocartilage
• Calcification calcification (white arrows) and hyaline cartilage calcification
(gray arrow).
B. Lateral radiograph shows complete loss of patellofemoral
CPPD Crystal Deposition Disease: Knee joint space
[Figure 4-28-4]
• Meniscal calcification
• Hyaline cartilage calcification
• Patellofemoral arthropathy
• Subchondral cysts
• Osseous bodies
Figure 4-28-6
Hemochromatosis:
Pathologic/Radiologic Findings
[Figure 4-28-7]
• Iron in synovioblasts
• CPPD crystal deposition
• Osteoporosis
• Symphysis pubis calcification
• Hyaline cartilage calcification Hemochromatosis. Frontal radiograph shows narrowing of the
• Uniform MCP joint involvement second through fifth metacarpophalangeal joints as well as
multiple large hook-like osteophytes (arrows)
• Hook-like osteophytes
Neuropathic Osteoarthropathy
• Charcot joint
• Tabetic arthropathy
• Neurotrophic joint
• Neuropathic arthropathy
• Neuroarthropathy
Neuroarthropathy: Etiologies
• Diabetes mellitus
• Alcoholism
• Syringomyelia
• Syphilis Alkaptonuria. A. Lateral radiograph of the lumbar spine shows
• Leprosy uniform loss of disc height and associated bone sclerosis.
• Meningomyelocele There is disc calcification bridging all levels anteriorly except
• Congenital insensitivity to pain for L4-L5, which shows large osteophytes and a vacuum
• Steroid administration (intra-articular) phenomenon.
B. Frontal radiograph of the knee shows uniform joint space
loss and bone sclerosis
Figure 4-28-11
Articular Anatomy
• Capitellum-hemispherical-articulates with radius
• Trochlea-spool 300 degree arch-articulates with ulna
• Coronoid fossa-ant/sup to trochlea, small-articulates with
coronoid
• Olecranon fossa 180 degrees-art. with semilunar notch
• Lesser sigmoid notch- radial side of proximal ulna/PRUJ
Biomechanics
• Three articulations:
➢ Ulnar-tochlear
➢ Radiocapitellar Effusion and synovitis.
➢ Proximal radioulnar Note complex fluid in the joint
➢ 0-140 degrees flex/ext distending the anterior and posterior
➢ 75 pronation fat pads (arrows). The fat pads are
intracapsular but extrasynovial
➢ 80 supination
Cartilage Loss
• Difficult to see directly (cartilage thin)
• Subchondral marrow edema best sign
• Phytes-posterior/medial/coronoid
➢ Confirm cart loss / cause impingement
• Associated with effusion and bodies
Synovial Folds
• Embryologic remnant
• Several locations
➢ Posterior/lateral catches
➢ Medial (meniscoid) most common
• May mimic bodies clinically and on MR
Epicondylitis
• Medial: golfer’s elbow (common flexor origin)
• Lateral: tennis elbow (common extensor origin) Enlargement of the ulnar nerve (arrow) with
• Spectrum from degeneration to partial to completetear surrounding soft tissue inflammation in a
• Increased T1 signal patient with
• Increased STIR, T2 signal cubital tunnel syndrome
• Linear vs. diffuse
• Histologically- angioblastic changes/ fibrillar collagen degeneration
Biceps: Anatomy
• Long head: superior glenoid
• Short head: coracoid
• Two heads merge distal to the bicipital groove
• Insertion onto radial tuberosity at elbow
• Intimate with brachialis
• Proximal synovial sheath
• Distally paratenon, bicipitoradialis bursa and lacertus fibrosus
Biceps Pathophysiology
• Degeneration
➢ Primary (overuse injury) Lateral epicondylitis (tennis elbow) with
➢ Or direct frictional effect focal fluid signal (arrow) at the common
extensor tendon origin indicating a partial tear
• Mechanical-pronation leads to impingement between radius and
ulna
• Hypovascular-critical zone
distally like rotator cuff
Figure 4-29-6
Biceps Tendinosis
• Common, but rare to image
• Imaging/ clinically overlap with partial tear, bursitis
• Very distal at insertion
Biceps-Partial Tears
• Attritional
• Pain
• No pop, usually no ecchymosis
• More marrow edema and bursitis
• Surgery not usually needed unless large
Muscle Disorders
• Tears
• DOMS
• Neuropathy-Parsonage Turner Syndrome “edema-like” muscle
signal
• Infection
Olecranon bursitis
Osseous Injury [Figure 4-29-8]
• Effusion on Xray: presumed fx Figure 4-29-8
• F/U X-ray vs MR
• Bone marrow edema after trauma: Bone bruise vs. fracture
➢ T1: focal low signal (linear) = fracture
➢ No line, ill-defined edema = bruise
Avulsion
• Chronic avulsive stress
➢ Tendinopathy
➢ Usu subtle edema at enthesis
• Avulsion fx
➢ Ligamentous or tendinous
➢ Thin, longitudinally oriented edema at cortical margin
Osteochondral Impaction
• Analogous bruises from ACL tears
• Transient disloc/sublux
• Often both sides of joint
Fracture Complications
• OA
• Bodies Occult radial neck fracture
• Capsular fibrosis
• Non union / malunion
• Associated ligament injury/instability (e.g., Essex Lopresti)
• AVN
• Pain
• Limited ROM
• Instability
Ligament Disorders
• Medial
• Lateral
Lateral Ligaments
• Components
➢ Lateral collateral ligament proper (LCL) (Radial collateral
ligament)
➢ Annular ligament
➢ Lateral ulnar collateral ligament (LUCL)
Annular Ligament
• Fibro-osseous ring that encircles and stabilizes the radial head
• Attaches on the anterior and posterior edges of the lesser sigmoid
notch Medial collateral ligament tear (arrow) and
• Anterior portion taught in supination and posterior portion taught lateral ulnar collateral ligament tear
in pronation (arrowhead) in a
patient with recent elbow dislocation
Radial Collateral Ligament
• Extends from the lateral epicondyle and attaches to the annular ligament
• Immediately deep to the common extensors
• About half to a third size of MCL
• Maintains humeroradial apposition in the presence of varus stress
LUCL INJURIES
• Caused by a fall on an outstretched hand
• Iatrogenic injury during release or repair of lateral epicondylitis
MR Arthrography Indications
• Bodies
• MCL injuries
• OCDs
• Subtle cartilage loss
Elbow MRA
• Ligament tear
➢ Extracapsular leakage of contrast
➢ Medial or lateral collateral ligament tear
• IA bodies
➢ Anterior, posterior recesses
• OCD
➢ Same dx as knee
➢ Esp capitellum
References
1. Jbara M, Patnana M, Kazmi F, Beltran J. MR imaging: arthropathies and infectious conditions of the elbow, wrist,
and hand. Magn Reson Imaging Clin N Am. 2004 May;12(2):361-379.
2. Bordalo-Rodrigues M, Rosenberg ZS. MR imaging of entrapment neuropathies at the elbow. Magn Reson Imaging
Clin N Am. 2004 May;12(2):247-263.
3. Potter HG, Ho ST, Altchek DW. Magnetic resonance imaging of the elbow. Semin Musculoskelet Radiol. 2004
Mar;8(1):5-16
4. Chung CB, Kim HJ. Sports injuries of the elbow. Magn Reson Imaging Clin N Am. 2003 May;11(2):239-53.
5. Steinbach LS, Palmer WE, Schweitzer ME. Special focus session. MR arthrography. Radiographics. 2002 Sep-
Oct;22(5):1223-1246.
6. Zou KH, Carrino JA. Comparison of accuracy and interreader agreement in side-by side versus independent evaluations
of MR imaging of the medial collateral ligament of the elbow. Acad Radiol. 2002 May9(5):520-5.
7. Jbara M, Patnana M, Kazmi F, Beltran J. MR imaging: arthropathies and infectious conditions of the elbow, wrist,
and hand. Magn Reson Imaging Clin N Am. 2004 May;12(2):361-79
8. Bordalo-Rodriguez M, Rosenberg ZS. MR Imaging of entrapment neuropathies at the elbow. Magn Reson Imaging
Clin N. Am. 2004 May; 12(2):247-63.
9. Chung CB, Chew FS, Steinbach L. MR imaging of tendon abnormalities of the elbow. Magn Reson Imaging Clin
N. Am. 2004 May;12(2):233-45.
10. Kaplan LJ, Potter HG. MR imaging of ligament injuries to the elbow. Magn Reson Imaging Clin N. Am. 2004
May;12(2):221-32, v-vi.
11. Fowler KA, Chung CB. Normal MR imaging anatomy of the elbow. Magn Reson Imaging Clin N. Am. 2004
May;12(2):191-206, v.
12. Potter HG, Ho St, Altchek DW. Magnetic resonance imaging of the elbow. Semin Musculoskeletal Radiol. 2004
Mar;8(1):5-16.
13. Savnik A, Jensen B, Norregaard J, Egund N, Danneskiold-Samsoe B, Bliddal H. Magnetic resonance imaging in the
evaluation of treatment response of lateral epicondylitis of the elbow. Eur Radiol. 2004 June;14(6):964-9. Epub
2003 Dec 11.
Hypertrophic Osteoarthropathy
• Classic Triad
• Joint swelling, 30%–40% patients
• 5% patients with lung cancer
• Cause? – may be paraneoplastic, due to a growth hormone releasing factor
Ivory Vertebra(ae):
Differential Diagnosis [Figure 4-30-5] Figure 4-30-5 Figure 4-30-6
• #1 Paget’s 50%
• #2 Hodgkin’s 30%
• #3 Metastasis 20%
Breast Carcinoma
• The most common source of
bone mets in women
• Spine #1 site
• 65% lytic, 25% mixed,
10% blastic
59 year old woman with multiple ivory 76 year old man with florid
vertebrae secondary to breast cancer periosteal reaction around distal
metastases fibula metastasis
Figure 4-30-7
Thyroid Cancer
• 8% of patients have metastases
• Lytic
Myeloma Types
• MGUS – monoclonal gammopathy of undetermined significance
(1% of all SPEPs)
• Asymptomatic myeloma (no bone lesions)
• Symptomatic multiple myeloma
(classic, generalized, osteosclerotic [POEMS], multiple myeloma
with osteosclerosis, leukemic)
• Non-Secretory myeloma – 3% of all cases
• Solitary plasmacytoma in bone – 3%-5% of cases
• Extramedullary plasmacytoma – 5%
65 year old man with solitary rib
Myeloma: Pathologic Features abnormality on whole body bone
• Plasma cells proliferate in erythropoietic areas scan, proven to be esophageal
• Grossly – dark red, tan; soft cancer metastasis
• Histology – sheets of malignant plasma cells obliterate the
marrow
• Special studies – markers for light chains
• Amyloid – 10%
• Osteoclast stimulating factor
Osteoclast-Stimulating Factor
• A cytokine (lymphotoxin alpha)
• Similar to O-AF
• Produced by myeloma cells, T cells
• Interferon is a cytokine antagonist
• Bisphosphonates used to counter osteoclastic resorption
Cancer 1997; 80:1557-63
Figure 4-30-12
Plasmacytoma
Differential Diagnosis [Figure 4-30-14]
• Metastasis: thyroid, renal
• Primary: Fibrosarcoma, MFH
Figure 4-30-15
56 year old man with myeloma,.
skull radiograph shows typical
“punched out” lytic lesions
Summary – PLB
• Usually has an aggressive appearance
➢ CT or MRI showing large soft tissue mass without large
cortical holes is typical
• Wide range of appearances
➢ Normal x-rays Large lytic lesions with soft tissue
➢ Geographic lesions mass and sequestra should put PLB
➢ “Blow out” lesions high up in the differential diagnosis
➢ Blastic lesions
References
1. Durie et al. Myeloma management guidelines: a consensus report. The Hematology Journal 2003; 4: 379-398
2. Mirels H. Metastatic disease in long bones. Clin Orthop Relat Res 1989;249:256-264
3. Mulligan M et al. Skeletal Metastatic Disease. In: Pope et al, Imaging of the Musculoskeletal System.
Philadelphia: Elsevier, 2006
4. Mulligan M. Imaging techniques used in the diagnosis, staging, and follow-up of patients with myeloma. Acta
Radiologica 2005;46:716-724
5. Mulligan M, McRae G, Murphey M. Imaging features of primary lymphoma of bone. AJR 1999; 173: 1691-1697
6. Roodman GD. Mechanisms of bone metastasis. N Engl J Med 2004;350:1655-1664
7. Weber K et al. An approach to the management of the patient with metastatic bone disease. Instr Course Lect
2004;53:663-676
Objectives
• To identify some of the common hematologic disorders
• To describe the clinical and epidemiological aspects of these
entities
• To demonstrate the most significant MSK imaging findings
Hematologic Disease
• Hereditary anemias
➢ Sickle cell anemia
➢ Thalassemia
➢ Rare anemias: Fanconi’s, thrombocytopenia with absent
radii syndrome (TAR)
• Coagulation disorders
➢ Hemophilia
➢ Myelofibrosis
Figure 4-31-5
Figure 4-31-6
Types of Thalassemia
• Alpha
➢ Least severe:
❖ Silent carrier = loss of 1 alpha globulin gene - often
incidental finding
❖ Most severe:
❖ Hydops fetalis = loss of 4 alpha globulin genes - die in
utero
• Beta:
➢ Spectrum
❖ Minor = slight anemia
❖ Major = life-threatening anemia requiring transfusions
❖ Risk of Fe++ overload
Figure 4-31-10
Figure 4-31-9
Gaucher’s Disease
• Ashkenazic Jews of Eastern European descent
• Defect of beta glucosidase
• Accumulation of glycosyl ceramide in the RE cells of BM,
spleen, and liver
• Hepatosplenomegaly, yellow skin, scleral pigmentation, acid and
alkaline phosphatase elevation
Imaging features
• AVN of the hip and femoral head
• Osteoporosis
• Marrow expansion with cortical thinning
• Erlenmeyer flask deformity
• Lytic lesions and sometimes periostitis Erlenmeyer flask deformity
Extramedullary Hematopoiesis
[Figures 4-31-13 and 4-31-14]
• Blood production in fetal regions
➢ Liver, spleen, adrenal, thymus, heart, lung, “Erlenmyer flask” deformity in Gaucher’s disease.
nodes, renal pelvis, GI tract, dura mater (almost “Crumpled tissue paper” cytoplasm on histology
anywhere !)
• Major causes:
Figure 4-31-13
➢ Hematologic disease (SS and
thalassemia)
➢ Myelofibrosis
➢ Leukemia
➢ Hodgkin’s
➢ Hyperparathyroidism
➢ Rickets
➢ Carcinomatosis
Hemophilia
• Oldest known bleeding disorder
• First noted in offspring of Queen Victoria of England
• Mutation in Queen Elizabeth’s X chromosomes
• Group of X-linked recessive disorders
• Gene carried by women and expressed in men
• All races affected TAR with absent radii syndrome: Note that the
• 20, 000 hemophiliacs in US thumb is present
• 400 new cases/year Figure 4-31-17
• Severity – related to lack of clotting factor
• 70% have < 1% of normal clotting factor
Knee [Figures 4-31-17 and 4-31-18] Marked articular space narrowing and cartilage
• Dense effusions destruction with massive subchondral cyst
• Juxtaarticular osteoporosis formation
• Subchondral irregularity
• Epiphyseal overgrowth
• Squaring of inferior pole of patella (20%-30%)
Figure 4-31-21
Review
• Sickle Cell
➢ Vaso-occlusion
❖ “Hand-Foot” syndrome
❖ AVN and medullary bone infarcts
❖ “H-shaped” (“Lincoln log”) vertebral bodies
❖ “Bone within a bone” appearance
❖ Salmonella infection
• Thalassemia
➢ “Hair on end”
➢ “Pseudohemangiomatous” appearance
➢ “Erlenmeyer flask” deformity (differential-Gaucher’s)
➢ “Rodent” facies
• Hemophilia
➢ Wide intercondylar notch
➢ Erosions
➢ Medial slope of distal tibia at ankle
➢ “Pseudotumor”
• Myelofibrosis
➢ Primary and secondary forms
➢ Diffusely dense bones
➢ Hepatosplenomegaly
➢ BM bx to make dx
References
1. "What is Sickle Cell Disease". Sickle Cell Information Center. December 16, 2003. Copyright © 1997. The
Georgia Comprehensive Sickle Cell Center at Grady Health System, The Sickle Cell Foundation of Georgia, Inc.,
Emory University School of Medicine, Department of Pediatrics, Morehouse School of Medicine.
http://www.scinfo.org/sicklept.htm
2. Funaki B. "Sickle cell anemia: Bone manifestations", "Bone within a bone". Chorus: Collaborative Hypertext of
Radiology. (Kahn CE ed). July 2004. Medical College of Wisconsin. February 1995.
http://chorus.rad.mcw.edu/doc/01060.html
3. Kahn CE. " Erlenmeyer flask deformity". Chorus: Collaborative Hypertext of Radiology. (Kahn CE ed). May
2004. Medical College of Wisconsin.
< http://chorus.rad.mcw.edu/doc/00648.html>
4. Kerr R. Imaging of musculoskeletal complications of hemophilia. Semin Musculoskelet Radiol 2003; 7:127-136.
5. Lonergan GJ, Cline DB, Abbondanzo SL. Sickle cell anemia. Radiographics 2001; 21:971-994.
6. Park JS, Ryu KN. Hemophilic pseudotumor involving the musculoskeletal system: spectrum of radiologic findings.
AJR Am J Roentgenol 2004; 183:55-61.
7. Wong AL, Sakamoto KM, Johnson EE. Differentiating osteomyelitis from bone infarction in sickle cell disease.
Pediatr Emerg Care 2001; 17:60-63; quiz 64.
Outline of Diseases
• Osteoporosis (and its sequelae)
• Osteogenesis imperfecta
• Neurofibromatosis
• Collagen vascular-like diseases
➢ SLE
➢ Scleroderma
➢ Polymyositis/dermatomyositis
Disuse osteoporosis in a 76 yo with left sided CVA
Terminology
• Osteopenia – “paucity of bone”
• Osteoporosis
➢ Decreased bone mineral density
➢ Normal in quality
➢ Decreased in quantity
• 30%-50% of cancellous bone must be gone to recognize
Types of Osteopenia
• Localized
• Regional or segmental
• Generalized or diffuse
Localized Osteopenia/Osteoporosis
• Focal areas of bone loss
• Differential diagnosis:
➢ Infection
➢ Arthritides
Figure 4-32-2
Regional
Osteopenia/Osteoporosis
• Segmental area of
decreased BMD
• Differential diagnosis:
➢ Disuse (immobilization)
➢ Chronic regional pain
syndrome (CRPS)
(RSD (Reflex
sympathetic dystrophy)
[Figure 4-32-2]
Chronic regional pain
➢ Transient osteoporosis syndrome (Reflex
(bone marrow edema) sympathetic dystrophy)
➢ Regional migratory
osteoporosis Note the increased
radionuclide accumulation
on the early and late views
of the bone scan
Generalized Osteopenia/Osteoporosis
• Diffuse decreased BMD
• Differential diagnosis:
➢ Senile osteoporosis
➢ Medications (Steroids, heparin)
➢ Systemic diseases (Deficiency states)
❖ Scurvy
❖ Malnutrition
❖ Calcium deficiency
BMD Terms
• BMD measured in gm/cm2
• T-score: Patient’s BMD compared to normative data (Normal = 25 yo women)
• Z-score: Patient’s BMD compared to her aged-matched controls
• World health organization uses T scores to classify a patient’s bone mineral
status
A = subcapital
B = neck
C = basicervical
D = intertrochanteric
E = subtrochanteric
Figure 4-32-11
Garden Type I [Figure 4-32-11]
Intertrochanteric Fractures
• Extracapsular
• Periosteum present
• Low incidence of nonunion or AVN (~1%)
• Distinction from basicervical often difficult (no clinical
concern)
• Most comminuted, 15% severely
• GT/LT may be displaced by gluteus or iliopsoas
• May have other non-suspected injuries in pelvis
Garden I type of femoral neck fracture treated with
Osteogenesis Imperfecta (OI) [Figure 4-32-12] Knowles’ pins
• Skeletal, skin, sclera and dentin abnormality
• 1/30K affected Figure 4-32-12
• 1/50K severely
• 20-50K in US
• 85% AD
• Major types:
➢ Congenita
➢ Tarda
OI vs Child Abuse
• Metaphyseal corner fx’s uncommon in OI
• Sternal, rib, scapular, skull and bucket handle fx’s Congenital type of Osteogenesis Imperfecta
common
• Fx’s continue to occur in protective custody
• Other non-MSK findings not present: Figure 4-32-13
➢ Retinal hemorrhage
➢ Visceral intramural hematomas
➢ Intracranial bleeding
➢ Pancreatitis
➢ Splenic trauma
Neurofibromatosis (NF)
• Described first by Tiresius (1773) and Smith (1849)
• Named for von Recklinghausen - noticed association of neural and cutaneous
elements in 1882!!
• Defects of all three cell layers = phakomatosis
• 1/3000 births
• Estimated ~100,000 in US
• One of humanity’s most common genetic disorders
• Mutation rate is 1/10,000 gametes/generation
• Greater than that for ALL OTHER COMMON GENETIC DISORDERS
• AD with variable gene expression (FH in 60%)
• Equal incidence in male and female and Caucasian and non-Caucasian
Neurofibromatosis (NF)
• Two distinct clinical forms:
➢ NF-1 (vonRecklinghausen’s) - Café-au-lait spots, neurofibromas, skeletal
deformities
➢ NF-2 - Acoustic neuromas
• Can lead to disfigurement, blindness, deafness, dermal/brain/spinal tumors,
loss of limbs, malignancies, learning disabilities
• WAS NOT “Elephant Man’s Disease”…John Merrick had Proteus Syndrome
(cell growth disturbance with hemihypertrophy and macrodactyly)
Figure 4-32-19
Figure 4-32-18
Symmetric Polyarthritis
• Articular symptoms and signs common-75%-90% of
patients Non-deforming nonerosive arthropathy of SLE
• Frequently bilateral and symmetric (differential diagnosis is post-Streptococcal
• 5%-40% with disease (Jacoud’s) arthropathy
• Hands > knees > wrists > shoulders
• ST swelling, periarticular osteopenia
• Reversible and little functional effect
• !!Cartilage and osseous destruction rare without underlying osteonecrosis!!
Scleroderma
• Unknown cause
• F:M (4:1)
• 3rd to 5th decade
• < 20 cases/million/year
• Variable prognosis
• Up to 65% MSK involvement at presentation
• Death: Lung, heart and renal involvement
Sclerodactyly
• Replacement of the normal connective tissue with dense collagen bundles
• Skin = thin, appears smooth and is tightly bound
• Fingers narrow and taper distally
Telangiectasia
• Permanent dilatation of capillaries and venules
• Face, lips, tongue and fingers
“Floppy thumb” of
dermatomyositis/polymyositis
Dermatomyositis with extensive soft
tissue calcification
Remember!
• PM, DM, Scleroderma, SLE, mixed CVD and overlap syndromes
may all look alike
➢ ST calcification
➢ Articular and osseous abnormalities
References
1. Bohndorf K, Imhof H, Pope TL (eds). Musculoskeletal Imaging: A Concise Multimodality Approach. New York,
NY, Thieme Medical Publishers, 2001
Outline
• Biomechanical considerations
• Historical perspective
• Epidemiology and clinical manifestations
• Anatomic approach with examples
➢ Stress injury “look alikes”
• Avulsive and muscular “tug” injuries
• Unusual activities causing stress injury
• Recommended work-up
“Bone Fatigue”
• 1922 - Muller
➢ Isolated a segment from the radius of a dog
➢ Created a fatigue fracture of the ulna
• 1949/50 - Rutishauser/Majno
➢ First description of the histologic aspects of fatigue fractures
Muller W. Bruns Beitr. klin. Chir. 127:251-290, 1922
R/M. Schweiz. med. Wschr. 79: 281-88, 1949. 6:333-42, 1950.
Historical Perspective
• 1855 - Breithaupt - Prussian military surgeon
➢ Clinical features of painful feet on long marches
• 1887 - Pauzet - army doc
➢ Exostoses on PE from bone proliferation soldiers’ feet
• 1897 - Stechow - Prussian guard
➢ First imaging in 36 cases of MT stress fractures
• 1905 – Blecher
➢ First femoral neck stress fracture
• 1921 – Deutschlander - German physician
➢ Comprehensive study of stress lesions in > 50 yo
• 1936 - Asal – German
➢ First large series of 590 stress fractures in German troops
Stress injuries
• Most common in lower extremities
• Dissipation of ground reaction forces (GRF) (running, walking, marching,
jumping)
• Bone exposed to stress (ie load) and strain (ie deformation) with weight-
bearing
• Factors influencing bone response:
➢ Bone geometry and bone density
• Jumping and landing – GRF up to 12 X body weight
Epidemiology
• 20% of all injuries seen in sports medicine clinics
• Between 4.7% and 15.6% of injuries in runners
• 20-25% of stress injuries in tibia, fibula or MT
• Females: 49% with very irregular menstruation, 39% with
irregular menstruation
• Study of 320 athletes with stress injury:
➢ 69% runners
➢ 8% fitness class participants
➢ 5% racket sports
➢ 4% basketball players Grade 4 Stress injury of the tibia,
• Track athletes have highest incidence pathological fracture of the fibula in
patient with RA on steroids
Clinical Features of Stress Injury Condensation of cancellous bone
• Pain associated with activity Perpendicular to the long axis
• Pain resolves without activity
• Pain in characteristic location associated with activity
• PE: ST swelling, point tenderness
Anatomic approach
• Lower extremity: Foot (MT, navicular, calcaneus), tibia, femur
• Pelvis (Insufficiency and adolescent)
• Upper extremity
• Unusual causes of stress injury
• Mimics of stress injury
• Recommended workup
Figure 4-33-3
Figure 4-33-4
Figure 4-33-5
Figure 4-33-7
Figure 4-33-8
Figure 4-33-19
Figure 4-33-20
Figure 4-33-21
References
1. Chamay A. Mechanical and morphological aspects of experimental overload and fatigue in bone. J Biomech 1970;
3:263-270.
2. Craig JG, Widman D, van Holsbeeck M. Longitudinal stress fracture: patterns of edema and the importance of the
nutrient foramen. Skeletal Radiol 2003; 32:22-27.
3. Müller W. Bruns Beitr. klin. Chir. 127:251-290, 1922
4. Rutishauser E, Majno G. [Lesions of normal and pathological bones due to overstrain.]. Bull Schweiz Akad Med
Wiss 1950; 6:333-342.
5. Tschantz P, Rutishauser E. [The mechanical overloading of living bone: initial plastic deformations and adaptation
hypertrophy]. Ann Anat Pathol (Paris) 1967; 12:223-248.
Lateral compression
• Most common mechanism of pelvic injury
• Lateral blow to the side of the pelvis Lateral compression Type I injury-STABLE
• Three types depending on severity (Note the disruption of the sacral foraminal
• “KEYS TO THIS INJURY:” (arcuate) lines-arrows)
➢ Horizontal fx’s of pubic ramus/rami
➢ Crush (buckling) fx of sacrum
Figure 4-34-4
Lateral compression - Young-Burgess
classification [Figures 4-34-3 to 4-34-5]
• I – Ipsilateral sacral compression fx (stable)
• II- I + associated iliac wing fx
➢ Rotationally unstable
Vertically stable
• III – I + II with contralateral “open book” appearance
(“windswept pelvis”)
Figure 4-34-6
“Windswept” pelvis
Lateral compression Type I injury
AP Compression
• Blows to front of pelvis
• MVA
• Three types depending on which ligaments involved
• Increases volume of pelvis
• Major risk = hemorrhage
• Often brain/abdominal injuries
• KEYS TO THIS INJURY:
➢ Vertical fx inf pubic rami (one or both sides)
➢ > 50% post acetabular wall
➢ < 10% sacral fx
Vertical Shear
• Fall from height or head and back trauma
• Least common
• KEYS TO THIS INJURY:
➢ Disruption of SP or SIJ
➢ Cephalad or caudad displacement of pelvis (best seen on
OUTLET film)
• Rotationally, vertically and posteriorly UNSTABLE
Acetabular fractures
• Letournel and Judet classification, 1993
• Ten different patterns
➢ Five elementary (run in single plane)
➢ Five associated (combination of elementary)
• Difficult to remember
• Most common:
➢ Posterior wall
➢ Transverse with posterior wall
➢ Both column (most common type)
• Add T-shaped and transverse = 90% Pelvic CT anatomy (see Harris et al: AJR
2004;182:1363-75)
Figure 4-34-15
Posterior wall acetabular fracture
Figure 4-34-16
Hip Trauma
• Dislocations
• Hip fx’s
➢ Common injury in multi-trauma
➢ Common in the elderly
❖ Osteoporosis and cerebrovascular disease
❖ Prone to falls
Hip Dislocations
• 5% of all dislocations
• High energy trauma (MVA, MCA, etc.)
• ~90+% posterior
• Commonly associated with femoral shaft, patella and post acetabular fx’s
• Clinically
➢ Limb shortening, internally rotated and adducted
➢ 10-15% transient sciatic nerve palsy (direct impingement)
Hip Fractures
• Intracapsular
➢ Subcapital
➢ Mid cervical
➢ Basicervical
• Extracapsular
➢ Intertrochanteric
➢ Subtrochanteric
• Femoral neck fx’s 3-6X > women
• Intertroch fx = frequency
Subtrochanteric Fractures
• Fracture line extends between LT and point 5 cm distally
• Direct trauma
• Older patient, less force required
• High incidence of malunion or nonunion
➢ ? secondary to greater proportion of cortical bone to trabecular bone in this
region
• Rx: Intramedullary rod
Schatzker Classification
• I=split fx (younger)
• II=split + depression of LTP (older)
• III=depression - splitting
• IV=MTP +/- depression
• V=split fx through MTP and LTP
• VI=dissociation of TP from underlying diaphysis
Maisonneuve fracture
• External rotation of ankle
• Fibular fx
• Serious injury
• Requires ORIF with screws
• Removed 8-12 weeks after injury
Ankle Fractures
• Common injuries
• Soft tissue changes (STS, effusion)
• Classification schemes
➢ Lauge-Hansen
❖ Difficult to remember
❖ Not very reproducible
➢ Danis-Weber (AO)
❖ Easy to remember
❖ Reproducible
Danis-Weber Classification
• Type A: Horizontal avulsion fx below mortise, stable, Rx: Closed reduction
and casting (without displaced MM fx)
• Type B: Spiral fibular fx – level of mortise, external rotation, stable or unstable,
Rx: Closed reduction unless fragments displaced
• Type C: Above mortise, disruption of lig attachment of tibia/fibula distal to fx,
unstable, Rx: ORIF
Figure 4-34-21
Coronal reconstruction
CT of calcaneal fracture of CT of calcaneal
fracture
Sanders Classification
• I = Non-displaced
➢ Non-operative
• II = 2 parts (split)
➢ ORIF
• III = 3 parts (split and depression
➢ ORIF
• IV = Comminuted
➢ Defies open reduction
• Measures height of PF
• A = most cephalic point of tuberosity to posterior
border of subtalar joint
• B = posterior border of subtalar joint to anterior
process
• Normal: 20 - 40º
Anatomy of the tarsal joints (Bohndorf K, Imhoff H,
Foot Injuries Pope T: Synopsis of MSK Imaging: A
• 5th MT Multimodality Approach, Thieme)
➢ Avulsion (pseudo-Jones or tennis fracture)
➢ Jones
➢ Stress fx (fatigue or insufficiency)
Figure 4-34-23
• LisFranc
Jones Fracture
• Transverse fx
• 2-3 cm distally
• Displaces on weight bearing
• 35%-50% persistent non-union
Google Search: Sponsored links (Jones Fracture lawsuits-Recover medical
expenses-Find attorneys and help nationwide-personal-injury-lawyer.com)
References
1. Bohler L: Diagnosis, pathology, and treatment of fractures of the os calcis. J Bone Joint Surg 13:75-89, 1931.
2. Bohndorf K, Imhof H, Pope TL (eds). Musculoskeletal Imaging: A Concise Multimodality Approach. New York,
NY, Thieme Medical Publishers, 2001
3. Borrill J, Funk L, Deakin S. Orthoteers: The guiding light in orthopaedic education. 2006.British Orthopaedic
Association.. <http://www.orthoteers.org/>
4. eMedicine (James WD, Adler J, Lutsep HL, Lorenzo CT, Lin EC, Ho SSW, Roy H, Gellman H, Meyers AD eds)
Symptomatic side
T1 T2
PAGET DISEASE
• Common – 3% of people over 40 years
• Lytic, blastic or mixed phases
• Most frequent to involve: spine, skull, pelvis
• Trabecular thickening – bone enlargement
T1
T2
T2
T1
T1
T1 T2
T1 T2
RADIOLOGIC DIFFERENTIATION OF
CHONDROSARCOMATOUS LESIONS
• Aggressive chondroid lesion with soft tissue mass
➢ High grade conventional chondrosarcoma
➢ Dedifferentiated chondrosarcoma
➢ Mesenchymal chondrosarcoma
• Large fluid component bone or soft tissue
➢ Myxoid chondrosarcoma
• Change in appearance or foci of more aggressive nature
➢ Diagnosis: Dedifferentiated chondrosarcoma
T1
T2 Fat Sat
T1 GD
T2 FAT SAT
First Radiograph
T2
T1
T1 STIR
T1
T1
T2
T1 STIR
STIR
STIR
T1 T2 T2
STIR
I1
Blastic Disease 814 Calcific
Blastic Lesions 967 Myelitis 792
Blastic Phase 812 Tendinitis 952
Blastomycosis 835 Tendonitis 930
Blount 911 Tendonitis (Glenohumeral) 943
Blow out lesions 967 Calcified falx cerebri 853
BMD 978 Calcified Soft Tissue Mass 1012, 1015
BMD (WHO Classification) 979 Calcinosis 984
Bohler 1003 Calcitonin 818
Bone Autograft 706, 707, 710 Calcium deficiency 977
Bone bruise 865, 879, 958 Calcium hydroxyapatite 718, 792, 949
Bone enlargement 814 Cancellous (Osteoid Osteoma) 746
Bone Graft Complications 708 Candidiasis 835
Fracture 709 Candle flame 813
Joint Instability 709 Cap thickness 758
Nonunion and Pseudarthrosis 708 Capillary hemangioma 809
Resorption 709 Capitate (Dislocation) 946
Bone Graft Substitutes 710 Capitellum 955
Bone Infarct 769, 906, 1024 Capsulorapphy 938
Osteonecrosis 769 Carcinomatosis 971
Bone Island 743 Carpal Dislocations 946
Bone Metastases 961 Carpal Stability 874
Bone Production 914 Carpal Tunnel 872, 876
Bone scan 744 Syndrome 877
Bone Tumors 720 Cartilage metaplasia 799
Cartilage 720 Cartilage nodules 799
Histiocytic 721 Cartilaginous Lesions 757
Marrow 720 Chondroblastoma 757
Notochord 721 Chondromyxoid fibroma 757
Osteoid 720 Chondrosarcoma 757
Unknown Origin 721 Enchondroma 757
Vascular 721 Juxtacortical chondroma 757
Bone Tumors (Incidence) 722 Osteochondroma 757
Important Factors in the Diagnosis of 723 Caseating necrosis 830
Primary Benign 722 Cavernous hemangiomas 761
Primary Malignant 722 Cavernous spaces 806
Bone within Bone 970 Cellulitis 826
Botryoid odontogenic cyst 852 Cementoblastoma 854
Bouchard nodes 923 Central giant cell granuloma 852
Bowing of long bones 901 Cervical Burst Fracture 846
Boxer’s Fracture 948 Cervical Spine Trauma 839
Brachial artery 944 Cervical spondylosis 848
Brachial nerve injury 944 Charcot joint 953
Breast Carcinoma 962 Chondroblastoma 720, 1008, 1024
Bristow procedure 938 Codman Tumor 763
Brodie abscess 748, 824, 1007, 1026 Chondroblasts 764
Brown tumor 711, 853, 1013 Chondrocalcinosis 950, 1021
Brucella 829 Chondroid 738
Brucellosis 829 Chondroid Lesion 1024
Bucket handle 861, 862 Chondroid Matrix (Enchondroma) 761
Bumpy (Soft Tissue Swelling) 912 Chondroid Matrix (Intramedullary Chondrosarcoma) 765
Bursae (Knee) 870 Chondromyxoid Fibroma 720, 1024
Bursitis (Bicipital Radialis) 957 Chondrosarcoma 762, 764, 1024
Bursitis (septic) 826 Dedifferentiated 769
Burst Fracture 846 Extraskeletal 768
Button osteophyte 922 Mesenchymal 768
Cafe-au-lait spots 773, 981 Myxoid 768
Calcaneal Fractures 1002 Chondrosarcomatous Lesions 1024
Calcaneofibular 881 Chordoma 721, 786
Calcaneus 995 Christmas disease 972
Chronic ACL Tear 867
Chronic Granulomatous Disease of Childhood 827
I2
Chronic hematoma 796 Decubitus ulcers 825
Chronic infection 818 Dedifferentiated Chondrosarcoma 764, 769
Chronic Osteomyelitis 825, 852 Deep Endosteal Scalloping 765
Chronic Recurrent Multifocal Osteomyelitis (CRMO) 827 Deforming nonerosive arthropathy 983
Chronic regional pain syndrome 976 Degenerative Joint Disease 951
Chronic renal failure 793 Dental Anatomy 849
Chronic sclerosing osteomyelitis 856 Dentigerous cyst 852
Chronic symmetric plasma cell osteomyelitis 827 Dentition 849
Clavicle Deoxyhemoglobin 848
Clay Shoveler Fracture 843 DeQuervain’s Syndrome 876
Clear Cell Chondrocytes 767 Dermatofibrosarcoma Protuberans (DFSP) 771, 781, 782, 802
Clear Cell Chondrosarcoma 763, 764, 767, 1008 Dermatofibrosis lenticularis disseminata 744
Clear Cell Sarcoma 792, 803 Dermatomyositis 976
Cleidocranial dysplasia 1007 DeSmet 860
Clutton joints 834 Desmoid 746
Coach’s Finger 948 Extraabdominal 779
Coccidioidomycosis 835 Desmoplastic fibroma 771, 777
Codman Tumor 763 DEXA 978
Collagen Vascular Diseases 793, 907, 1012 Diabetes 825
Collagen vascular-like diseases 976 Insipidus 892
Collateral ligament 869 Mellitus 773, 825, 953
Collateral ligaments 859 Diffuse sclerosis 1010
Colles fracture 945 Diphoshonates 818
Column Fracture (Pelvis) 1000 Direct implantation 820
Complete pelvic instability 997 Discitis 828
Compression Fracture 841 Discography 828
Congenital insensitivity to pain 953 Discoid 860
Congenital Syphilis 834 DISI deformity 874
Contiguous spread 820 Distal radial buckle fracture 945
Contusion 865 Distal radioulnar joint 872
Cooley’s anemia 970 Distal Tuft Fracture 948
Coracoid 942 Disuse/Immobilization Osteoporosis 977
Coronoid fossa 955 Double Axillary Pouch Sign 934
Cortical Double line sign 908
Osteoid Osteoma 746 Doughnut sign 785
Desmoid 777 Drug Abusers 827
Fibrous Dysplasia 775 Du Toit & Roux 938
Involvement 738, 739 Dual Energy X-ray Absorptiometry (DEXA) 978
Lucency/Central Calcification 1005 Dupuytren Exostosis 759
Resorption 712 Durie/Salmon PLUS Staging (Myeloma) 965
Thickening (Chondrosarcoma) 765 Dysbaric disorders 907
Cotton wool 814 Dysplasia Epiphysealis Hemimelica: Trevor Disease 759
CPPD 718, 949 Dysplastic Thoracolumbar Junction 1020
Arthropathy 792 Dysprosium 165 795
Deposition/arthropathy 1021 Early focal cemento-osseous dysplasia 850
Cranial Sclerosis 744 Echinococcus 837
Craniotabes 901 ECU tendon sheath 875
CREST Syndrome 984 Ehlers-Danlos 1016
Cretinism 1007, 1020 Elbow 955
Crohn's disease 912 Dislocations and Fractures 944
Cruciate ligaments 859 Embolization 748, 808
Cryptococcosis 836 Enchondroma 720, 760, 769, 1024
Crystal deposition (Thalassemia) 971 Enchondroma vs. Chondrosarcoma 769
Crystal Deposition Disease 718, 949 Enchondromatosis 1017
Cushing syndrome 773 Endocrinopathies 773
Cyst (Paralabral) 938 Endodontic procedures 854
Cystic hygroma 808 Endosteal scalloping 770
Cystic Masses (Knee) 870 Enostosis 720, 743
Cysticercosis 837 Enteropathic arthritis 912
Dactylitis 830, 834, 969, 1010 Enthesopathy 914
Dagger sign 918 Enucleation 852
Danis-Weber Classification 1001
I3
Eosinophilic Granuloma 721, 887, 890, 967 Focal cemento-osseous dysplasia 855, 857
LCH 1008 Focal scerosing osteomyelitis 854
Epicondylitis (Elbow) 956 Foot 879, 995
Epidermoid Carcinoma 826, 834 Injuries 1003
Epidermoid Inclusion Cyst 784, 790 Fracture (First MC) 947
Epidural hematoma 848 Fractures 816
Epiphyseal Lesions 1008 Fractures (Pathologic) 961
Dysgenesis 1021 Frieburg 911
Dysplasia 1020 Full thickness (Rotator Cuff Tear) 928
Epiphysis 767 Galeazzi 945
Epithelial nests 776 Ganglia 870
Epitrochlear Lymph Node 960 Ganglia (Knee) 870
Erlenmeyer flask deformity 971 Ganglion 792
Erosions 913 Ganglion/Synovial Cyst 1031
Erosive Osteoarthritis 917 Ganglion/synovial cyst/bursa 796
Erupting teeth 854 Gardner Syndrome 852, 856
Essex-Lopresti 945, 1003 Gardner Syndrome (Osteoma) 746
Ewing Sarcoma 721, 887, 964, 967 Gastrocnemius 869
Ewing Sarcoma (Intergroup Study) 888 Gastrocnemius/ Semimembranosus 870
Exophthalmos 892 Gaucher disease 818, 907, 971
Exostoses 856 GCT 769
Exostosis (Subungual - Dupuytren Exostosis) 759 Geodes 790
Extensor Carpi Ulnaris Sheath 875 Geographic Contusion (Knee) 866
Extensor tendons 859 Geographic Pattern (Bone Tumors) 725
Extent of Musculoskeletal Neoplasm 738 Geographic 1A: Differential Diagnosis 725
Extra-abdominal Desmoid Fibromatosis 778 Geographic IB: Differential Diagnosis 726
Extra-articular erosions (Gouty Arthritis) 950 Geographic IC: Differential Diagnosis 726
Extramedullary Hematopoiesis 971 Giant Bone Island 743
Extraskeletal Chondrosarcoma 764, 768 Giant Cell (Reparative) Granuloma 780
Facet 840 Giant Cell Tumor 721, 784, 1008
Fallen fragment sign 787 Giant Cell Tumor Tendon Sheath (GCT-TS) 794
Familial vitamin D res rickets 903 Giant Cells 784
Fanconi syndromes 903, 968 Gigantism 1029
Fanconi’s Anemia 972 Glad Lesion 936
Felon 825 Glenohumeral 932
Felty Syndrome 914 Instability 932
Femur 995 Joint 932
Fibrocartilage Calcification 951 Ligaments 932
Fibroma molluscum 1029 Glenohumeral Internal Rotation Deficit (GIRD) 936
Fibromas 746 Glenohumeral Labroligamentous complex 932
Fibromatosis 771, 778 Glenohumeral ligament (avulsion) 935
Fibromatosis: Types 778 Glenoid labrum 932
Fibrosarcoma 771, 780, 781, 802 Glomus 721
Fibrosarcoma/MFH 748 Glomus Tumor 805, 808
Fibrosis Histiocytoma 773 Gnathic Osteosarcoma 754
Fibrous cortical defect 771 Golfer’s elbow 956
Fibrous dysplasia 771, 773, 856, 944, 1017 Goltz syndrome 744, 784
Fibrous Histiocytoma (Malignant) 721 Gorham 809
Fibrous medullary defect 771 Gorlin syndrome 853
Fibroxanthoma (Nonossifying fibroma) 771 Gout 718, 817, 949, 1010, 1012
Fibular (lateral) 869 Gouty arthritis 949, 950
Fibular collateral lig complex 881 Gouty tophus 804
Fibular collateral ligament 867 Gracilis 869
Filariasis 837 Granulomatous Disease of Childhood 827
Finger (Trauma) 948 Grashey view 942
First MC (Fracture) 947 Greater Tuberosity Fracture 935
Flexion Teardrop Fracture 843 Ground glass 774
Flexor Digitorum (Avulsion) 948 Group B strep 822
Flipped (meniscal tear) 862 Guinea worm (dracunculosis) 837
Florid cemento-osseous dysplasia 856 Gumma 834
Fluid - fluid level 764, 785, 802 Guyon’s canal 872, 877
Fluorosis 818 HA Crystal Deposition Disease 952
I4
Hagl Lesion 935 Hypercementosis 854
Hajdu-Cheney Syndrome 1008 Hyperextension 840
Hallux 924 Hyperextension Dislocation 844
rigidus 924 Hyperextension Injuries 843
valgus 924 Hyperextension: Teardrop Fracture 845
Hamartoma 743 Hyperflexion 840
Hamate Fracture 947 Hyperflexion Injuries 840
Hand-Foot syndrome 969 Hyperflexion Sprain 840
Hand-Schüller-Christian disease 887, 892 Hyperparathyroidism 711, 773, 852, 856, 950, 971, 1007,
Hangee Fracture 845 1012, 1021
Hangman Fracture 845 Hyperthyroidism 773
Hanover 1003 Hypertrophic Osteoarthropathy 962
Hawkins classification of talar neck fractures 1002 Hypophosphatasia 904, 1007
Hawkins sign 1002 Hypothyroidism 1020, 1021
Heberden nodes 923 Idiopatic osteosclerosis 854
Hemangioendothelioma (HE) 721, 805, 810 Ifosfamide 903
Hemangioma 721, 804, 805, 1012 Iliotibial band 867
Arteriovenous 805 Iliotibial tract 869
AV malformation 852 Imaging for Staging Musculoskeletal Neoplasm 738
Capillary 805, 809 Immature cementoblastoma 850
Cavernous 805 Immature periapical cemental dysplasia 850
Venous 805 Impingement Syndrome 927
Hemangiopericytoma (HPC) 721, 768, 805, 810 anterolateral 881
Hematogenous Osteomyelitis: Adult 824 Infantile dermal/digital fibromatosis 778
Hematogenous Osteomyelitis: Child 822 Infantile myofibromatosis 778
Hematogenous Osteomyelitis: Infant 822 Infarction 969
Hematogenous Vascular Supply 820 Infection 1006
Hematologic Disease 968 Infectious Spondylodiscitis 1023
Hemochromatosis 949, 950, 952, 1021 Inferior Glenohumeral Labroligamentous complex 932
Hemodialysis elbow 718 Inferior Glenohumeral Ligament 933
Hemoglobinopathy 907 Inflammatory 780
Hemophilia 968, 972 Infrapatellar 870
Hemophiliac pseudotumor 973 Infrapatellar cleft 870
Hemorrhage 781, 790 Insufficiency fractures 979, 983
Hereditary Hyperphosphatasia: Juvenile Paget Disease 818 Interbody Fusion 710
Hereditary multiple exostoses (HME) 757, 760, 1017 Intermedius 869
Heterotopic Bone Formation: Myositis Ossificans 800 Interosseous ligament 880
High - Grade Surface 754 Interosseous syndrome (Elbow) 956
High output congestive failure 812 Interspinous widening 840
Hill-Sachs Lesion 934, 943 Intertrochanteric Fractures 980
Hip Intraarticular Bodies (Elbow) 956
Fractures 1000 Intra-Articular Hydroxyapatite Crystal Deposition Disease
Joint instability 999 952
Trauma 1000 Intracortical fibrous dysplasia 775
Histoplasmosis 836 Intramedullary (Chondrosarcoma) 764
HLA B27 916 Intramedullary Extent 738
Hodgkin 966, 971 Intramedullary Hemorrhage 848
Hook of hamate 877 Intranuclear inclusions 812
Hoop stresses 860 Intraosseous ganglion 784, 790, 1008
H-Shaped Vertebral Bodies 970 Intrasubstance Tear (Rotator Cuff) 929
H-type vertebrae 1010 Invisible Margin (Bone Tumors) 728
Human/animal bites 825 Involucrum 820
Humeral Fractures 943 Irradiation 907
Humphrey 859 Irregular Epiphyses (multiple) 1020
Hutchinson triad 834 Isolated Fractures Radius: Galeazzi 945
Hyaline cartilage cap 757, 758 Isolated Fractures Ulna: Monteggia 945
Hyaluronic acid 795 Isolated Tendon Injuries 948
Hydrops Fetalis 808 ITB Friction Syndrome 869
Hydroxyapatite 715 Ivory vertebra 814, 962
Hydroxyapatite Crystal Deposition 952 Differential Diagnosis 962
Hydroxyproline 812 Jaccoud arthropathy 1016
Hygroma 808 Jaffe-Campanacci syndrome 773
I5
Jaws 849 Laminar Fractures 843
Jefferson Fracture 846 Langerhans Cell Histiocytosis (LCH) 748, 887, 890, 1013,
Jersey Finger 948 1008, 1017
Joint Arthroplasty (Complications of ) 699 Laser therapy 808
Dislocation / Abnormal Alignment 702 Lateral compression (Pelvis Trauma) 996
Fractures and Nonunion 702 Lateral Epicondylitis (Elbow) 957
Heterotopic Bone Formation 699, 703 Lateral inferior geniculate artery 863
Loosening and/or infection 699 Lateral Meniscus 859
Radionuclide Evaluation 700 Lateral Process of Talus Fractures 1002
Small Particle Disease 699, 701, 702 Lateral Stabilizers 869
Joint involvement 738, 739 Lateral Tendons (Ankle and Foot) 884
Abscess 741 Lateral Ulnar Collateral Ligament 959
Bursitis 741 Lauge-Hansen 1001
Diabetic muscle ischemia 741 LCL-Biceps Femoris 870
Fibromatosis 741 Ledderhose disease 780
Gadolinium 742 Legg-Calvé-Perthes 911
Hematoma 741 Leiomyosarcoma 781, 802
intraarticular resection 739 Leprosy 829, 833, 953
Lymphocele 741 Lesion matrix 738
Muscle flap 741 Letournel and Judet classification 998
Myositis ossificans 741 Letterer-Siwe disease 887, 892
Myxoid liposarcoma 741 Leukemia 971
Post-Operative Imaging (Bone Neoplasm) 741 Ligament and Tendon Involvement 739
Radiation necrosis 741 ligament(ous) injury 840
Reactive lymph node 741 Limb Salvage Procedures 737
Seroma 741 Lipoblastoma 896
Soft Tissue Mass - Benign 740 Lipoma 720, 804, 1015
Soft Tissue Mass - Malignant 740 Lipoma Arborescens 798
Subtraction MRI 742 Lipoma Intramuscular 895
Synovial cell sarcoma 741 Lipomatosis 897
Joint Replacement 699 Liposarcoma 720, 781, 802, 893, 897, 1015
Jones Fracture 1003 Atypical 898
JRA 919 Dedifferentiated 898
Polyarticular 920 Higher Grade Lesions 898
Still Disease: Pauci or Monoarticular 920 Myxoid Lesions 898
Jumpers Knee 870 Pleomorphic Liposarcoma 899
Juvenile aponeurotic fibroma 778 Well-Differentiated 897
Juvenile Chronic Arthritis 912, 919, 973, 1016 Loa loa 837
Juvenile Paget Disease 818 Location in Bone: Axial (Bone Tumors) 724
Juvenile-onset adult type RA 920 Locked facets 842
Juvenile-onset ankylosing spondylitis 919 Long Head of Biceps Tendon 929
Juxtaarticular Osteoporosis 912 Long Head of the Biceps Tendon 932
Juxtacortical Chondroma 720, 762, 767 Longitudinal Tibial Stress Fracture 992
Juxtacortical Chondrosarcoma 767 Loose Bodies 871
Juxtacortical Osteosarcoma 752 Looser zones (Osteomalacia) 715
Kaplan 860 Looser’s zones 902
Kaposi sarcoma 837 Lower Extremity Trauma 995
Kasabach - Merritt 809 Low-Grade Chondroid Lesion 769
Keloid formation 744 Low-Grade chondrosarcoma 769
Keratocyst 852 Lumpy 912
Kienböck 911 Lunate 946
Kienböck’s Disease 911 Lung Cancer 963
Klippel-Trenaunay-Weber 809 Lunotriquetral Instability 875
Knee 995 Lyme disease 834, 835
Knee Injury 1001 Lymphangioma 721, 805
Knee Stabilizers 867 Lymphoma 720, 748, 961, 964
Köehler 911 Lymphoma of Bone (Primary Lymphocytic) 966
Kohler Disease 1006 Lytic Patterns (Bone Tumors) 728
Kyphosis 830, 840 lytic phase 812
Labral Repair 938 Lytic Phase 813
Labrum 932 Lytic Skull Lesions 1013
Lamina dura 850 Macho-Macho 852
I6
Madura Foot 837 Multiple enchondromatosis 760, 761
Maffucci syndrome 760, 761, 809 Multiple Myeloma 964
Magic Angle Phenomenon 876 Multiple myeloma with sclerosis or POEMS syndrome 965
Magnuson Stack 938 Multiple tori and exostoses 856
Malignant Bone Tumors: Age Distribution by Decade 723 Musculoskeletal Infection 820
Malignant Fibrous Histiocytoma (MFH) 721, 771, 780, 781 Musculoskeletal Neoplasm - Extent 738
Malignant melanoma of soft parts 803 Musculoskeletal Neoplasm - Staging - Surgical Implications
Malignant myositis 801 737
Malignant transformation (Multiple Enchondromatosis) 761 Musculoskeletal Tumors - Staging 734
Mallet Finger 948 Histologically Benign 735
Malnutrition 977 Histologically Malignant 736
Marrow Edema (Osteoid Osteoma) 747 Mycetoma 837
Marrow hyperplasia 969 Mycobacteria 829
Massive Osteolysis of Gorham 809 Mycobacterium 833
Mastocytosis 818 Mycobacterium Leprae 833
Matrix Formation 723 Myelitis (Calcic) 792
Matrix Formation (Bone Tumors) 729 Myelofibrosis 818, 968, 971, 974
Mazabraud syndrome 773 Myelography 840
McCune Albright syndrome 773 Myeloma 720, 961, 964, 1013
Medial Collateral Ligament (MCL) 867 Myeloma/plasmacytoma 786
Injuries 868 Myelomalacia 848
Medial Collateral Ligament (Elbow) 959 Myeloproliferative diseases 949
Medial Meniscus 859 Myositis 837, 983
Medial migration (Osteoarthritis: Hip) 923 Myositis Ossificans 792, 800, 1012
Medial Tendons (Ankle and Foot) 884 Myotendinous (Rotator Cuff Tear) 928
Median nerve 872, 877 Myotendinous Tear of Pectoralis 931
Impingement 956 Myxoid 780
Melorheostosis 744 Myxoid Chondrosarcoma 764, 768
Meningoceles 983 Myxoma 773, 792
Meningomyelocele 953 Myxomatous neoplasms 796
Meniscal Cyst 798, 870 Narrow Disk Space 1023
Meniscal Flap 862 Nasopalatine duct cyst 850
Meniscal tears 798, 858, 861 Navicular 880
Menisci (Calcification) 951 Neck of the scapula 942
Menisci (Post-surgical) 863 Necrosis - Avascular 719
Meniscofemoral ligaments 863 Neoplasm (Paget Disease) 817
Meniscus homologue 875 Nerve Impingement (Elbow) 956
Mesenchymal cells 768 Nerve root avulsion 840
Mesenchymal Chondrosarcoma 764, 768 Neuroarthropathy 953
Metabolic Bone Disease 900 Neuroblastoma 963, 964, 967
Metachronous Osteosarcoma 750 Neurofibromatosis (NF) 976, 981
Metaphyseal chondrodysplasia 904 Neurofibromatosis (Type 1) 773, 1017, 1020, 1029
Metastases 748, 768, 1013 Neurogenic tumor 786
Skeletal 961 Neuropathic 834
Metastatic lymphoma 967 Joint 1017
Methemoglobin 848 Osteoarthropathy 949, 953
MFH (Malignant Fibrous Histiocytoma) 802 Shoulder-Syrinx 1027
MFH/ fibrosarcoma 769 Neurovascular involvement 738, 739
Middle Glenohumeral Ligament 933 Nevoid basal cell carcinoma syndrome 853
Milk - Alkali syndrome 793 NF (Neurofibromatosis) 981
Milwaukee Shoulder 952 NF-1 (vonRecklinghausen’s) 981
Mithramycin 818 NF-2 - Acoustic neuromas 981
Mixed Connective Tissue Disease (MCTD) 1016 Nidus (Osteoid Osteoma) 746
Mixed/Blastic Disease 814 Night Stick Fracture 944
Monostotic 773, 812 Nocardia 833
Monteggia 945 Nodular Fasciitis 792, 801
Morton’s Neuroma 885 Non-Hodgkin 966
Motheaten (Bone Tumors) - Differential Diagnosis 727 Non-Insertional Achilles Tendon Pathology 883
Mucoepidermoid carcinoma 852 Nonossifying fibroma (NOF) 771, 981
Mucopolysaccharidosis 1020 Nonosteogenic fibroma 771
Mucormycosis 836 Nonspecific spindle cell sarcoma 781, 802
Multidirectional Instability (Glenohumeral) 939 O’Donoghue’s Triad 867
I7
Oblique meniscomeniscal ligament 863 Osteosarcoma 743, 750, 751, 769, 857, 1012
Occult fracture 865 Intramedullary 751
OCD 955 Juxtacortical 752
Odontogenic cyst 852 Parosteal 753
Odontogenic keratocyst 852 Telangiectatic 752
Odontogenic myxoma 852 Osteosarcoma (Sclerosing) 754
Odontoid Fracture 847 Osteosarcoma: Low Grade Intramedullary 754
Odontoma 855, 857 Osteosarcoma: Soft Tissue 755
OI (Osteogenesis Imperfecta) 980 Extraskeletal 755
Olecranon bursitis 949, 958 Osteosarcoma : Intracortical 756
Olecranon fossa 955 Osteosarcomatosis 755
Ollier disease 760 Osteosclerosis 711, 714
Ollier Syndrome 762 Overhanging edge 914
Oncogenic osteomalacia 773 Overhanging edge (Gouty Arthritis) 950
Os Acromiale 928, 942 Oxalosis 718
Os odontodeum 847 Oxyhemoglobin 848
Os Trigonum 880 P V N S 793
Osgood-Schlatter 911 Paget Disease 812, 1013, 1017
Osler-Weber-Rendu 809 Paget’s disease 856
Osseous bowing 812 Pain (Congenital Insensitivity) 953
Osseous deformity 816 Palmar Fibromatosis 779
Osseous Lesions both Sides of Joint 1006 Palmer 1003
Osseous Neoplasm 733 Pancreatitis 907
Ossicle 860 Panne 911
Ossifying fibroma 775, 855, 857 Panner’s disease 959
Osteitis deformans 812 Paralabral Cyst 937
Osteoarthritis 920 paramyxovirus (measles) 812
Osteoarthritis (secondary) 826 Parathormone (PTH) 711
Osteoarthropathy (Hypertrophic) 962 Paravertebral soft tissue 828
Osteoarthropathy (Neuropathic) 949, 953 Paronychia 825
Osteoblastic Metastasis 743 Parosteal Osteosarcoma 753
Osteoblastoma 720, 743, 748, 763, 855, 857, 1008, 1024 Parrot Beak 862
Osteochondral fracture 879 Parsonage Turner Syndrome 958
Osteochondral Lesion 879 Partial thickness (Rotator Cuff Tear) 928
Osteochondritis 834 Patellar Dislocation 866
Osteochondritis Dissecans 799, 865, 879, 910 Patellar Retinacula 867, 869
Osteochondroma 720, 757 Patellar Tendinitis 870
Osteochondroses 911, 1006 Patellar tendon 869
Osteochondrosis 906 Patellofemoral Joint 870
Osteoclast 962 Patellofemoral Syndrome 870
Osteofibrous dysplasia 771, 775, 776 Pathologic Fractures 961
Osteogenesis Imperfecta (OI) 976, 980, 1007 Pattern of Bone Destruction and Lesion Margin 725
Osteoid 738 Geographic 725
Osteoid Osteoma 720, 743, 746, 748, 763, 1005, 1008 Motheaten 725
Osteolysis (Post-Traumatic - Clavicle) 941 Permeative 725
Osteolysis of Gorham 809 Transition Zone 725
Osteoma 720, 743, 745, 857 PCL 867, 868
Osteomalacia 711, 714, 809, 900 PCL Tear 868
Osteomyelitis 718, 748, 821, 824, 825, 827, 830, 856, 967, Pectoralis Major Tear 931
1026 Pedicle erosion 981
Osteomyelitis (salmonella) 1010 Pedicle sclerosis 749
Osteonecrosis 769, 906, 999 Pedicolaminar Fracture-Separation 844
Osteonecrosis (Spontaneous) 910 Pelvic Ring Disruption 998
Osteopathia striata 744 Pelvic Ring Fractures 995
Osteopenia 714, 900, 979, 1010 Pelvic Stress Injury 993
Osteopetrosis 856 Pelvis Trauma 995
Osteophyte (button) 922 Pencilling (Long Bones) 981
Osteophyte formation 921 perched facets 842
Osteopoikilosis 744 Percutaneous ablation (radiofrequency) 748
Osteoporosis 711, 900, 976, 979, 1008 Percutaneous removal (Osteoid Osteoma) 748
Osteoporosis (transient) 909 Embolization 748
Osteoporosis circumscripta 813 Radiofrequency 748
I8
Periapical cemento-osseous dysplasia 854 Posterolateral Rotatory Instability (Elbow) 960
Periapical cyst 850 Post-traumatic cyst 784, 790
Periapical granuloma 850 Pregnancy 907
Periarticular Calcification 715 Prepatellar 870
pericapsular fat planes 826 Primary Lymphocytic Lymphoma of Bone 966
Periodontal ligament 850 Primary Lymphoma 966
Periosteal Osteosarcoma 753, 1014 Primary Periarticular HA Crystal Deposition Disease:
Periosteal reaction 723 (Calcific Tendinitis) 952
Periosteal Reaction (Intramedullary Chondrosarcoma) 765 Prostaglandin (Osteoma) 746
Periosteal reaction (PTH) 711 Prostate Carcinoma 962
Periosteal Reaction: Aggressive 731 Pseudarthrosis (Tibia) 981
Codman triangle 731 Pseudogout 950
Hair-On-End 731 Pseudomonas 821
Laminated 731 Pseudotumor (Hemophiliac) 973
Sunburst 731 Pseudoxanthoma Elasticum 792
Periosteal Reaction: Nonaggressive 730 Psoriasis 916
Buttressing 730 Psoriatic arthritis 912, 916, 1009
Expansion 730 Psoriatic Sacroiliitis 1010
Septation 730 Pubic fracture 998
Solid 730 Pulley Injuries 948
Periosteal/juxtacortical (Chondrosarcoma) 764 Puncture wounds 825
Periostitis 914 Putti Platt 938
Permeative (Bone Tumors) - Differential Diagnosis 727 PVNS 792, 973, 1006
Peroneus Brevis 884 Pyknodysostosis 1007
Peroneus Brevis Split Syndrome 885 Pyomyositis 826
Peroneus Longus and Brevis 884 Pyrophosphate arthropathy 950, 951
Peroneus Quartus 886 Quadriceps tendon 869
Perthes Lesion 934 Quadrilateral Space Syndrome 930
Pes anserine 870 RA 869
Phemister triad 832 Rachitic rosary 901
Phlebolith 806 Radial Collateral Ligament 959
Picture frame 814 Radial Fracture 945
Pigmented Villonodular Synovitis (PVNS) 793 Radial head 944
Pillar Fracture 844 Radial head dislocation 945
Pisotriquetral joint 872 Radial nerve impingement 956
Plantar Fascia 882 Radial Styloid Hutchinson’s/ Chauffer’s Fracture 945
Plantar Fasciitis 882 Radial tunnel syndrome 956
Plantar Fibromatosis 780, 882 Radiation 757
Plantaris Tendon 884 Radiation - internal synovectomy 795
Plasmacytoma 720, 966 Radiation Induced Chondrosarcoma 764
PNET 964, 967 Radiocapitellar Line 944
POEMS syndrome 964, 965 Radiolucent Lesions
Polyarthritis 983 Multilocular (Macho-Macho) 852
Polymyositis 976 Periapical 850
Polyostotic 773, 812 Pericoronal 852
Polyostotic Lesions 732 Radiopaque and Mixed Lesions
Angiomatous lesions 732 Ground Glass 856
Malignant 732 Interradicular 855
Neurofibromatosis (type 1) 732 Multifocal Confluent 856
Paget disease 732 Periapical 854
Popliteus hiatus 870 Target Lesion, Dense 857
Popliteus tendon 859 Radioulnar ligaments 875
Positive Rim Sign 943 Raynaud’s phenomenon 984
Posterior Dislocation (Glenohumeral) 943 Reactive Arthritis 917
Posterior Impingement (Elbow) 956 Rectus femoris 869
Posterior Instability (Glenohumeral) 935, 943 Recurrent Multifocal Osteomyelitis 827
Posterior recesses 870 Reflex sympathetic dystrophy 976
Posterior Superior Glenoid Impingement 936 Reiter Disease 912, 916, 917, 1010
Posterior talofibular 881 Renal Cell Carcinoma 963
Posterior Tibial Tendon 884 Renal disease 869
Posterior tibiofibular ligament 880 Renal Insufficiency - Chronic (MSK Manifestations) 711
Posterior Vertebral Scalloping 1020 Renal Osteodystrophy 711, 903
I9
Renal Tubular Disorders 903 Serpentine sclerosis 907
Rhabdomyosarcoma 769, 781, 802, 964, 967 Serpentine vessels 806
Rheumatoid Arthritis 797, 817, 912, 914, 941 Sever 911
Rheumatoid arthritis, JRA 748 Shepherd’s Crook 774
Ribbon ribs 1029 Shiny corner sign 918
Rickets 714, 900, 971 Sickle cell anemia 818, 968, 1010
Acetabuli Protrusio 714 Simple Bone Cyst 786
Basilar invagination 714 Sinding-Larsen-Johansson 911
Triradiate pelvis 714 Sinus lesions 745
Rim Rent Tear (Rotator Cuff) 929 Sinus Tarsi Syndrome 882
Ring sequestra 825 Sinus tracts 822
Rolando Fracture 947 Skeletal Metastases 961
Romanus and Andersson lesion 918 Skull: beveled edge, button sequestrum 891
Rotator cuff 932 SLAC Wrist 874
Atrophy 930 SLAP Tears 936
Tears 915, 925 SLE 869, 976
Types 928 SLE (Systemic Lupus Erythematosis) 983
Rowe 1003 Slipped Epiphyses 715, 826
Saber shin 834 Small cell carcinoma 964
Sacral Lesions: Differential Diagnosis 786 Smith Fracture (Reverse Colles) 945
Sacroiliac disease 918 Soft Tissue abscess 826
Sacroiliitis 1010 Soft Tissue Chondroma 800
Sacrospinous ligaments 997 Soft tissue chondrosarcoma 1012
Sacrotuberous ligament 997 Soft Tissue Ganglion 795
Saddle nose 834 Soft Tissue Hemangioma 805
Salmonella 821 Soft Tissue infection 825
Salter-Harris Fracture 1011 Soft Tissue Lipomatous Tumors 893
Sanders Classification 1003 Soft Tissue Masses Differential Diagnosis 804
SAPHO 827 Soft Tissue Neoplasm 733
Sarcoid 837 Angiomatous lesions 733
Sarcomatous transformation 817 Elastofibroma and fibromatosis 733
Sartorius 869 Lipomatous lesions 733
Saucerization (Juxtacortical Chondroma) 762 Neurogenic tumors 733
Saunders 1003 PVNS and ganglion 733
Sausage digit 912 Soft Tissue Sarcoma Incidence 781
Scaphoid fracture 945 Solitary Focus Bone Scan 964
Scapholunate Ligament 946 Souer and Remy 1003
Disruption 946 Sphenoid 745
Scapular “Y” View 942 Spina ventosa 830
Scapular Fractures 942 Spinal cord edema/hematoma 848
Schatzker Classification (Tibial Plateau Fractures) 1001 Spine Infections 828
Scheuermann Disease 911 Spinoglenoid Notch Entrapment 930
Sclerodactyly 984 Spirochetes 834
Scleroderma 793, 976, 985 Spondylitis 918
Sclerosing osteomyelitis of Garre 825 Spondyloarthropathies 912, 916
Sclerosing Osteosarcoma 754 Spondylodiscitis 828, 830, 1023
Scoliosis 901, 981 Spondylolisithes 845
Scurvy 900, 904, 977 Spontaneous healing (Osteoid Osteoma) 748
Secondary chondromatosis - trauma 799 Spontaneous osteonecrosis 865, 910
Secondary Chondrosarcoma 764 Sporotrichosis 836
Secondary osteoarthritis 826 Squamous cell carcinoma 852
Segond fracture 807, 1001 Staph aureus 821, 828
Semimembranosus 869, 870 Stener Lesion 947
Semitendinosus 869 Sterno-clavicular Joint 941
Senile osteoporosis 977 Steroid administration 953
Septic Arthritis 718, 748, 825 Steroids 869, 907
Septic bursitis 826 Steroids (Osteopenia/Osteoporosis) 977
Septic tenosynovitis 826 Stewart-Treve syndrome 810
sequestra 824, 967 Still Disease 919
Sequestra-Like Appearance 1005 Storioform 780
Sequestrum 820 Stress fracture 748
Seronegative Spondyloarthropathy 1009 Femur 1027
I 10
Stress Injuries 987 Thrombocytopenia 809
Subacute osteomyelitis 748, 824, 1007, 1026 Thrombocytopenia with Absent Radii (TAR) 968, 972
Subchondral cyst 784, 790, 921, 1008 Thumb Injury 947
Subchondral cyst/intraosseous ganglion 763 Thyroid Cancer 963
Subchondral Resorption 713 Tibial collateral 870
Subchondral Sclerosis 923 Tibial Plateau Fractures 1001
Sublabral Foramen 933 Tile 995
Subligamentous extension 830 Tile Classification 995
Subligamentous/Subtendinous Resorption 713 Tophi 950
Subperiosteal (Osteoid Osteoma) 746 Tori 856
Subperiosteal abscess 822, 823 Torus/ Buckle fracture 945
Subperiosteal Resorption 712 Transchondral fracture 879
Subscapularis (Avulsion) 935 Transient Osteoporosis 909
Subscapularis (Disruption) 935 Transient Osteoporosis Hip 1015
Subscapularis Muscle 932 Transient Regional Osteoporosis 977
Subscapularis Tears 929 Transverse Fractures (Pelvis) 999
Subtrochanteric Fractures 1000 Transverse ligament 863
Subungual Exostosis 759 Trap shooter’s shoulder 942
Sunburst 967 Trauma 839
Super bone scan 718 Trauma (Dysbaric Disorders) 907
Superior Glenohumeral Ligament 933 Trauma (Pelvis and Lower Extremity) 995
Superolateral migration (Osteoarthritis - Hip) 923 Trauma (Upper Extremity) 941
Supinator syndrome (Elbow) 956 Traumatic bone “cyst” 850
Supracondylar fracture 944 Traumatic Spondylolisithes 845
Suprapatellar “bursa” 870 Trevor Disease 759, 1020
Suprascapular Nerve Entrapment 930 Triangular Fibrocartilage (Calcification) 951
Supraspinatus Tendon (Tear) 935 Triangular Fibrocartilage Complex 875
Swan-Neck, Boutonniere deformities 914 Triceps Injuries 958
Symmetric Polyarthritis 983 Triquetrum Fracture 947
Symphysis pubis (Calcification) 951 Triradiate pelvis 901
Synchronous Osteosarcoma 750 Trochlea 955
Syndesmophyte 918 Trochlear sulcus 956
Synovial Chondroma 792 Trolley track sign 918
Synovial Chondromatosis 792, 799, 1006 Tropical ulcer 834
Synovial Trough Sign 943
Cyst 790, 792 T-score 978
Folds (Elbow) 956 Tuberculosis 829, 973
Lipoma 792, 798 Tuberculous
Osteochondromatosis 799 Arthritis 748, 832
Plica 871 Osteomyelitis 830
Sarcoma 781, 792, 793, 795, 802, 1012 Spondylodiscitis 830
Synovitis (Postoperative - Glenohumeral) 939 Tubulation (Osteochondroma) 758
Syphilis 834, 953 Tumoral Calcinosis 792, 1012
Syringomyelia 848, 953 Turner syndrome 808
Systemic Lupus Erythematosis (SLE) 983, 1016 UCL and ulnocarpal ligaments 875
Tabetic arthropathy 953 Ulcer (tropical) 834
Talar Neck Fractures 1002 Ulcerative Colitis 912
Talus 995 Ulcers 825
Tarsal Coalition 880 Ulnar
Tarsal joints 1003 fracture 945
Tarsal Tunnel Syndrome 885 nerve 872
Telangiectasia 984 Tunnel Syndrome 877
Telangiectatic Osteosarcoma 751 Unicameral bone cyst (UBC) 784, 944
Tendinitis (Calcific) 952 Unilateral Facet Injury 841
Tendon Sheath 794 Unusual infection 818
Tennis elbow 956 Upper Extremity Trauma 941
Tenosynovitis 876 Van Neck 911
Tenosynovitis (septic) 826 Vanishing Bone Disease 809
Tetracycline 748 Vastus lateralis 869
TFCC 872 Vastus medialis 869
Thalassemia 968, 970 Ventral (anterior) SIJ ligament 997
Thickened trabeculae 815 Vertebra Plana 891
I 11
Vertebral scalloping 981
Vertebroplasty 808
Vertical shear (Pelvic Trauma) 996
VISI deformity 875
Vitamin D: Prohormone 900
Volar Plate Avulsion 948
Voorhoeve Disease (Osteopathia Striata) 744
Wall Fracture (Pelvis) 999
West Point View 942
Whipple 912
Whiskering 914
Widened hip joint 826
Wimberger sign 834
Wormian Bones 1007
Wrisberg 859
Wrist 872
Wrist Subluxations 1019
Xenograft 709
X-linked hypophosphatasia 903
Yaws 834
Young-Burgess 995
Young-Burgess Classification 996
Young-Burgess vs Tile Classifications 995
Yttrium 90 795
Zonal pattern 801
Zonal phenomena 801
Z-score 978
I 12
Radiologic
Pathology
Fifth Edition
VOLUME 3
Neuroradiology and Pediatric
Radiologic Pathology Correlation
2006
Editors
2007
Ellen M. Chung, LTC, MC, USA
Chief, Pediatric Radiology
Jeffrey R. Galvin, MD
Chief, Chest Radiology
Kelly K. Koeller, MD
Chief, Neuroradiology
Mark D. Murphey, MD
Six Week Course Director
Chief, Musculoskeletal Radiology
All rights reserved. No part of this publication may be reproduced or transmitted in any form
or by any means: electronic, mechanical, photocopy, recording, or any other information
storage and retrieval system without written permission of the publisher.
Great care has been taken to guarantee the accuracy of the information contained in this
volume. However, neither the American Registry of Pathology, Armed Forces Institute of
Pathology, nor the editors and contributors can be held responsible for errors or for any
consequences arising from the use of the information contained herein.
The opinions and assertions contained herein are the private views of the authors and are
not to be construed as official nor as representing the views of the Departments of the Army,
Air Force, Navy, or Defense.
987654321
ISBN 1-933477-00-8
Preface
The Armed Forces Institute of Pathology’s Radiologic Pathologic Correlation
course presented by the Department of Radiologic Pathology enters its 59th year
of educating radiology residents worldwide. For the fifth year, our staff and visiting
lecturers have contributed their lecture material and images to compile Radiologic
Pathology 2006 – 2007, continuing the tradition of presenting richly illustrated
material that teaches the pathologic basis of disease to improve our understanding
of the imaging appearance of disease. We hope the efforts of our authors and
editors have once again accomplished our goal of bringing the outstanding and
unique Radiologic Pathologic Correlation course to your fingertips.
Acknowledgements
iii
Faculty – VOLUME 3
iv
Table of Contents – VOLUME 3
Neuroradiology
Kelly K. Koeller, MD, FACR
Imaging of Demyelinating Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1037
Lymphoma and Uncommon Neuroepithelial Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1045
Cerebral Intraventricular Neoplasms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1058
Imaging of the Temporal Bone: Anatomy and Congenital Lesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1068
Imaging of the Temporal Bone: Infectious and Neoplastic Lesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1076
Imaging of the Orbit: The Globe and Conal Lesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1088
Imaging of the Orbit: Intraconal and Extraconal Lesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1097
James G. Smirniotopoulos, MD
Patterns of Location: Infratentorial and Supratentorial . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1106
Patterns of Enhancement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1126
The WHO 2000 Brain Tumor Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1137
Non-Astrocytic Gliomas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1149
Extraaxial Tumors: Other Non-Glial Lesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1158
Neoplasms of the Meninges . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1164
Pinealomas and, other Pineal Region Masses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1175
The Phakomatoses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1184
Mary E. Jensen, MD
Subarachnoid Hemorrhage and Intracranial Aneurysms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1210
Intracranial Vascular Malformations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1220
Intracranial Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1231
Paranasal Sinuses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1240
Sella and Parasellar Region . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1250
Erin Simon Schwartz, MD
Congenital Spinal Anomalies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1260
Wendy R. K. Smoker, MS, MD, FACR
Imaging of the Suprahyoid Neck: Superficial, Parapharyngeal and Carotid Spaces . . . . . . . . . . . . . . . . .1266
Imaging of the Suprahyoid Neck: Masticator and Parotid Spaces . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1274
Imaging of the Suprahyoid Neck: Pharyngeal Mucosal Space and Oral Cavity . . . . . . . . . . . . . . . . . . . .1282
Spine: Degenerative Disease and Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1290
Spinal Tumors, Cysts, and Mimics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1298
Congenital Abnormalities of the Brain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1307
Kelly K. Koeller, MD, FACR
Neuroradiology Seminar 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1318
Neuroradiology Seminar 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1322
Pediatric Radiology
Ellen M. Chung, LTC, MC, USA
Childhood Urinary Tract Infection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1329
Neonatal GI Tract Obstruction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1341
Acute GI Disorders of Infants and Children . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1353
Diseases Affecting The Pediatric Airway . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1363
Vascular Rings and Slings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1374
Cystic Renal Disease of Childhood . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1381
Marylin J. Siegel, MD
Pediatric Renal Tumors: Infancy and Young Children . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1390
Pediatric Adrenal Masses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1402
Pediatric Pelvic Masses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1414
Bone Marrow Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1425
Congenital Lung Malformations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1435
Lung Diseases in Neonates . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1444
Pediatric Cardiac Imaging Part I: Vascular Anomalies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1453
Pediatric Cardiac Imaging Part II: Congenital Heart Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1463
v
Gael J. Lonergan, MD
Congenital Heart Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1472
Forensic Radiology of Child Abuse . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1491
Dorothy I. Bulas, MD
Neonatal Brain: Radiologic Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1501
vi
Neuroradiology
Imaging of Demyelinating Diseases
Kelly K. Koeller, MD, FACR
Imaging Hallmarks
• White matter location
➢ May involve basal ganglia
• Little or no mass effect
• Usually no calcification
• May or may not enhance
Figure 5-1-1
Normal Lesions [Figure 5-1-1]
• Virchow-Robin spaces
➢ Perivascular space of deep penetrating vessels
➢ Follows CSFsignal intensity
• Ependymitis granularis
➢ Frontal horn
Demyelinating Disorders
• Multiple sclerosis
• Vascular
• Viral / post-viral demyelination
• Toxic / metabolic encephalopathies
• Iatrogenic white matter degeneration Figure 5-1-2
Multiple Sclerosis
• Unknown etiology
➢ Viral: measles, Epstein-Barr virus (EBV)
➢ Genetic: chromosome 6, human lymphocyte antigens (HLA)
loci
➢ Autoimmune: associations with Graves’, myasthenia gravis,
ulcerative colitis, Crohn's, SLE
• Females (60%): especially with optic neuritis
• 95% cases: 18-50 years old
• Cooler climates: northern Europe, North America; southern South
America
Multiple Sclerosis
• Relapsing-remitting: 70%
➢ Numbness, dysesthesia, burning sensations
➢ 2 clinical attacks from 2 separate lesions
❖ At least 24 hours and at least 30 days apart Ependymitis granularis
➢ Partial or complete remission for months or years
• Progressive: 20%
➢ Primary progressive: slow onset without distinct attacks
➢ Secondary progressive: relapsing-remitting form with progressive disability
• “Monosymptomatic demyelinating”: 10%
McDonald et al, Ann Neurol 2001: 50-121-127
Arteriosclerosis
• Long penetrating end arteries
➢ Few or no collateral vessels
• Pons, thalami, basal ganglia, deep white matter
• Prevalence increased with age and history of stroke
Venous Collagenosis
• Noninflammatory stenosis
• Occlusion of subependymal veins
• Associated with periventricular white matter changes Senescent white matter changes.
Note subcortical location
Moody et al, Radiology 1995; 194:469-476
HIV Encephalitis [Figure 5-1-12] PML with relative lack of mass effect
and sparing of cortical gray matter
• Much less common with anti-retroviral therapy
• Deep white matter and gray matter
• Psychomotor slowing, mental status changes, memory problems, apathy Figure 5-1-12
• Direct or indirect infection of oligodendrocytes
• Demyelination and vacuolation
➢ Axonal loss and microglial nodules
Thurnher et al AJNR 2001; 22:977-984
HIV Encephalitis
• Imaging often normal early in course
• Diffuse mild cerebral atrophy
➢ Cortical first, then central
• Ill-defined patchy areas
➢ Central white matter, basal ganglia, thalamus
➢ Bilaterally symmetric
➢ Usually no necrosis or edema
➢ No enhancement
HIV encephalitis with characteristic
Thurnher et al AJNR 2001; 22:977-984; Olson et al, Radiology 1988; cortical atrophy
169:445-448
Toxic Demyelination
• Alcohol
• Ion balance disorders
➢ Osmotic myelinolysis
➢ Extrapontine myelinolysis
• Organic toxins (lipophilic solvents)
• Carbon monoxide poisoning (“interval” form)
• Drug abuse (poisoned heroin)
Figure 5-1-15
Summary
• Normal
➢ Virchow-Robin spaces: follow CSF
➢ Ependymitis granularis: frontal horn
• Multiple Sclerosis
➢ Periventricular
➢ Clinical diagnosis
• Vascular demyelination
➢ Senescent white matter changes Radiation necrosis mimicking appearance of a
❖ Subcortical, do not involve corpus callosum glioblastoma multiforme
➢ Posterior Reversible Encephalopathy Syndrome
(PRES)
• Viral / postviral demyelination
➢ ADEM
➢ PML
➢ HIV encephalitis
• Toxic / metabolic demyelination
➢ Alcohol
➢ Osmotic myelinolysis: centra pons
• Iatrogenic demyelination
➢ Chemotherapy and radiation injury
References
1. Arbelaez A, Pajon A, Castillo M. Acute Marchiafava-Bignami disease: MR findings in two patients. AJNR Am J
Neuroradiol 2003; 24:1955-1957.
2. Baqi M, Kucharczyk W, Walmsley SL. Regression of progressive multifocal encephalopathy with highly active
antiretroviral therapy. Aids 1997; 11:1526-1527.
CNS Lymphoma
• 6.6%-15.4% of all primary brain tumors
➢ Only GBM, meningioma, and low-grade astrocytoma are more common
• Less than 1% of all body lymphomas
• Primary lymphoma much more common than secondary
Miller et al, Cancer 1994; 74:1383-1397; Henry et al, Cancer 1974; 34:1293-1302
Clinical
• Wide age range
➢ Peak: 4th to 5th decades
➢ Smaller peak: 1st decade (AIDS)
• Nonspecific clinical presentation
➢ Expanding mass lesion
➢ Encephalitis
➢ Stroke Figure 5-2-1
➢ Cranial nerve palsies
Koeller et al, Radiographics 1997; 17:1497-1526
Immunocompromised Patients
• “Opportunistic neoplasm”
➢ Incidence much higher than in
immunocompetent patients
• AIDS-defining diagnosis in HIV+ patients
• 2% of AIDS patients develop CNS lymphoma
• CNS mass lesion in AIDS patient
➢ Toxoplasmosis #1, lymphoma #2
➢ Lymphoma: #1 in pediatric AIDS patient
Rosenblum et al, Ann Neurol 1988: 23:S13-S16;
Koeller et al, Radiographics 1997; 17: 1497-1526
Two masses, both lymphoma, with one located
Gross Pathology [Figure 5-2-1] around the ventricle while the other arises from
• Intra-axial nodule the leptomeninges
➢ Grayish-pink, homogeneous, circumscribed
➢ Multifocal: 50%
• Leptomeningeal Figure 5-2-2
• Uveal
• Intradural spinal
Koeller et al, Radiographics 1997; 17:1497-1526
Figure 5-2-4
Lymphoma with characteristic
CT hyperdensity and T2 hypointensity
Figure 5-2-5
Lymphoma of right
basal ganglia
Neuroepithelial Tumors
• Astrocytic
➢ Pleomorphic xanthoastrocytoma Toxoplasmosis or lymphoma ?
• Oligodendroglial PET image shows hypermetabolic activity consistent with
• Mixed glial lymphoma
• Ependymal
• Choroid plexus
• Pineal parenchymal
• Neuroblastic
• Glial of uncertain origin
• Neuronal and mixed neuronal-glial
➢ Ganglioglioma / Gangliocytoma
➢ Desmoplastic Infantile Ganglioglioma
➢ Dysplastic cerebellar gangliocytoma
➢ Dysembryoplastic neuroepithelial tumor
➢ Cerebellar Liponeurocytoma
• Embryonal
➢ Supratentorial PNET
➢ Atypical teratoid / rhabdoid tumor
Ganglioglioma / Gangliocytoma
• About 1% of all brain tumors
• Children and young adults
➢ 80% <30 years old; peak: 10-30 years of age
➢ Males slightly more common
• Most common tumor seen in chronic temporal lobe epilepsy
➢ 15%-25% of medically refractory seizures
• Cerebral hemisphere predilection
➢ Temporal lobe: most common (38%)
➢ Optic nerves, pituitary and pineal glands, spinal cord, ventricles, cranial
nerve (1 report)
Johnson et al, Pediatr Neurosurg 1997; 27:203-207; Athale et al, Neuroradiology
1999; 16:790-792
Ganglioglioma
• Positron Emission Tomography (PET): heterogeneous metabolic activity
• MR Spectroscopy: increased choline-creatine ratio
Provenzale et al, AJR 1999; 172:1103-1107; Kumabe et al, Figure 5-2-10
Neurosurgery 1999; 45:183-187
Desmoplastic Infantile
Ganglioglioma / Astrocytoma
• First described in 1987
➢ “Superficial cerebral astrocytoma”
➢ “Desmoplastic cerebral astrocytoma of
infancy”
• Rare: 0.6% of brain tumors
➢ 16% of all infant brain tumors
➢ Vast majority: less than 1 year (range:
up to 17 years) Ganglioglioma in temporal lobe
➢ Males more common (2:1)
• Rapid onset: increasing head circumference
• Usually more than one lobe: typically frontal and parietal
VandenBerg et al, J Neurosurg 1987; 66:58-71; Taratuto et al, Cancer 1984; Figure 5-2-12
54:2505-2512
Figure 5-2-11
Cerebellar Liponeurocytoma
• No gender predilection
• Cerebellum or cerebellopontine angle
• WHO grade I or II
➢ Well-differentiated neuronal cells
➢ Focal lipomatous differentiation
➢ Low mitotic activity
• Good overall prognosis but few cases
➢ No role for radiation therapy or chemotherapy?
Kleihues et al, WHO classification 2000, 110-111
Pleomorphic Xanthoastrocytoma
• Originally described in 1979 (Kepes et al)
➢ 12 cases of supratentorial tumors involving the
leptomeninges
• Believed to arise from subpial astrocytes of the cortex
• Less than 1% of all brain neoplasms
• Importance: characteristic imaging appearance, highly
amenable to surgical resection
Kepes et al, Cancer 1979:44:1839-1852
Figure 5-2-24
Peripheral Mass
• Ganglioglioma
➢ Variable size with common calcification
➢ Most common cause of chronic temporal lobe epilepsy
➢ Gangliocytoma: lacks glial component
• Dysembryoplastic neuroepithelial tumor (DNT)
➢ Almost always involves cortical margin
➢ Uncommon calcification
➢ Temporal lobe: 62%
➢ “Soap bubble” appearance
Cerebellar Mass
• “Striated” cerebellar mass
➢ Dysembryoplastic cerebellar gangliocytoma (Lhermitte-Duclos)
• With fat content
➢ Cerebellar liponeurocytoma
References
Ependymoma
• Arise from ependymal cells of ventricular wall
➢ Also central canal of spinal cord
• 3%-9% of all neuroepithelial tumors
➢ 6%-12% of pediatric brain tumors
➢ 30% of all brain tumors in children < 3 years of age
• No gender predilection
3rd WHO classification, 2000
Ependymoma
• Increased intracranial pressure and hydrocephalus
• Adults: 5-year survival rate = 57%, 10-year = 45%
• Less favorable prognosis
➢ Children: especially those under 2 years of age
➢ Fourth ventricle location
• Recurrence common
• Gross total resection “curative”
➢ Radiation therapy in partial resection cases
3rd WHO classification, 2000; Childs Nerv Syst 1990; 6:375-378;
Neurosurgery 1995; 37:655-667; Neurosurgery 1993; 32:169-175
Ependymoma
• Well-circumscribed mass
• May extend into brain
• Fourth ventricle: foraminal extension common
3rd WHO classification, 2000
Subependymoma
• First described in 1945
• Arise from subependymal glial layer
• Incidence: 0.4 (asymptomatic) - 0.7%
(symptomatic)
• Most smaller than 2 cm diameter
➢ Symptomatic: 3-5 cm
• Hydrocephalus (80%), focal
neurologic deficit (27%), seizures
(9%), subarachnoid hemorrhage
(4.5%)
J Neurosurg 1945; 2:232-240; Acta
Neurochir 1989; 96:15-25;
AJR 1995; 165:1245-1250; Neurosurgery Ependymoma with foraminal extension on MR
1986; 19:594-598
Subependymoma
• Males more common
• Older than 15 years of age: 82%
• Fourth ventricle: > 50%
➢ Lateral ventricle: ~ 45%
• Well-circumscribed avascular mass
➢ Pedicular attachment to ventricular wall
Neurosurgery 1986; 19:594-598; J Neurosurg 1978: 49:689-696
Subependymoma
• Expansive but not infiltrative
• WHO grade I
➢ Dense fibrillary matrix
➢ Cysts and nests
➢ Low mitotic activity
• Low recurrence rate
• 10% mixed with ependymoma or other tumor
Neurosurgery 1986; 19:594-598; 3rd WHO classification, 2000
Central Neurocytoma
• First described in 1982
➢ Confusion with intraventricular oligodendroglioma
• “Central”: lateral and third ventricles
➢ “Extraventricular central neurocytoma” for those located
elsewhere (brain, cerebellum, spinal cord)
• 0.25%-0.5% of all intracranial tumors
• No gender predilection
Acta Neuropathol 1982;56:151-156; 3rd WHO classification, 2000;
Brain Pathol 1993; 3:297-306
Central Neurocytoma
• Broad age range: 8 days to 67 years
➢ Mean age: 29 years
➢ 50%: 20-30 years of age
➢ 75%: 20-40 years of age
• Short clinical course (mean: 3 months)
➢ Increased intracranial pressure, mental status changes, visual
deficits
3rd WHO classification, 2000; Brain Pathol 1993; 3:297-306
Central Neurocytoma
• Arise from septum pellucidum or ventricular wall
• Lateral ventricle near foramen of Monro: 50%
➢ Lateral and third ventricles: 15%
➢ Bilateral: 13%
➢ Third ventricle alone: 3% Subependymoma of right lateral
Surg Neurol 1998: 49:197-204; 3rd WHO classification, 2000 ventricle on axial T1-weighted
pre-contrast and post-contrast
images
Colloid Cyst
• Most common neuroepithelial cyst: probably arises
from endoderm
• Young to middle-aged adults
• Positional headache: acute CSF obstruction
• Antero-superior third ventricle
• Variable composition: mucoid material with old
blood, cholesterol crystals, serous fluid,
paramagnetic ions
Lach et al, J Neurosurg 1993; 78:101-111;
Shaungshotti et al, Arch Pathol Lab Med 1965; 80:214-
224
Intraventricular Meningioma
• CT: well-defined globular mass
➢ Hyperattenuated compared to brain
➢ Calcification: 50%
Neurosurgery 1987: 20:465-468; AJNR 1995; 16:1378-1381;
Surg Neurol 1994: 42:41-45
Summary
• Fourth Ventricle
➢ Ependymoma
➢ Subependymoma
➢ Choroid Plexus Papilloma
• Third ventricle
➢ Colloid Cyst Choroid plexus metastasis
➢ All the others: less common from renal cell carcinoma
• Lateral Ventricle (anterior half)
➢ Subependymoma
➢ Central Neurocytoma
➢ Subependymal Giant Cell Astrocytoma
➢ Ependymoma
➢ Astrocytoma
References
1. Baron Y, Barkovich AJ. MR imaging of tuberous sclerosis in neonates and young infants. AJNR Am J Neuroradiol
1999; 20:907-916.
2. Bolen JW, Jr., Lipper MH, Caccamo D. Intraventricular central neurocytoma: CT and MR findings. J Comput
Assist Tomogr 1989; 13:495-497.
3. Chiechi MV, Smirniotopoulos JG, Jones RV. Intracranial subependymomas: CT and MR imaging features in 24
cases. AJR Am J Roentgenol 1995; 165:1245-1250.
4. Coates TL, Hinshaw DB, Jr., Peckman N, et al. Pediatric choroid plexus neoplasms: MR, CT, and pathologic
correlation. Radiology 1989; 173:81-88.
5. Darling CF, Byrd SE, Reyes-Mugica M, et al. MR of pediatric intracranial meningiomas. AJNR Am J Neuroradiol
1994; 15:435-444.
6. Ellenbogen RG, Winston KR, Kupsky WJ. Tumors of the choroid plexus in children. Neurosurgery 1989; 25:327-
335.
7. Furie DM, Provenzale JM. Supratentorial ependymomas and subependymomas: CT and MR appearance. J Comput
Assist Tomogr 1995; 19:518-526.
8. Hassoun J, Gambarelli D, Grisoli F, et al. Central neurocytoma. An electron-microscopic study of two cases. Acta
Neuropathol (Berl) 1982; 56:151-156.
9. Hassoun J, Soylemezoglu F, Gambarelli D, Figarella-Branger D, von Ammon K, Kleihues P. Central neurocytoma:
a synopsis of clinical and histological features. Brain Pathol 1993; 3:297-306.
10. Healey EA, Barnes PD, Kupsky WJ, et al. The prognostic significance of postoperative residual tumor in
ependymoma. Neurosurgery 1991; 28:666-671; discussion 671-672.
11. Hoeffel C, Boukobza M, Polivka M, et al. MR manifestations of subependymomas. AJNR Am J Neuroradiol 1995;
16:2121-2129.
12. Kahn EA, Luros JT. Hydrocephalus from overproduction of cerebrospinal fluid, and experiences with other
parillomas of the choroid plexus. J Neurosurg 1952; 9:59-67.
13. Killebrew K, Krigman M, Mahaley MS, Jr., Scatliff JH. Metastatic renal cell carcinoma mimicking a meningioma.
Neurosurgery 1983; 13:430-434.
14. Kleihues P, Cavenee WK eds. World Health organization Classification of Tumours, Pathology & Genetics:
Tumours of the Nervous System. IARC, Lyon, France, 2000.
15. Kudo H, Oi S, Tamaki N, Nishida Y, Matsumoto S. Ependymoma diagnosed in the first year of life in Japan in
collaboration with the International Society for Pediatric Neurosurgery. Childs Nerv Syst 1990; 6:375-378.
16. Lach B, Scheithauer BW, Gregor A, Wick MR. Colloid cyst of the third ventricle. A comparative
immunohistochemical study of neuraxis cysts and choroid plexus epithelium. J Neurosurg 1993; 78:101-111.
17. Lang I, Jackson A, Strang FA. Intraventricular hemorrhage caused by intraventricular meningioma: CT appearance.
AJNR Am J Neuroradiol 1995; 16:1378-1381.
18. Lobato RD, Sarabia M, Castro S, et al. Symptomatic subependymoma: report of four new cases studied with
computed tomography and review of the literature. Neurosurgery 1986; 19:594-598.
19. Majos C, Cucurella G, Aguilera C, Coll S, Pons LC. Intraventricular meningiomas: MR imaging and MR
spectroscopic findings in two cases. AJNR Am J Neuroradiol 1999; 20:882-885.
20. Matsumura A, Ahyai A, Hori A, Schaake T. Intracerebral subependymomas: clinical and neuropathological
analyses with special reference to the possible existence of a less benign variant. Acta Neurochir Wien 1989;
96:15–25.
21. McConachie NS, Worthington BS, Cornford EJ, Balsitis M, Kerslake RW, Jaspan T. Review article: computed
tomography and magnetic resonance in the diagnosis of intraventricular cerebral masses. Br J Radiol 1994;
67:223-243.
22. McGirr SJ, Ebersold MJ, Scheithauer BW, Quast LM, Shaw EG. Choroid plexus papillomas: long-term follow-up
results in a surgically treated series. J Neurosurg 1988; 69:843-849.
23. Menor F, Marti-Bonmati L, Mulas F, Poyatos C, Cortina H. Neuroimaging in tuberous sclerosis: a
clinicoradiological evaluation in pediatric patients. Pediatr Radiol 1992; 22:485-489.
24. Morantz RA, Kepes JJ, Batnitzky S, Masterson BJ. Extraspinal ependymomas. Report of three cases. J Neurosurg
1979; 51:383-391.
25. Morrison G, Sobel DF, Kelley WM, Norman D. Intraventricular mass lesions. Radiology 1984; 153:435-442.
26. Palma L, Celli P, Cantore G. Supratentorial ependymomas of the first two decades of life. Long-term follow-up of
20 cases (including two subependymomas). Neurosurgery 1993; 32:169-175.
Middle Ear
• Epitympanum
➢ Malleus head
➢ Short process of incus
• Mesotympanum
➢ Muscles: tensor tympani (V3), stapedius (VII)
➢ Ossicles: rest of malleus and incus, stapes
➢ Ligaments
➢ Nerves: chorda tympani (VII), Jacobson’s nerve (IX)
Figure 5-4-4
Superior portion of internal auditory canal
with labyrinthine canal containing the
facial nerve on its way to the geniculate
ganglion and tympanic facial segment
along medial wall of middle ear
Figure 5-4-5
Superior portion of cochlea and internal
auditory canal. Note vestibular aqueduct
arising from posterior margin of temporal
bone
Figure 5-4-8
Basilar turn of cochlea. Internal carotid
artery is seen anterior to the cochlea and
is delimited from the middle ear by a
bony plate. Eustachian tube arises just
lateral to the artery and heads along an
anteromedial pathway towards the
nasopharynx
Figure 5-4-10
Figure 5-4-11
Cochlea is separated by cochlear
promontory from middle ear. Anterior
portion of internal auditory canal is just
coming into view. Scutum is well seen
along superior margin of medial external
auditory canal
Figure 5-4-12
Mid-portion of internal auditory canal with
crista falciformis along its lateral margin.
Vestibule now appears with lateral and
superior semicircular canals. Facial
nerve is located immediately inferior to
lateral semicircular canal and above oval
window
Figure 5-4-13
Figure 5-4-14
Congenital Anomalies
• Outer ear
• Middle ear
• Inner ear
• Vascular
➢ Internal carotid artery
➢ Jugular vein
• Cholesteatoma
• Encephalocele
Congenital Malformations
• External and middle ear (1st and 2nd branchial arch) develop independent of
inner ear (ectodermal)
• IAC development separate from inner ear development
• Anomalies of all 3 parts are rare
➢ Dysplasias and trisomies 13, 18, 21
Fisher and Curtin, Otolaryngol Clin North Am 1994; 27:511-531
Figure 5-4-25
1. Caldemeyer KS, Mathews VP, Azzarelli B, Smith RR. The jugular foramen: a review of anatomy, masses, and
imaging characteristics. Radiographics 1997; 17:1123-1139.
2. Couloigner V, Grayeli AB, Bouccara D, Julien N, Sterkers O. Surgical treatment of the high jugular bulb in patients
with Meniere's disease and pulsatile tinnitus. Eur Arch Otorhinolaryngol 1999; 256:224-229.
3. Dahlen RT, Harnsberger HR, Gray SD, et al. Overlapping thin-section fast spin-echo MR of the large vestibular
aqueduct syndrome. AJNR Am J Neuroradiol 1997; 18:67-75.
4. Davidson HC, Harnsberger HR, Lemmerling MM, et al. MR evaluation of vestibulocochlear anomalies associated
with large endolymphatic duct and sac. AJNR Am J Neuroradiol 1999; 20:1435-1441.
5. Gao PY, Osborn AG, Smirniotopoulos JG, Harris CP. Radiologic-pathologic correlation. Epidermoid tumor of the
cerebellopontine angle. AJNR Am J Neuroradiol 1992; 13:863-872.
6. Gavilan J, Trujillo M, Gavilan C. Spontaneous encephalocele of the middle ear. Arch Otolaryngol 1984; 110:206-
207.
7. Gottlieb MB, Blaugrund JE, Niparko JK. Imaging quiz case 1. Tegmental encephalocele. Arch Otolaryngol Head
Neck Surg. 1998 Nov;124(11):1274, 1276-7.
8. Jackler RK, De La Cruz A. The large vestibular aqueduct syndrome. Laryngoscope 1989; 99:1238-1242;
discussion 1242-1233.
9. Jackler RK, Luxford WM, House WF. Congenital malformations of the inner ear: a classification based on
embryogenesis. Laryngoscope 1987; 97:2-14.
10. Keen JA. Absence of both internal carotid arteries. Clin Proc 1945-1946;4:588
11. Mafee MF, Charletta D, Kumar A, Belmont H. Large vestibular aqueduct and congenital sensorineural hearing
loss. AJNR Am J Neuroradiol 1992; 13:805-819.
12. Martinez-Granero MA, Martinez-Bermejo A, Arcas J, et al. [Unilateral agenesis of the internal carotid artery in
childhood: description of a case]. Rev Neurol 1997; 25:1207-1209.
13. Mayer TE, Brueckmann H, Siegert R, Witt A, Weerda H. High-resolution CT of the temporal bone in dysplasia of
the auricle and external auditory canal. AJNR Am J Neuroradiol 1997; 18:53-65.
14. Overton SB, Ritter FN. A high placed jugular bulb in the middle ear: a clinical and temporal bone study.
Laryngoscope 1973; 83:1986-1991.
15. Paparella MM. Mondini's deafness. A review of histopathology. Ann Otol Rhinol Laryngol Suppl 1980; 89:1-10.
16. Pappas DG, Jr., Hoffman RA, Cohen NL, Holliday RA, Pappas DG, Sr. Petrous jugular malposition (diverticulum).
Otolaryngol Head Neck Surg 1993; 109:847-852.
17. Peron DL, Schuknecht HF. Congenital cholesteatomata with other anomalies. Arch Otolaryngol 1975; 101:498-
505.
18. Robson CD, Robertson RL, Barnes PD. Imaging of pediatric temporal bone abnormalities. Neuroimaging Clin N
Am 1999; 9:133-155.
19. Romo LV, Casselman JW, Robson CD. Temporal Bone: Congenital Anomalies. In: Som P.M., Curtin H.D. (eds)
Head and Neck Imaging, 4th edn. Mosby-Year Book Inc., St. Louis, 2003, pp: 1275-1360.
20. Sinnreich AI, Parisier SC, Cohen NL, Berreby M. Arterial malformations of the middle ear. Otolaryngol Head
Neck Surg 1984; 92:194-206.
21. Smith ME, Fisher C, Weiss SW. Pleomorphic hyalinizing angiectatic tumor of soft parts. A low-grade neoplasm
resembling neurilemoma. Am J Surg Pathol 1996; 20:21-29.
22. Thiers FA, Sakai O, Poe DS, Curtin HD. Persistent stapedial artery: CT findings. AJNR Am J Neuroradiol 2000;
21:1551-1554.
23. Valvassori GE, Clemis JD. The large vestibular aqueduct syndrome. Laryngoscope 1978; 88:723-728.
Inflammatory Disease
• Mechanism
➢ Eustachian tube dysfunction
➢ Decreased intratympanic pressure
➢ Children: otitis media
➢ Adults: nasopharyngeal carcinoma
• Thin-section CT: soft tissue and fluid look alike
➢ Hounsfield units not helpful
Nemzek and Schwartz in Som and Curtin,
Head and Neck Imaging, 4th ed, 2003, Mosby
Artist rendition of retraction pocket at
superior tympanic annulus caused by
Acquired Cholesteatoma [Figures 5-5-1 to 5-5-5]
negative intratympanic pressure
• Exfoliated keratin within sac of stratified squamous epithelium
• 98% of middle ear cholesteatomas
➢ Probably from retraction pocket in pars flaccida
• Prussak’s space: ossicles displaced medially
• Bone destruction Figure 5-5-2
➢ Scutum and ossicles:coronal plane best
➢ Pars tensa: lateral semicircular canal, axial plane best
Buckingham and Valvassori, Otolaryngol Clin North Am 1973; 6:363
Figure 5-5-3
Bilateral exostoses
Figure 5-5-14
Figure 5-5-15
Figure 5-5-16
Focal enhancement of deep portion of
internal auditory canal secondary to
arteriovenous malformation (not
vestibular schwannoma)
Longitudinal Transverse
Frequency 80% 20%
Axis Long Short
Blow Temporoparietal Occipital
Middle ear injury Likely Rare
Inner ear injury Rare Common
Facial paralysis 10–20%, usually 40–50%, usually
incomplete & acute & complete
delayed
Tegmen tympani Common Less common
disruption
Schwartz and Curtin in Som and Curtin,
Head and Neck Imaging, 4th ed., Mosby, 2003
Figure 5-5-26
Chondrosarcoma
Otosclerosis
• Primary endochondral bone within otic capsule replaced by
spongy vascular bone (“otospongiosis”)
• Slowly progressive
• Presents 10–30 years old with tinnitus
➢ Hearing loss later
• Females more common (70%)
• Bilateral 80% (usually asynchronous)
Valvassori, Otolaryngol Clin North Am, 1973; 6:379-389;
Reudi, Arch Otolaryngol 1963; 78:469-477
Otosclerosis
• Fenestral type (80%): CHL
➢ Begins at anterior oval window
• Cochlear type (20%): SNHL
➢ Almost always with fenestral type
➢ “Double Ring” sign
Ossicular derangement
• Demineralized areas: active disease
• Chronic disease: may appear normal
• MR: punctate enhancement
Mafee et al, Radiology 1985; 156:703-708; Swartz et al, Radiology 1985; 155:147-
150; Sakai et al, Am J Otolaryngol 2000; 21:116-118
Summary
• Challenging complex anatomy
• Facial nerve course: critical for pre-operative evaluation
• Bony plate between hypotympanum and ICA canal
• Tegmen tympani
• Cholesteatoma: bone erosion
• Cerebellopontine Angle: “AMEN”
➢ Vestibular schwannoma: most common
➢ Meningioma
➢ Epidermoid
➢ Non-acoustic schwannoma
• Jugular foramen
➢ Paraganglioma
➢ Schwannoma
• Petrous apex
➢ Cholesterol granuloma vs. epidermoid
➢ Chondrosarcoma, Chordoma, Metastasis
• Otosclerosis
• Radiologist’s Goals
➢ Define extent of lesion
References
1. Berger MS, Wilson CB. Epidermoid cysts of the posterior fossa. J Neurosurg 1985;
62:214-219.
Figure 5-6-4
Imaging of the Orbit: The Globe and Conal Lesions 1088 Neuroradiology
Globe [Figure 5-6-5] Figure 5-6-5
• Retina
➢ Neural sensory inner layer (photoreceptors)
➢ Retinal pigmented epithelium (RPE) outer layer
➢ Ora serrata
• Uvea: choroid (vascular); Bruch’s membrane
➢ Iris
➢ Ciliary body
• Sclera: fibrous layer; cornea anteriorly
• Tenon’s capsule (bulbar fascia)
• Normal: only one “layer” seen
Figure 5-6-8
Neuroradiology 1089 Imaging of the Orbit: The Globe and Conal Lesions
Cranial Nerves III, IV, VI Figure 5-6-9
• Motor control of EOMs
• Cranial Nerve III: all EOMs except
➢ Lateral rectus: Cranial Nerve VI
➢ Superior oblique: Cranial Nerve IV
➢ “LR6SO4”
• Sensory control: V1 primarily, V2 (infraorbital region)
Leukocoria
• Retinoblastoma
• Persistent hyperplastic primary vitreous (PHPV)
• Retinopathy of prematurity (ROP)
• Congenital cataract Choroidal detachment, with typical U-
• Coats’ disease shape created by anchor points at
• Toxocariasis ciliary body and vessels away from
• Total retinal detachment the optic disk
Mafee, in Som and Curtin, Head and Neck Imaging, 4th ed., Mosby, 2003
Retinoblastoma – Pathology
• Neuroectodermal origin: primitive embryonal retinal cells
(retinoblasts)
• Rosettes: Flexner-Wintersteiner or Homer-Wright type
• Highly malignant: necrosis, mitotic figures
• Calcification
Kyritsis et al, Nature 1984; 307:471-473
Retinoblastoma - Imaging [Figure 5-6-12]
• CT: imaging study of choice Retinoblastoma with characteristic
➢ Calcification: >90% of cases calcification on CT
❖ Child < 3 y/o: highly suggestive for diagnosis
• Tri- / tetralateral retinoblastoma with pineal and/or suprasellar masses
• MR: not as specific as CT
➢ Hyperintense on T1WI and PD
➢ Hypointense on T2WI
➢ May miss lesions as large as 4mm
➢ Better for intracranial extension, extraocular spread
Char, Ophthalmology 1984; 91:1347-1350; Mafee, Radiol Clin North Am 1987;
25:667-681; Mafee et al, Ophthalmology 1989; 96:965-976
Toxocariasis
• Chorioretinitis: Toxocara canis (nematode)
• Granuloma: eosinophilic abscess Persistent hyperplastic primary vitreous (PHPV)
• CT: homogeneous intravitreal density with hyaloid canal
➢ Retinal detachment, organized vitreous,
inflammatory exudate
➢ Irregular thickening of uveoscleral coat
• MR: subretinal exudate, variably hyperintense on all sequences
Margo et al, Pediatr Ophthalmol Strabismus 1983; 20: 180-184; Wilder, Trans Am
Acad Ophthalmol Otolaryngol 1950; 55:99-104 Figure 5-6-14
Uveal Melanoma
• Uvea
➢ Choroid, ciliary body, iris
➢ Derived from mesoderm & neuroectoderm
➢ Most highly vascular part of eyeball
• Melanoma: most common neoplasm of choroid
• Whites (15:1)
➢ Incidence increases with age
• Arises from choroid, elevates and may rupture Bruch’s
membrane (mushroom shape)
Yanoff and Fine, Ocular Pathology, Harper and Row, 1975; Mafee,
Radiol Clin North Am 1998; 36:1083-1099
Gross photograph of Coats Disease
Uveal Melanoma [Figure 5-6-15]
• Metastasis: liver > lung > bone > kidney > brain
• Diagnosis usually made by ophthalmoscopy or US
• CT: elevated, hyperdense, sharply marginated (usually) solid mass
• MR
➢ Hyperintense on T1WI and PDW
➢ Hypointense on T2WI
• Moderate enhancement
Duffin et al, Arch Ophthalmol 1981; 99:1827-1830; Enochs et al, Radiology 1997; Figure 5-6-15
204:417-423; Mafee in Som
and Curtin, Head and Neck
Imaging, 4th ed., Mosby,
2003
Uveal melanoma
Figure 5-6-17
Figure 5-6-18
Blow-out fracture
Neuroradiology 1091
1093 Imaging of the Orbit: The Globe and Conal Lesions
Conal Lesions
• Graves
• Pseudotumor
• Others
➢ Lymphoproliferative disease
➢ Metastasis: 7%, breast carcinoma, nodular
➢ Arteriovenous fistula or vascular congestion
➢ Acromegaly
➢ Amyloid
➢ Cysticercosis / Trichinosis
Graves Disease
• Most (up to 80%) patients are or will be hyperthyroid
➢ Euthyroid (10%)
• Family history: 30%
• Range: 15–86 years old (peak: 30–50)
• Females much more common (4:1)
• Males, patients > 50y/o: more severe disease
Kendler et al, Arch Ophthalmol 1993; 111:197-201
Graves Disease
• Acute phase
➢ Inflammatory reaction: congestion, hypertrophy, fibrosis of Graves Disease
orbital fat / muscles
➢ Mucopolysaccharides accumulate in EOMs Figure 5-6-20
• Chronic phase: exophthalmos (34%–93%)
➢ Fibrosis
➢ Restrictive myopathy
➢ Diplopia
Rubin and Sadun in Yanoff and Duker, Ophthalmology, Mosby, 1999
Pseudotumor: EOM
• Tendons involved (unlike Graves disease)
• Ragged “fluffy” muscle border
• Inward bowing of muscle contour at globe insertion
• “Dirty” retrobulbar fat
• May extend intracranially (apical orbital inflammation) or onto
optic nerve (ON) sheath (perineuritis)
• Bone destruction rare
Pseudotumor with tendinous
Trokel and Hilal, Am J Ophthalmol 1979; 87:503-512; involvement and rapid response to
Flanders et al, J Comput Assist Tomogr 1989; 13:40-47 steroid therapy on follow-up
Neuroradiology 1093
1095 Imaging of the Orbit: The Globe and Conal Lesions
References
1. Abramson DH, Ellsworth RM, Kitchin FD, Tung G. Second nonocular tumors in retinoblastoma survivors. Are
they radiation-induced? Ophthalmology 1984; 91:1351-1355.
2. Abramson DH, Ellsworth RM, Tretter P, Javitt J, Kitchin FD. Treatment of bilateral groups I through III
retinoblastoma with bilateral radiation. Arch Ophthalmol 1981; 99:1761-1762.
3. Blodi FC, Gas JD. Inflammatory pseudotumour of the orbit. Br J Ophthalmol 1968; 52:79-93.
4. Char DH, Hedges TR, 3rd, Norman D. Retinoblastoma. CT diagnosis. Ophthalmology 1984; 91:1347-1350.
5. Coats G, Lond R. Forms of retinal diseases with massive exudation. Ophthalmol Hosp Rep 1908; 17:440-525.
6. Duffin RM, Straatsma BR, Foos RY, Kerman BM. Small malignant melanoma of the choroid with extraocular
extension. Arch Ophthalmol 1981; 99:1827-1830.
7. Edward DP, Mafee MF, Garcia-Valenzuela E, Weiss RA. Coats' disease and persistent hyperplastic primary
vitreous. Role of MR imaging and CT. Radiol Clin North Am 1998; 36:1119-1131, x.
8. Eller AW, Jabbour NM, Hirose T, Schepens CL. Retinopathy of prematurity. The association of a persistent hyaloid
artery. Ophthalmology 1987; 94:444-448.
9. Ellsworth RM. The practical management of retinoblastoma. Trans Am Ophthalmol Soc 1969; 67:462-534.
10. Enochs WS, Petherick P, Bogdanova A, Mohr U, Weissleder R. Paramagnetic metal scavenging by melanin: MR
imaging. Radiology 1997; 204:417-423.
11. Flanders AE, Mafee MF, Rao VM, Choi KH. CT characteristics of orbital pseudotumors and other orbital
inflammatory processes. J Comput Assist Tomogr 1989; 13:40-47.
12. Hunt WE, Meagher JN, Lefever HE, Zeman W. Painful opthalmoplegia. Its relation to indolent inflammation of the
carvernous sinus. Neurology 1961; 11:56-62.
13. Jakobiec FA, Tso MO, Zimmerman LE, Danis P. Retinoblastoma and intracranial malignancy. Cancer 1977;
39:2048-2058.
14. Kaufman LM, Mafee MF, Song CD. Retinoblastoma and simulating lesions. Role of CT, MR imaging and use of
Gd-DTPA contrast enhancement. Radiol Clin North Am 1998; 36:1101-1117.
15. Kendler DL, Lippa J, Rootman J. The initial clinical characteristics of Graves' orbitopathy vary with age and sex.
Arch Ophthalmol 1993; 111:197-201.
16. Kodilinye HC. Retinoblastoma in Nigeria: problems of treatment. Am J Ophthalmol 1967; 63:469-481.
17. Kyritsis AP, Tsokos M, Triche TJ, Chader GJ. Retinoblastoma--origin from a primitive neuroectodermal cell?
Nature 1984; 307:471-473.
18. Mafee MF, Goldberg MF, Cohen SB, et al. Magnetic resonance imaging versus computed tomography of
leukocoric eyes and use of in vitro proton magnetic resonance spectroscopy of retinoblastoma. Ophthalmology
1989; 96:965-975; discussion 975-966.
19. Mafee MF, Goldberg MF, Greenwald MJ, Schulman J, Malmed A, Flanders AE. Retinoblastoma and simulating
lesions: role of CT and MR imaging. Radiol Clin North Am 1987; 25:667-682.
20. Mafee MF, Goldberg MF. Persistent hyperplastic primary vitreous (PHPV): role of computed tomography and
magnetic resonance. Radiol Clin North Am 1987; 25:683-692.
21. Mafee MF, Peyman GA. Retinal and choroidal detachments: role of magnetic resonance imaging and computed
tomography. Radiol Clin North Am 1987; 25:487-507.
22. Mafee MF. The eye. In: Som PM, Curtin HD, eds. Head and neck imaging. 4th ed. St. Louis: Mosby–Elsevier
Science; 2003
23. Mafee MF. Uveal melanoma, choroidal hemangioma, and simulating lesions. Role of MR imaging. Radiol Clin
North Am 1998; 36:1083-1099
24. Margo CE, Katz NN, Wertz FD, Dorwart RH. Sclerosing endophthalmitis in children: computed tomography with
histopathologic correlation. J Pediatr Ophthalmol Strabismus 1983;20:180-184
25. Pendergrass TW, Davis S. Incidence of retinoblastoma in the United States. Arch Ophthalmol 1980; 98:1204-1210.
26. Reese AB. Telangiectasis of the retina and Coats' disease. Am J Ophthalmol 1956; 42:1-8.
27. Rubin RM, Sadun AA. Ocular myopathies. In: Yanoff M, Duker JS, eds. Ophthalmology. St. Louis: Mosby; 1999.
28. Tolosa E. Periarteritic lesions of the carotid siphon with the clinical features of a carotid infraclinoidal aneurysm. J
Neurol Neurosurg Psychiatry 1954; 17:300-302.
29. Trokel SL, Hilal SK. Recognition and differential diagnosis of enlarged extraocular muscles in computed
tomography. Am J Ophthalmol 1979; 87:503-512.
30. Weber AL, Romo LV, Sabates NR. Pseudotumor of the orbit. Clinical, pathologic, and radiologic evaluation.
Radiol Clin North Am 1999; 37:151-168, xi.
31. Wilder HC. Nematode endophthalmitis. Trans Am Acad Ophthalmol Otolaryngol 1950:99-109.
32. Yanoff K, Fine BS, Ocular Pathology . Hagerstown: Harper & Row, 1975.
Schwannoma
• 1% of all orbital tumors: usually intraconal
➢ Arise from cranial nerves, not optic nerve
➢ Isolated or neurofibromatosis association
• Benign with slow growth
➢ Well-encapsulated
• Painless proptosis
• Compresses or engulfs optic nerve
Carroll et al, Radiol Clin North Am 1999; 37:195-202
Orbital Lymphoma
• Lymphoid tumors: 10%-15% of orbital masses
➢ Lymphoma, pseudolymphoma, lymphoid hyperplasia
• 10% of all lymphomas as primary site
➢ 75% have or will have systemic lymphoma
➢ Lacrimal gland: most common site
➢ EOMs rarely involved
• Non-Hodgkin’s (B-cell): majority
• Proptosis, ptosis, diplopia
• Rubbery firm masses
Valvassori et al, Radiol Clin North Am 1999; 37:135-150; Flanders et
al, Radiol Clin North Am 1997; 25:601-612;
Schwannoma
Figure 5-7-7
Malignant fibrous histiocytoma
Neuroradiology 1097
1099 Imaging of the Orbit: Intraconal and Extraconal Lesions
Arteriovenous Fistula [Figure 5-7-8] Figure 5-7-8
• Usually post-trauma
➢ Spontaneous less common (Ehlers-Danlos, osteogenesis
imperfecta, pseudoxanthoma elasticum)
• Orbital bruit, proptosis, chemosis
• CT/MR: dilated superior ophthalmic vein
• Angiography diagnostic
• Endovascular occlusion: treatment of choice
Tan et al, Radiol Clin North Am 1987; 25:849-861
Carotid-cavernous
Extraconal Lesions fistula with enlarged
• Lymphangioma* superior ophthalmic
• Metastasis* vein. Lateral view from
• Rhabdomyosarcoma* cerebral angiogram
• Dermoid/epidermoid shows abnormal flow
• Paranasal sinus disease through cavernous
➢ Infection sinus, petrosal
➢ Neoplasm sinuses, and superior
*commonly “intercompartmental” ophthalmic vein
Figure 5-7-9
Figure 5-7-10
Rhabdomyosarcoma
• Superior orbit predilection Figure 5-7-12
• Homogeneous mass
• CT: isoattenuated to muscle
➢ Bone destruction common in larger lesions
➢ Necrosis, calcification, hemorrhage uncommon
• T1WI: hypointense
• T2WI: hyperintense
• Moderate to marked enhancement
Mafee et al, Radiol Clin North Am 1998; 36:1215-1227
Neuroradiology 1099
1101 Imaging of the Orbit: Intraconal and Extraconal Lesions
Figure 5-7-13 Figure 5-7-14
Fungal sinusitis
Figure 5-7-18
Neuroradiology 1101
1103 Imaging of the Orbit: Intraconal and Extraconal Lesions
Summary
• Retinoblastoma: most common intraocular malignancy of childhood
• Uveal melanoma: most common malignancy of the globe in adults
• Uveal metastasis: frequently bilateral
• Most common diseases of the orbit
➢ 1. Graves: no tendon involvement
➢ 2. Lymphoma
➢ 3. Pseudotumor: involves tendon
• Intraconal lesions
➢ Optic nerve tumors
❖ Glioma
❖ Nerve sheath meningioma
➢ Cavernous hemangioma
➢ Nerve sheath tumors
➢ Lymphoma
➢ Fibrous histiocytoma
➢ Varix
➢ Carotid-cavernous fistula
• Extraconal lesions
➢ Lymphangioma
➢ Metastases: 10% of orbit masses
➢ Rhabdomyosarcoma
➢ Dermoid
➢ Sinus disease
• Lacrimal gland lesions
➢ “The 50% gland”
➢ 50% inflammatory/lymphoproliferative
➢ 50% neoplasms
❖ 50% benign, 50% malignant
• Lacrimal sac lesions: most are malignant
References
1. Azar-Kia B, Naheedy MH, Elias DA, Mafee MF, Fine M. Optic nerve tumors: role of magnetic resonance imaging
and computed tomography. Radiol Clin North Am 1987; 25:561-581.
2. Bilaniuk LT. Orbital vascular lesions. Role of imaging. Radiol Clin North Am 1999; 37:169-183, xi.
3. Carroll GS, Haik BG, Fleming JC, Weiss RA, Mafee MF. Peripheral nerve tumors of the orbit. Radiol Clin North
Am 1999; 37:195-202, xi-xii.
4. Chandler JR, Langenbrunner DJ, Stevens ER. The pathogenesis of orbital complications in acute sinusitis.
Laryngoscope 1970; 80:1414-1428.
5. Daniels DL, Williams AL, Syvertsen A, Gager WE, Harris GJ. CT recognition of optic nerve sheath meningioma:
abnormal sheath visualization. AJNR Am J Neuroradiol 1982; 3:181-183.
6. Eustis HS, Mafee MF, Walton C, Mondonca J. MR imaging and CT of orbital infections and complications in acute
rhinosinusitis. Radiol Clin North Am 1998; 36:1165-1183, xi.
7. Flanders AE, Espinosa GA, Markiewicz DA, Howell DD. Orbital lymphoma. Role of CT and MRI. Radiol Clin
North Am 1987; 25:601-613.
8. Font RL, Hidayat AA. Fibrous histiocytoma of the orbit. A clinicopathologic study of 150 cases. Hum Pathol 1982;
13:199-209.
9. Haik BG, Saint Louis L, Bierly J, et al. Magnetic resonance imaging in the evaluation of optic nerve gliomas.
Ophthalmology 1987; 94:709-717.
10. Jakobiec FA, Yeo JH, Trokel SL, et al. Combined clinical and computed tomographic diagnosis of primary lacrimal
fossa lesions. Am J Ophthalmol 1982; 94:785-807.
11. Kaufman LM, Villablanca JP, Mafee MF. Diagnostic imaging of cystic lesions in the child's orbit. Radiol Clin
North Am 1998; 36:1149-1163, xi.
12. Mafee MF, Haik BG. Lacrimal gland and fossa lesions: role of computed tomography. Radiol Clin North Am 1987;
25:767-779.
13. Mafee MF, Pai E, Philip B. Rhabdomyosarcoma of the orbit. Evaluation with MR imaging and CT. Radiol Clin
North Am 1998; 36:1215-1227, xii.
14. Mafee MF, Putterman A, Valvassori GE, Campos M, Capek V. Orbital space-occupying lesions: role of computed
tomography and magnetic resonance imaging. An analysis of 145 cases. Radiol Clin North Am 1987; 25:529-559.
Neuroradiology 1103
1105 Imaging of the Orbit: Intraconal and Extraconal Lesions
Patterns of Location: Infratentorial and
Supratentorial
James G. Smirniotopoulos, MD
PATTERN ANALYSIS
• Basic Approach
➢ Where is the lesion ?
❖ Intraaxial
❖ Extraaxial
❖ Intraventricular
➢ Where is the lesion ?
❖ Supratentorial
❖ Infratentorial
➢ How old is the patient ?
❖ Child
❖ Adult
➢ What about Sex ?
INTRA-AXIAL
• Cortex
• Gray-white Junction
• Deep White Matter
• Deep Gray Matter
• Glioma
• Medulloblastoma
• Hemangioblastoma
• Metastases
• Infarct/hematoma
• AVM/congenital
• Abscess/inflammation
EXTRA-AXIAL LESIONS
• Subarachnoid
• Subdural
• Epidural
• Calvarium (Skull Base)
• Subgaleal
• Scalp (Soft-tissues)
• Meningioma
• Pituitary adenoma
• Craniopharyngioma
• Schwannoma
• Chordoma
• Dermoid/epidermoid, cyst, lipoma
• Hematoma, metastasis, infection
BASIC APPROACH
CLASSIC LOCATIONS
• Foramen magnum
• Cerebellopontine angle (CPA)
• Fourth ventricle/Cerebellum
• Sella/parasellar/suprasellar
• Basal ganglia/Third ventricle
• Lateral ventricle/Pineal region
• Deep hemispheric/periventricular
• Cortical and subcortical
• Convexity Extraaxial
Patterns of Location: Infratentorial and Supratentorial 1104
1106 Neuroradiology
Cranial Nerves Figure 5-8-1
• Olfactory (I)
• Optic (II)
• Oculomotor (III)
• Trochlear (IV)
• Trigeminal (V)
• Abducens (V)
When looking into the IAC
• Facial (VII)
(internal auditory canal) notice
• Vestibulocochlear (VIII)
that
7 is UP and Coke (cochlear) is
Internal Auditory Canal
DOWN
[Figures 5-8-1 and 5-8-2]
• S – Schwannoma (8th >> > 5th)
• A – aneurysm, arachnoid cyst
• M – meningioma, mets
• E – epidermoid, ependymoma, CPP
Vestibular Schwannoma
Figure 5-8-3
[left] T2W image shows CSF, normal nerve, and round mass.
[right] T1WGd image shows enhancement of mass. The
normal 7th and 8th nerves do NOT enhance in this location
Neuroradiology 1105
1107 Patterns of Location: Infratentorial and Supratentorial
Young Schwannoma – Old Schwannoma [Figure 5-8-4] Figure 5-8-4
• Benign Cystic Degeneration
Vestibular Schwannoma
• IAC origin
➢ IAC involved
➢ IAC Enlarged (70%)
• Spherical Mass
➢ encapsulated
• Heterogeneous if large
➢ > 20 mm
• Enhance “always”
Figure 5-8-6
Hyperostosis
Meningioma
Figure 5-8-7
Tentorial Meningioma
Central Masses [Figure 5-8-10] Schematic of central posterior fossa mass: Did it
begin in the 4th ventricle, in the medullary velum,
CHILD - CEREBELLAR/IVth or in the cerebellum?
• Medulloblastoma (PNET)
• Astrocytoma (usu. Pilocytic) Figure 5-8-10
• Ependymoma
• Post fossa cysts
ADULT - CEREBELLAR/IVth
• Metastasis
• Hemangioblastoma
• Hemorrhage, infarct
• Glioma
➢ Ependymoma
➢ Astrocytoma
• Abscess
Neuroradiology 1107
1109 Patterns of Location: Infratentorial and Supratentorial
Medulloblastoma [Figures 5-8-11 and 5-8-12] Figure 5-8-11
• ‘Homogeneous’
➢ finely irregular
• Cyst and Hemorrhage are uncommon
<10%
• Hyperdense on NCT
➢ up to 75%
➢ densely cellular
➢ sm. Round blue-cells
• Center is behind 4th vent
• Rounder not angular
Pilocytic Astrocytoma
[Figures 5-8-13 to 5-8-16]
• Cyst and Mural Nodule
➢ balanced morphology
• Wall may not enhance
• Cyst fluid with protein Medulloblastoma, hyperdense on plain CT
• Nodule low density on CT
➢ may calcify up to 25%
• No increase in vascularity Figure 5-8-12
• WHO Grade 1
• Peak at ~10 yrs
Figure 5-8-13
Figure 5-8-18
Figure 5-8-19
Neuroradiology 1109
1111 Patterns of Location: Infratentorial and Supratentorial
Expansile Mass in Brainstem Figure 5-8-20
[Figure 5-8-20]
Figure 5-8-21
Figure 5-8-22
Ependymoma.
Copyright 2005
Ependymoma
CLASSIC LOCATIONS
• Foramen magnum
• Cerebellopontine angle
• Fourth ventricle/Cerebellum
• Sella/parasellar/suprasellar
• Basal ganglia/Third ventricle
• Lateral ventricle/Pineal region
• Deep hemispheric/periventricular
• Cortical and subcortical
• Convexity Extraaxial
Elevated Prolactin
• Microadenoma
➢ < 10mm diameter
➢ Entirely intrasellar
• Macroadenoma
➢ > 10 mm
• Stalk Effect
➢ Blocks Prolactin Inhibitory Factor
➢ 40-150 ng PRL vs. 28 for nl.
• Hypothyroidism
➢ “Cross Reaction” from TSH
• Exogenous
• Pharmacologic
Neuroradiology 1111
1113 Patterns of Location: Infratentorial and Supratentorial
Macroadenoma [Figure 5-8-28] Figure 5-8-28
Craniopharyngioma – 2 Types
• Child
➢ Adam Ant – inomatous
❖ enamel organ of tooth
➢ Commonly Cystic
➢ ‘Machine Oil’
➢ Commonly Calcified
➢ Adherent to brain
❖ pilocytic astrogliosis
• Adult
➢ Squamous and Papillary
➢ Commonly Solid
➢ Calcification less common Pituitary macroadenoma with hyperintensity from old
➢ Easier to resect hemorrhage
Figure 5-8-29
Figure 5-8-30
Craniopharyngioma,
expansile remodeling of sella
turcica
Craniopharyngioma
Figure 5-8-33
Figure 5-8-34
SELLA/PARASELLAR
• Differential Features: Figure 5-8-35
➢ ADULT – Pituitary adenoma
➢ CHILD – Craniopharyngioma or
Glioma (hypothalamus or optic ) >
EG, etc
➢ SELLA NORMAL – NOT pituitary
➢ Ca++ – Craniopharyngioma, but...
➢ HYPEROSTOSIS – Meningioma (
exp. “blistering” )
➢ CLIVUS – Chordoma, mets, NP Ca
➢ Remember – rule out vascular
lesions (aneurysms)
Neuroradiology 1113
1115 Patterns of Location: Infratentorial and Supratentorial
• Lateral ventricle/Pineal region Figure 5-8-36
• Deep hemispheric/periventricular
• Cortical and subcortical
• Convexity Extraaxial
Colloid cyst
Differential Diagnosis – 3rd ventricle.
Copyright 2005
Figure 5-8-39
Figure 5-8-40
Aqueduct Obstruction
Non-traumatic hemorrhage
[Figures 5-8-43 and 5-8-44]
Non-traumatic hemorrhage in the right thalamus Non-traumatic hemorrhage in the right thalamus.
Copyright 2006
Neuroradiology 1115
1117 Patterns of Location: Infratentorial and Supratentorial
Hypertensive Hemorrhage Figure 5-8-45
ARTERIOLOSCLEROSIS
CLASSIC LOCATIONS
• Foramen magnum Figure 5-8-49
• Cerebellopontine angle
• Fourth ventricle/Cerebellum
• Sella/parasellar/suprasellar
• Basal ganglia/Third ventricle
• Lateral ventricle
• Pineal Region
• Deep hemispheric/periventricular
• Cortical and subcortical
• Convexity Extraaxial
Patterns in Neuroradiology
• Cerebello-Pontine Angle
• Fourth Ventricle/Cerebellum
• Sella/Parasellar
• Basal Ganglia/Third Ventricle
• Lateral Ventricle
• Pineal Region
• Deep Hemispheric/Periventricular
• Cortical/Subcortical
• Convexity Extraaxial
Intraventricular Neoplasms
• Ependymoma (and subependymoma)
• Choroid plexus papilloma
• Subependymal giant cell astro.
Toxoplasmosis
• Meningioma
• Colloid cyst (3rd)
• Medulloblastoma (4th)
• Dermoid/epidermoid
• Central neurocytoma
• Mets, lymphoma, Germ Cell
Neuroradiology 1117
1119 Patterns of Location: Infratentorial and Supratentorial
Lateral Ventricle @ f. Monro Figure 5-8-50
• Lateral Ventricle/caudate
➢ Subependymal Giant Cell Astro.
❖ TUBEROUS SCLEROSIS, Enhances &
Ca++
➢ Subependymoma
❖ Variant of Ependymoma
❖ No Ca++, no enhancement
➢ Central Neurocytoma
❖ Septum pellucidum
➢ Cyst/Cavum septum pellucidum
➢ Huntington Chorea
❖ Atrophy
Trigone or Atrium
CSF Overproduction?
Central Neurocytoma
• Central
➢ Often centered on septum pellucidum
➢ Extension into both lateral ventricles
➢ Hyperdense on CT
➢ Gray matter on MR
➢ Spontaneous Bleed
➢ Calcifications
CLASSIC LOCATIONS
• Foramen magnum
• Cerebellopontine angle
• Fourth ventricle/Cerebellum
• Sella/parasellar/suprasellar
• Basal ganglia/Third ventricle
Pineal Cyst
CLASSIC LOCATIONS
• Foramen magnum
• Cerebellopontine angle
• Fourth ventricle/Cerebellum Pineal cyst
• Sella/parasellar/suprasellar
• Basal ganglia/Third ventricle
• Lateral ventricle/Pineal region
• Deep hemispheric/periventricular
• Cortical and subcortical
• Convexity Extraaxial
Figure 5-8-54
Figure 5-8-55
Figure 5-8-57
PCNSL: Immunocompetent
Cytomegalovirus – note the thin rim of abnormal
RIM PHOMA enhancement cause by ependymitis
(Courtesy Vince Mathews, M.D.)
CMV [Figure 5-8-57]
Time is Brain !
• Therapeutic Windows:
• 3 hours for IV tPA
• 6 hours for IA thrombolysis
• 9 hours for IV ‘Bat Spit’?
➢ an enzyme known as
desmoteplase or DSPA
➢ isolated from the saliva of
Desmodus rotundus
➢ vampire bat, Central and
South America, 1oz
NOTE: Clock starts with last time
patient was observed ‘normal’. If
you wake with a stroke, that PCA Infarct Lights up like a lightbulb
might be bedtime … unless you on MRI DWI
get up at night
Neuroradiology 1121
1123 Patterns of Location: Infratentorial and Supratentorial
CVA : Progression of CT findings Figure 5-8-62
Old Infarct
• Wallerian Degeneration
CLASSIC LOCATIONS
• Foramen magnum
• Cerebellopontine angle
• Fourth ventricle/Cerebellum
• Sella/parasellar/suprasellar
• Basal ganglia/Third ventricle
• Lateral ventricle/Pineal region
• Deep hemispheric/periventricular DNET – Usually a cortical lesion, often wedge-
• Cortical and subcortical shaped
• Convexity Extraaxial
Epidural Metastasis
Schematic of epidural (left) and subdural (right)
localization.
Subdural = Epi-arachnoid [Figure 5-8-66] Copyright 2006
Subdural Metastasis
Neuroradiology 1123
1125 Patterns of Location: Infratentorial and Supratentorial
Patterns of Enhancement
James G. Smirniotopoulos, MD
Figure 5-9-1
Why Give Contrast?
Contrast Enhancement
• Vascularity
➢ Blood Volume (rCBV)
Perfusion MTT
➢ Blood Flow (rCBF)
➢ Arteries & veins > capillary
• Permeability Blood
➢ Capillary (leakage) Brain
Barrier
Breakdown
Figure 5-9-5
Neuroradiology 1125
1127 Patterns of Enhancement
The Berlin Wall and the BBB [Figure 5-9-8] Figure 5-9-8
• Who built the Berlin Wall?
➢ The East Germans
• Why?
➢ To keep out the West Germans
• But … the barrier works in BOTH directions
• Some things are kept out
➢ Drugs, Contrast material
• Some things are kept in:
➢ Hemosiderin
➢ Vasogenic Edema
Physiologic Why?
• Why do we have a BBB?
➢ To protect the brain
➢ To create the ionic environment for nerve conduction
• Why do we have tastebuds?
➢ So that we eat things good for us
❖ Salt
❖ Sweet
❖ Sour
❖ Umami (MSG)
❖ Bitter
Normal Enhancement
• Choroid Plexus
• Pineal
• Pituitary Stalk
• Pituitary Gland (anterior and posterior)
➢ Hypophyseal Portal System
• Cavernous sinus and dural reflections
• Nasal turbinates
• Sinonasal mucosa
• Extracranial muscles and mucosa
Nasal Cycle
• Vasocongestion ~/~ vasoconstriction
• 6 – 8 hour cycle alternation
• Humidify and warm the air
• Secrete mucus (1 – 2 liters/day)
• Chronic vasocongestion would cause submucosal edema
• Breathe mostly through the vasoconstricted side (~ 75%-85%)
• Yogi’s can control which nostril
• So can Tom Cruise (Minority Report)
Contrast Enhancement
• Morphologic Patterns
➢ Homogeneous (solid)
➢ Heterogeneous (non-uniform)
➢ Ring (unilocular/multilocular)
➢ Serpentine ("Gyriform“)
❖ Serpiginous?
Serpiginous
• “A creeping skin eruption.”
Contrast Enhancement
• Location
➢ SUPERFICIAL (CORTICAL/GYRAL)
➢ GREY-WHITE JUNCTION
➢ DEEP WHITE MATTER
➢ PERIVENTRICULAR, EPENDYMAL
Neuroradiology 1127
1129 Patterns of Enhancement
Contrast Enhancement Figure 5-9-11
• Cortical/Gyriform
➢ Cerebral Ischemia / Infarction
➢ CSF or sub-pial spread
➢ Meningo-encephalitis
➢ S.A.H.
➢ Leptomeningeal Malformation (SW)
➢ Meningioangiomatosis (NF2)
Pachymeningeal Enhancement
[Figure 5-9-14]
• Intracranial Hypotension
Figure 5-9-14
Pachymeningeal
enhancement
(Courtesy Laszlo Mechtler,
DNI)
H&P
• Pt is a 25 yo woman, PMHx of BCP, presenting w/
acute mental status changes, afebrile
Actually…
• Pt is a 34 yo marine stationed at Guantanamo Bay
Cuba, presenting w/ acute mental status changes,
febrile
Figure 5-9-18
Herpes encephalitis
Dural Tail
• Curvilinear enhancement Meningioma - Dural Tail
• AKA “dural flair”
• First reported w/meningioma
• First reported to be neoplastic invasion
• What is it REALLY?
➢ Thickening of the dura
➢ Vasocongestion of the dura
➢ Edema of the dura
Neuroradiology 1129
1131 Patterns of Enhancement
Contrast Enhancement [Figure 5-9-19] Figure 5-9-19
• Ring Lesion
➢ Circumferential or peripheral/marginal
enhancement, surrounding a central non-
enhancing region.
➢ In turn, this is often surrounded by a large area
of “edema”.
➢ May be unilocular or multilocular.
Contrast Enhancement
• Contrast leaks into interstitium from vessels without BBB
• Remains localized within millimeters of where it leaks out
• Not “simple diffusion” but rather “BULK FLOW” at a very slow rate
• (Glacier Not River)
Contrast Enhancement
• Ring Lesions Differential
➢ M – Metastasis, MS
➢ A – Abscess (Also Cerebritis)
➢ G – Glioblastoma, Granuloma
➢ I – Infarct (Esp. Basal Ganglia)
➢ C – Contusion (Rare)
➢ A – AIDS (Toxo, Etc.)
➢ L – Lymphoma (in Aids)
➢ D – Demyelination (Active)
➢ R – Resolving Hematoma
Radiation Change (Necrosis)
Contrast Enhancement
• Ring Lesion Features For Infection
➢ ORGANIZED ABSCESS
➢ thin and uniform wall (3-7mm.)
➢ smooth inner margin does not “fill in” on CT, MR, even after time delay
imaging
➢ CEREBRITIS (infection w/o organization):
➢ variable wall (may be smooth) smooth/variable inner margin
➢ often has “fill-in” on DDD
➢ (w/o fluid level)
Figure 5-9-22
Cerebral abscess in thalamus
Figure 5-9-23
Figure 5-9-24
Abscess
Neuroradiology 1131
1133 Patterns of Enhancement
Glioblastoma Multiforme Figure 5-9-25
Tumefactive Demyelination
[Figure 5-9-26]
References
1. Ahmadi J, Hinton DR, Segall HD, Couldwell WT. Surgical implications of magnetic resonance-enhanced dura.
Neurosurgery. 1994 Sep;35(3):370-7;discussion 377.
2. Aoki S, Sasaki Y, Machida T, Tanioka H. Contrast-enhanced MR images in patients with meningioma: importance
of enhancement of the dura adjacent to the tumor. AJNR Am J Neuroradiol. 1990 Sep-Oct;11(5):935-8.
3. Asari S, Yabuno N, Ohmoto T. Magnetic resonance characteristics of meningiomas arising from the falcotentorial
junction. Comput Med Imaging Graph. 1994 May-Jun;18(3):181-5.
4. Ekinci G, Akpinar IN, Baltacioglu F, et al. Early-postoperative magnetic resonance imaging in glial tumors:
prediction of tumor regrowth and recurrence. Eur J Radiol 2003; 45:99-107.
5. Goldsher D, Litt AW, Pinto RS, Bannon KR, Kricheff II. Dural "tail" associated with meningiomas on Gd-DTPA-
enhanced MR images: characteristics, differential diagnostic value, and possible implications for treatment.
Radiology. 1990 Aug;176(2):447-50. .
6. Helie O, Soulie D, Sarrazin JL, Derosier C, Cordoliani YS, Cosnard G. [Magnetic resonance imaging and
meningiomas of the posterior cerebral fossa. 31 cases] J Neuroradiol. 1995 Dec;22(4):252-70. French.
7. Henegar MM, Moran CJ, Silbergeld DL. Early postoperative magnetic resonance imaging following nonneoplastic
cortical resection. J Neurosurg 1996; 84:174-179.
8. Hutzelmann A, Palmie S, Buhl R, Freund M, Heller M. Dural invasion of meningiomas adjacent to the tumor
margin on Gd-DTPA-enhanced MR images: histopathologic correlation. Eur Radiol. 1998;8(5):746-8.
9. Hutzelmann A, Palmie S, Freund M, Buhl R, Heller M. [Dura thickening adjacent to intracranial, para-dural space-
occupying lesions in MRI. Histologic correlation] Aktuelle Radiol. 1997 Nov;7(6):305-8. German. PMID:
9467021
10. Hutzelmann A, Palmie S, Zimmer C, Benz T, Leweke F, Freund M. [The meningeal sign: a new appraisal] Rofo.
1996 Apr;164(4):314-7. German.
11. Ildan F, Tuna M, Gocer AP, Boyar B, Bagdatoglu H, Sen O, Haciyakupoglu S, Burgut HR. Correlation of the
relationships of brain-tumor interfaces, magnetic resonance imaging, and angiographic findings to predict cleavage
of meningiomas. J Neurosurg. 1999 Sep;91(3):384-90.
12. Kaufman BA, Moran CJ, Park TS. Computer tomographic scanning within 24 hours of craniotomy for a tumor in
children. Pediatr Neurosurg 1995; 22:74-80.
13. Kawahara Y, Niiro M, Yokoyama S, Kuratsu J. Dural congestion accompanying meningioma invasion into vessels:
the dural tail sign. Neuroradiology. 2001 Jun;43(6):462-5.
14. Lai PH, Ho JT, Chen WL, et al. Brain abscess and necrotic brain tumor: discrimination with proton MR
spectroscopy and diffusion-weighted imaging. AJNR Am J Neuroradiol 2002; 23:1369-1377.
Neuroradiology 1133
1135 Patterns of Enhancement
15. Martin-Duverneuil N, Sola-Martinez MT, Miaux Y, et al. Contrast enhancement of the facial nerve on MRI:
normal or pathological? Neuroradiology 1997; 39:207-212.
16. Masdeau JC, Moreira J, Trasi S, Visintainer P, Cavaliere R, Grundman M: The open ring. A new imaging sign in
demyelinating disease. J.Neuroimaging 1996; 6(2):104-107.
17. Masdeu JC, Quinto C, Olivera C, Tenner M, Leslie D, Visintainer P: Open-ring imaging sign: highly specific for
atypical brain demyelination. Neurology 2000; 54(7):1427-1433.
18. Nagele T, Petersen D, Klose U, Grodd W, Opitz H, Voigt K. The "dural tail" adjacent to meningiomas studied by
dynamic contrast-enhanced MRI: a comparison with histopathology. Neuroradiology. 1994 May;36(4):303-7.
19. Nakasu S, Nakasu Y, Matsumura K, Matsuda M, Handa J. Interface between the meningioma and the brain on
magnetic resonance imaging. Surg Neurol. 1990 Feb;33(2):105-16.
20. Nakau H, Miyazawa T, Tamai S, Tsuchiya K, Shima K, Shirotani T, Chigasaki H. Pathologic significance of
meningeal enhancement ("flare sign") of meningiomas on MRI. Surg Neurol. 1997 Dec;48(6):584-90; discussion
590-1.
21. Quekel LG, Versteege CW. The "dural tail sign" in MRI of spinal meningiomas. J Comput Assist Tomogr. 1995
Nov-Dec;19(6):890-2.
22. Sakai K, Tada T, Fukasaku K, Kyoshima K, Kobayashi S. Histological examination of the gadolinium-enhanced
dura mater around meningiomas on magnetic resonance imaging. Neurol Med Chir (Tokyo). 1993 Jul;33(7):429-
33.
23. Sato M, Matsumoto M, Kodama N. Meningeal enhancement surrounding meningiomas on Gd-DTPA MRI.
Fukushima J Med Sci. 1998 Jun;44(1):1-11.
24. Sato N, Bronen RA, Sze G, et al. Postoperative changes in the brain: MR imaging findings in patients without
neoplasms. Radiology 1997; 204:839-846.
25. Sekiya T, Manabe H, Iwabuchi T, Narita T. [The dura mater adjacent to the attachment of meningiomas: its
enhanced MR imaging and histological findings] No Shinkei Geka. 1992 Oct;20(10):1063-8. Japanese.
26. Takeguchi T, Miki H, Shimizu T, Kikuchi K, Mochizuki T, Ohue S, Ohnishi T. The dural tail of intracranial
meningiomas on fluid-attenuated inversion-recovery images. Neuroradiology. 2004 Feb;46(2):130-5. Epub 2004
Jan 28.
27. Wilms G, Lammens M, Marchal G, Van Calenbergh F, Plets C, Van Fraeyenhoven L, Baert AL. Thickening of dura
surrounding meningiomas: MR features. J Comput Assist Tomogr. 1989 Sep-Oct;13(5):763-8.
28. Yamaguchi N, Kawase T, Sagoh M, Ohira T, Shiga H, Toya S. Prediction of consistency of meningiomas with
preoperative magnetic resonance imaging. Surg Neurol. 1997 Dec;48(6):579-83.
Neuroradiology 1135
1137 The WHO 2000 Brain Tumor Classification
Pathologic – Radiologic Correlation
Pathology Radiology
Cellularity T2 SI, DWI & ADC
Endothelial proliferation Enhancement, PWI, and
and Vascularity Permeability Imaging
Necrosis Ring Lesion, MRS, DWI & ADC
Hemorrhage T1 and T2 SI
Labeling Indices MRS, Th 201 and FDG
Infiltration T1 and T2 SI, DTI
WHO Classification
• Defines Histologic Subtypes
• Grades Biologic Potential
• Allows International Cooperation
• Ascending scale of Aggression from 1-4
WHO Correlation
• Low Grade
➢ Long-Term Survival: Possible Cure
➢ Stable History (No Progression): Possible Cure
Normal
Circumscribed vs Diffuse
Pilocytic Astrocytoma
• Cystic Cerebellar Astrocytoma
Juvenile Pilocytic Astrocytoma
(“PA” or “JPA”)
Pilocytic Astrocytoma
• Synonyms: Polar Spongioblastoma, Cystic
Cerebellar Astrocytoma
• Cell of Origin: Astrocyte (bi-polar, hairlike)
• Associations: in ON w/ NF-1
• Incidence: 3%–6% of ALL Cranial, 32% of Child
• Age: 5–15 (Zulch 3–7) Sex: Slight F (11/9) Circumscribed astrocytoma, like pilocytic
• Location: Cerebellum, Chiasm/Hypothal, Optic astrocytoma, have “pushing margins” and are
• Treatment: Surgery, patience often fluid-secreting
• Prognosis: 77% at 5 yrs, 75% at 10 yrs, 75% at 15 yrs
Neuroradiology 1137
1139 The WHO 2000 Brain Tumor Classification
Figure 5-10-5 Figure 5-10-6
Pathology
• Biphasic pattern
➢ dense pilocytic glia
➢ Rosenthal fibers
➢ loose microcystic areas
• No necrosis
• Low grade
• Abnormal capillaries
➢ allow enhancement Pilocytic Astrocytoma
➢ fluid production
WHO Grade I
• Circumscribed Astrocytoma
➢ JPA (Pilocytic)
➢ SGCA (Subependymal Giant Cell)
• Ganglioglioma
• Meningioma
Subependymal Giant Cell Astro [Figure 5-10-10] Subependymal Giant Cell Astrocytoma
Astrocytomas
• “SPECIAL” ASTROCYTOMAS
➢ Circumscribed Growth:
❖ Pilocytic
❖ Subependymal Giant Cell
❖ Pleomorphic Xantho-Astrocytoma
Circumscribed Astrocytoma
Pleomorphic Xanthoastrocytoma
• Rare Variant of Astrocytoma
• Arises from Subpial Astrocytes
• Affects Superficial Cerebral Cortex and Meninges
• Skull erosion (scalloped excavation)
• Temporal > Frontal > Parietal
• WHO Grade 2,3
• 50% progress over time
Pleomorphic Xanthoastrocytoma
• IMAGING:
➢ CT APPEARANCE:
❖ Well-Circumscribed Hypodense or Cystic Mass
❖ Often Isodense Solid Nodule that Intensely Enhances
❖ May Mimic Juvenile Pilocytic Astrocytoma
❖ Calcifications Rare
Pleomorphic Xanthoastrocytoma
• MR APPEARANCE:
➢ Well-Circumscribed Mass of Variable Size
➢ Superficial Cortical Location
➢ T1: Low/Mixed Signal,
➢ T2: High/Mixed Signal
➢ Often with Cystic Component
➢ Solid Portion Intensely Enhances
➢ Adjacent Meninges May Enhance (Tail)
➢ Little or No Mass Effect
Neuroradiology 1139
1141 The WHO 2000 Brain Tumor Classification
Astrocytomas
• “Ordinary” Astrocytoma
➢ Diffuse Infiltration of WM by:
❖ Fibrillary Astrocytes
❖ Protoplasmic Astrocytes
❖ Gemistocytic Astrocytes
❖ WHO 2,3,4 (NOT 1)
❖ KS & Mayo Grades 1–4
KERNOHAN 1 2 3 4
(KS)
ANAPLASIA 0 Min >1/2 Marked
Astrocytoma: Diffuse
(Fibrillary, protoplasmic, etc.)
• “Adult type” or “Hemispheric” Astrocytoma
• Diffusely infiltrate brain, along WM tracts
• Continuum, from low-grade to high-grade
• Genetic Alterations 17 => 9 => 10
• Many Progress in Histology over time, changing
from WHO Gr. 2 => Gr. 3 => Gr. 4 (GBM)
• Imaging tends to correlate with histology, especially
at the ends of spectrum
Benign – Diffuse
• HOMOGENEOUS
➢ NO NECROSIS
➢ NO HEMORRHAGE
➢ INCREASED WATER
❖ DARK and Poorly Demarcated on CT
❖ Dark and Sharp on T1W
❖ BRIGHT and Sharp on T2W PD T2
➢ MICROCYST >>> MACROCYST Gr 2 Fibrillary Astrocytoma
(macrocysts occur in JPA, etc.)
Gr 2 Fibrillary Astrocytoma
[Figures 5-10-14 and 5-10-15]
Figure 5-10-15
T1- T1-
non gad
Gr 2 Fibrillary Astrocytoma – no enhancement
after gadolinium
Neuroradiology 1141
1143 The WHO 2000 Brain Tumor Classification
Gr 2 Astrocytoma: PWI [Figure 5-10-16] Figure 5-10-16
• Reduced perfusion
Figure 5-10-17
T2 T1-gad
Figure 5-10-18
Figure 5-10-19
Gliomatosis Cerebri – a diffuse astrocytoma
infiltrating two or more lobes of the brain
Figure 5-10-20
Gliomatosis Cerebri
Expanded Brain
GBM - Glioblastoma
“Malignant” Astrocytoma:
• Older patient
➢ 40’s and up
➢ exceptions (PNET)
➢ ~ 1/2 arise from previous low grade (2–3)
• Abnormal Vessels (neovascularity)
➢ BBB abnormality
➢ vasogenic edema
➢ contrast enhancement
➢ irregular vessels, shunting, etc.
• HETEROGENEOUS
➢ hemorrhage (old/new)
➢ tumor necrosis
➢ tumor itself
Neuroradiology 1143
1145 The WHO 2000 Brain Tumor Classification
Astrocytoma Gr4: Angiogenesis Figure 5-10-24
Figure 5-10-25
T1-gad T2
Mechanisms of Enhancement
Ultrastructure of BBB
• Neural capillary ABBB or Non-neural
➢ astrocytic feet no astrocytic feet
➢ continuous BM fenestrated BM
➢ tight junctions intercellular gaps
➢ no pinocytosis pinocytosis
GBM - Glioblastoma
Glioblastoma multiforme with pseudopalisading
Pseudopalisading Necrosis [Figure 5-10-27]
necrosis
Schematic of Glioblastoma
multiforme – there are neoplastic
cells infiltrating into the surrounding
white matter
Glioblastoma Multiforme
Neuroradiology 1145
1147 The WHO 2000 Brain Tumor Classification
X-Ray Perfusion Imaging [Figure 5-10-33] Figure 5-10-33
Glioblastoma Multiforme
1. Kadri H,Mawla AA, Murad L: Incidence of childhood brain tumors in Syria (1993-2002) Pediatric Neurosurgery
2005; 41:173-177
2. Levin VA, Leibel SA, Gutin PH. Neoplasms of the central nervous system.
In: DeVita VT Jr, Hellman S, Rosenberg SA, eds. Cancer: Principles & Practice of Oncology. Vol 2. 5th ed.
Philadelphia, Pa: Lippincott-Raven Publishers; 1997:2022-2082.
3. Parizek J, et al: Posterior cranial fossa surgery in 454 children. Childs' Nerv Syst 1998; 14:426-439.
4. Pobereskin LH, Chadduck JB: Incidence of brain tumours in two English counties: a population based study. J
Neurol Neurosurg Psychiatry 2000; 69: 464-471.
Neuroectodermal Tumors
• Astrocytoma
• Circumscribed Ependymoma – Gross Axial section
• Diffuse
• Ependymoma Figure 5-11-2
• Choroid Plexus Tumors
• Oligodendroglioma
• Medulloblastoma (PNET)
• Atypical Rhabdoid Tumor
• Ganglioglioma
• Central Neurocytoma
• Lhermitte-Duclos
• Dysembryoplastic Neuroepithelial Tumor
EPENDYMOMA
• WHO Classification Ependymoma – heterogeneous
➢ Ependymoma (WHO grade II) central mass
❖ Variants: cellular, papillary, clear cell, tanycytic, mixed
➢ Anaplastic ependymoma (WHO gr III) Figure 5-11-3
➢ Myxopapillary ependymoma
➢ Subependymoma
EPENDYMOMAS – Demographics
• 5%–6% of All Intracranial
• 70% occur in Males
• 70% arise in the Fourth Ventricle
• 70% present in Childhood
• 70% of All Intramedullary
• 5 year survival – 50%
Figure 5-11-5
Figure 5-11-6
Ependymoma – Tumor extends into
vallecula of cisterna magna
Figure 5-11-7
Figure 5-11-8
Neuroradiology 1149
1151 Non-Astrocytic Gliomas
Figure 5-11-13 Figure 5-11-14
Figure 5-11-15
CSF Homeostasis
OLIGODENDROGLIOMA
• Cell of origin
➢ Oligodendrocyte
➢ Makes central myelin
➢ 51% - 90% oligos, remainder astrocytes
• 1%–8% of ALL CNS primary
• Adults > Children (8:1)
• Age peak 35 – 45 yrs)
• Supratentorial – 85%
• Slow growth, Long Hx (10 years)
➢ Prognosis better with 1p and 19q mutations
OLIGODENDROGLIOMA – Radiology
• Heterogeneous Hemispheric Mass
➢ Ca++, Cysts – “myxoid change”, Blood products Oligodendroglioma. CT shows very dense
• Extend to Cortex and infiltrate GM calcifications, highly suggestive and characteristic
➢ Gyriform or dot-dash Ca++ of oligodendroglioma
➢ Scalloped erosion inner table
• 2/3 will enhance Figure 5-11-18
➢ +/– anaplasia
• MR +/- special pulse sequences for Ca++ detection
• MR Spectroscopy?
➢ Potential for tumor grade, but not subtype or
genetics
MR - What is it?
Oligo-astrocytoma
• Nothing Specific … Looks like Diffuse Astrocytoma
Oligodendroglioma – Heterogeneous peripheral
Oligodendroglioma [Figure 5-11-18] mass that involves the cortex with thick curvilinear
• CT Shows DENSE Ca++ calcifications
Figure 5-11-19
Neuroradiology 1151
1153 Non-Astrocytic Gliomas
Oligodendroglioma Figure 5-11-20
• Combined 1p/19q loss
➢ Associated with prolonged survival
➢ Response to PVC (procarbazine, vincristine
CCNU® [Lomustine]) chemotherapy
➢ 50% volume decrease in 100%
➢ Median survival 10 yrs vs 2 yrs
❖ 95% 5 yr survival
➢ Most powerful predictor on multivariate analysis
Cairncross et al. J NCI 1998;90:1473
Oligodendroglioma
MEDULLOBLASTOMA – Demographics
• 1st or 2nd most common cerebellar neoplasm in children
➢ 1/5 – 1/3 of ALL pediatric CNS
➢ M:F 1.1 – 2:1
• May be congenital (present at birth up to 60 days)
➢ most (1/2) < 15 yrs.
➢ however, 1/3 present from 15–35 yrs.
• 5 year survival >> 50% => approached 75%-85%
• Primitive Neuroectodermal Tumor
Figure 5-11-23
RADIATION CHEMOTHERAPY
• Dividing Cells
• Neovascularity
• Pharmaceuticals
➢ Tested against murine leukemia
➢ Small round blue cell tumor
➢ Cis-platinum
❖ Dividing cells
❖ Electrical field
❖ Platinum electrodes
Neuroradiology 1153
1155 Non-Astrocytic Gliomas
Fourth Ventricle - Schematic [Figure 5-11-24] Figure 5-11-24
Figure 5-11-25
Medulloblastoma
Medulloblastoma (PNET) [Figure 5-11-29] Figure 5-11-28
“Zuckerguss” or Sugar Icing (CSF dissemination)
CSF DISSEMINATION
• Neuroectodermal:
➢ PNET (medulloblastoma)
➢ GBM (reaches ventricle or pia)
➢ Ependymoma
➢ Oligodendroglioma (micro curiosity - no Sx)
➢ CPP and CPC
Medulloblastoma (PNET) – Rounded
mass in the central posterior fossa
Non-Astrocytic Gliomas 1154
1156 Neuroradiology
• Non-glial: Figure 5-11-29
➢ Germinoma
➢ Lymphoma (usually secondary)
➢ Leukemia
➢ Carcinomatous Meningitis
Medulloblastoma - Desmoplastic
CSF spread of Medulloblastoma (PNET)
• Lateral Hemispheric Location
• Older Patients More peripheral Figure 5-11-30
Summary
• Ependymoma
➢ Intraventricular, soft, heterogeneous
• Choroid Plexus Papilloma
➢ Very young, Hydrocephalus
➢ Very Small Papillae and Lobulations
• Oligodendroglioma
➢ Superficial, skull remodeling
➢ Dense Calcification: dot-dash and linear
• Medulloblastoma (PNET)
➢ Hyperdense on CT
➢ Central posterior fossa
References
1. Kadri H,Mawla AA, Murad L: Incidence of childhood CSF spread of Medulloblastoma (PNET)
brain tumors in Syria (1993-2002. Pediatric Neurosurgery
2005; 41:173-177
Figure 5-11-31
2. Parizek J, et al: Posterior cranial fossa surgery in 454
children. Childs' Nerv Syst 1998; 14:426-439.
3. Jenkinson MD, Smith TS, Joyce K, Fildes D, du Plessis
DG, Warnke PC, Walker C MRS of oligodendroglial
tumors: correlation with histopathology and genetic
subtypes. Neurology. 2005 Jun 28;64(12):2085-9.
4. Cairncross JG, Ueki K, Zlatescu MC, et al. Specific
genetic predictors of chemotherapeutic response and
survival in patients with anaplastic oligodendrogliomas. J
Natl Cancer Inst 1998; 90:1473-1479.
Figure 5-11-32
Neuroradiology 1155
1157 Non-Astrocytic Gliomas
Extraaxial Tumors:
Other Non-Glial Lesions
James G. Smirniotopoulos, MD
Notochord Embryology
Chordoma
CHORDOMA
• ORIGIN: Notochordal Rests Figure 5-12-3
• AGE: (30–60)
• LOCATION:
➢ Clivus 35%
➢ Spine 15% (esp. Cx)
➢ Sacrum 50%
CHORDOMA: Imaging
• Location: midline clivus
➢ Extend lateral, dorsal , ventral
• NCT: Bone destruction
➢ Heterogeneous Chordoma (left) and Thornwaldt cyst (right). The
➢ “Cysts”, Ca++ orange line is the embryologic location of the
• ECT: Heterogeneous notochord, the green triangle is the clivus
Chordoma
Chordoma – Destruction of the clivus, the basilar
Eccentric Growth [Figure 5-12-5] and vertebral arteries are stretched over a large
bulky, hypovascular mass. Air and contrast
Figure 5-12-5 remain from an earlier myelogram
Figure 5-12-6
Figure 5-12-8
Neuroradiology 1157
1159 Extraaxial Tumors: Other Non-Glial Lesions
T1 pre and post, T2 [Figure 5-12-9] Figure 5-12-9
Chordoma
Figure 5-12-10
Sacrococcygeal chordoma
Figure 5-12-11
DERMOID/EPIDERMOID
• True Cysts
• Inclusion Cysts
• Lined by an Epithelium
Chondrosarcoma
TRUE CYSTS OF THE CNS
• Epidermoid
• Dermoid
• Colloid
• Craniopharyngioma
• Rathke Cleft
• Ependymal
• Endodermal
TRUE CYSTS
• A fluid filled space, lined by an epithelium.
• Classified by the type of epithelial lining:
➢ Epidermoid
❖ squamous epithelium - ectoderm
➢ Dermoid
❖ squamous and dermal adnexa - ectoderm
➢ Colloid cyst
❖ ciliated cuboidal/columnar epithelium, mucus secreting cells - similar to
endoderm ?
❖ Craniopharyngioma (two types)
❖ Adamantinomatous - children, cystic, calcified
❖ Squamous and papillary - adult, solid
➢ Rathke Cleft cyst
❖ ciliated cuboidal/columnar epithelium - possibly endoderm ?
➢ Teratoma - a neoplasm of multipotential germ cells
NON-GLIAL MASSES
• Dermoid and Epidermoid
➢ MYTH OF THE MESODERM
DERMOID/EPIDERMOID: Histology
• 1. Epidermoid – Squamous Epithelium - ONLY
• 2. Dermoid – Sq. Epi PLUS Dermal Appendages
(hair, sebaceous, sweat glands, etc.)
• 3. Teratoma – Complex tissues, 2 or more germ
layers
Epidermoid Inclusion Cyst. Note: the lesion is
(often mainly ectoderm, “benign cystic”)
nearly, but not exactly, like CSF in signal. The
sagittal image demonstrates internal layers of
EPIDERMOID [Figure 5-12-12] keratin
• AGE: 4 – 6TH Decade
• Location: Midline or lateral (CPA)
• Composition: Sq. epithelium, keratin
Figure 5-12-13
• Thin wall, no Ca++ or Vascularity
• NCT: Lipid to Brain
➢ Ca++/enhance. rare
• MRI: Hetero., CSF to Brain
➢ NOT bright on T1W
➢ **Fluid/Fluid Level RARE
Pearly Tumor
Neuroradiology 1159
1161 Extraaxial Tumors: Other Non-Glial Lesions
Epidermoid [Figures 5-12-17 and 5-12-18] Figure 5-12-18
Figure 5-12-17
T1W Gd FLAIR
Figure 5-12-19
Epidermoid Inclusion Cyst. Faint peripheral
enhancement from gliosis. Internal wisps from
layers of keratin, and marked hyperintensity on the
FLAIR image
DERMOID
• AGE: 3rd Decade
• Location: Midline
• Composition: Sq. epi. & appendages
• Thick wall, Ca++ & Vascularity
• NCT: Lipid to Brain, Fluid/Fluid
➢ Ca++/enhance. often
Dermoid with hair and sebaceous
• MRI: Hetero., Lipid to Brain
material
➢ Bright on T1W
➢ **Dysraphism, Sinus tract
Figure 5-12-20
Dermoid Inclusion Cyst
Ruptured Dermoid
Figure 5-12-21
Epidermal surface, but with
sebaceous glands, hair shafts and
follicles – making this a dermoid
inclusion cyst
COLLOID CYST
• A benign mass, in a Malignant Location
Neuroradiology 1161
1163 Extraaxial Tumors: Other Non-Glial Lesions
Neoplasms of the Meninges
James G. Smirniotopoulos, MD
Educational Objectives
• Meningioma is the most common non-glial primary tumor
• Meningioma is the most common extraaxial neoplasm
• Most meningiomas have “typical imaging”
➢ Hemispheric, homogeneous, broad based on the dura, hyperostosis,
hormonally sensitive
• Some meningiomas have “atypical imaging”
• Hemangiopericytoma is NOT a meningioma
Meningioma
• 75% are histologically typical
• 75% are radiologically typical
• Not the same 75%
➢ CT
➢ MR
➢ Angiography
• Atypical Imaging =/= Atypical Histology
• “The atypical appearance of a common lesion may be seen more often than
the classic appearance of an uncommon lesion.”
Meningioma – Radiation
• Low Dose (<800 cGray)
➢ Immigrants to Israel (1940’s)
➢ Tinea Capitis (ringworm)
➢ Superficial radiation
➢ High Incidence of Meningioma
• High Dose (>2000 cGray = 2000 RADS)
➢ Used for Skull Base Tumors
➢ Pituitary Adenoma
Meningiomas
• 1/7 to 1/4 of all Intracranial Primary
➢ ~ 6/ 100k / year
➢ small ones in ~ 1.4% of autopsies
• 1/4 – 1/3 of all Intraspinal Tumors
• Middle age (40–60) Your current Age + Ten Years
• Female > Male
➢ Cranial 2–4:1 Figure 5-13-1
➢ Spinal 4–8:1
➢ Progesterone receptors in 2/3
➢ Estrogen receptors less common
Neuroradiology 1163
1165 Neoplasms of the Meninges
Incidental Meningioma [Figure 5-13-2] Figure 5-13-2
Not Incidental
Meningioma – Location
• Parasagittal 25%
• Convexity 20%
• Ant. Basal 40%
➢ Sphenoid 20% Small incidental meningioma of the
➢ Olfactory 10% tentorium cerebelli
➢ Suprasellar 10%
• Tentorial 10%
• Ventricular 5% Figure 5-13-3
Meningioma – CT Imaging [Figure 5-13-4]
• Non-Contrast
➢ Sharply Circumscribed
➢ Homogeneous
➢ Hyperdense (+/– Ca++)
➢ NOT from psammoma bodies !
➢ Broad Dural Surface
➢ Bone Changes (Hyperostosis)
• Enhanced CT
➢ Homogeneous Enhancement
Figure 5-13-4
Figure 5-13-5
Meningioma – with classic features of
hyperdensity and hyperostosis
Meningiomas – MR Imaging
• “Meningiomas are ISO-intense.” Bar graphs showing high frequency of
➢ Usually on T1W vasogenic edema with meningioma
➢ Vary pulse sequence to see
• EXTRA-axial Features
➢ Gray-matter buckling
➢ Pseudo-capsule of vessels
➢ Meningeal/dural “TAIL”
• GADOLINIUM ENHANCEMENT
Meningioma – Isointense to GM
[Figure 5-13-8]
Figure 5-13-9
Figure 5-13-8
Neuroradiology 1165
1167 Neoplasms of the Meninges
Meningioma [Figure 5-13-10] Figure 5-13-10
• Meningioma
• Tentorium or Dura
• IAC Normal
• Hemispherical
• Homogeneous
• Hyperostosis
Meningioma - Pseudocapsule
Figure 5-13-13
Figure 5-13-12
Meningioma - Transdural
Neuroradiology 1167
1169 Neoplasms of the Meninges
Intraventricular: ~ 5% [Figures 5-13-15 and 5-13-16] Figure 5-13-15
• Usually Adult
• F>M
• Usually Lateral Ventricle
• Usually Trigone/Atrium
• ALWAYS attached to Choroid Plexus
• Vascular pedicle from choroid
Figure 5-13-18
Figure 5-13-21
Meningioma Hyperostosis
• Does NOT mean invasion of bone Variable patterns of hyperostosis from
• Implies CHRONICITY meningioma
➢ and benign behavior
• Skull Base
➢ Invasion via HAVERSIAN CANALS
Figure 5-13-22
Neuroradiology 1169
1171 Neoplasms of the Meninges
Meningioma – Atypical Imaging Figure 5-13-23
(Yet, typical Histology) [Figure 5-13-23]
• Focal Lucency Outside (arachnoid cyst)
• Focal Lucency Inside (necrosis, cyst)
• Hypodensity (“humid”, lipoblastic)
• Focal Hyperdensity (metaplasia, hemorrhage)
• Heterogeneous
• Hyperintensity on T1W
• Hyperintensity on T2W
Fatty Metaplasia
Fatty Metaplasia [Figure 5-13-24] Meningioma with typical histology – yet aggressive
radiologic appearance
Meningioma – Cysts
• Inside of neoplasm Figure 5-13-24
➢ (rim enhancement)
• Between tumor and brain
➢ (”arachnoid cysts”)
• Inside Brain
➢ PIA separates tumor from brain
➢ ?? Results of chronic Edema
➢ Vacuolization of White Matter
“Malignant Meningioma”
• < 3% of all Meningioma
• Anaplastic (Malignant) Meningioma
• Papillary Meningioma
• “Benign” Metastasizing Meningioma
• Hemangio-Peri-Cytoma (HPC)
• Malignant Fibrous Histiocytoma (MFH)
Meningioma – One level shows typical
hemispheric shape, the next shows a peritumoral
“cyst”
Hemangiopericytoma – (HPC)
• Narrow dural base (“Mushrooming”)
• No Hyperostosis
• No Calcification in tumor
• Lobulated (not hemispheric)
• Internal Signal Voids (on MRI)
➢ irregular and multiple
• Hypervascular on Angio
➢ irregular patterns
Meningioma
• The 4H+ Tumor
➢ homogeneous
➢ hyperdense
➢ homogeneous enhancement
➢ hemispheric shape
➢ hyperostosis
➢ hormonally modulated
Meningioma
• 75% are histologically typical
• 75% are radiologically typical
• Not the same 75%
➢ CT
➢ MR
➢ Angiography
• Atypical Imaging =/= Atypical Histology
Neuroradiology 1171
1173 Neoplasms of the Meninges
References
1. Ahmadi J, Hinton DR, Segall HD, Couldwell WT. Surgical implications of magnetic resonance-enhanced dura.
Neurosurgery. 1994 Sep;35(3):370-7;discussion 377.
2. Aoki S, Sasaki Y, Machida T, Tanioka H. Contrast-enhanced MR images in patients with meningioma: importance
of enhancement of the dura adjacent to the tumor. AJNR Am J Neuroradiol. 1990 Sep-Oct;11(5):935-8.
3. Asari S, Yabuno N, Ohmoto T. Magnetic resonance characteristics of meningiomas arising from the falcotentorial
junction. Comput Med Imaging Graph. 1994 May-Jun;18(3):181-5.
4. Berger MS. Perfusion MR and the evaluation of meningiomas: is it important surgically? AJNR Am J Neuroradiol
2003; 24:1499-1500. (1)
5. Goldsher D, Litt AW, Pinto RS, Bannon KR, Kricheff II. Dural "tail" associated with meningiomas on Gd-DTPA-
enhanced MR images: characteristics, differential diagnostic value, and possible implications for treatment.
Radiology. 1990 Aug;176(2):447-50.
6. Helie O, Soulie D, Sarrazin JL, Derosier C, Cordoliani YS, Cosnard G. [Magnetic resonance imaging and
meningiomas of the posterior cerebral fossa. 31 cases] J Neuroradiol. 1995 Dec;22(4):252-70. French.
7. Hutzelmann A, Palmie S, Buhl R, Freund M, Heller M. Dural invasion of meningiomas adjacent to the tumor
margin on Gd-DTPA-enhanced MR images: histopathologic correlation. Eur Radiol. 1998;8(5):746-8.
8. Hutzelmann A, Palmie S, Freund M, Buhl R, Heller M. [Dura thickening adjacent to intracranial, para-dural space-
occupying lesions in MRI. Histologic correlation] Aktuelle Radiol. 1997 Nov;7(6):305-8. German.
9. Hutzelmann A, Palmie S, Zimmer C, Benz T, Leweke F, Freund M. [The meningeal sign: a new appraisal] Rofo.
1996 Apr;164(4):314-7. German.
10. Ildan F, Tuna M, Gocer AP, Boyar B, Bagdatoglu H, Sen O, Haciyakupoglu S, Burgut HR. Correlation of the
relationships of brain-tumor interfaces, magnetic resonance imaging, and angiographic findings to predict cleavage
of meningiomas. J Neurosurg. 1999 Sep;91(3):384-90.
11. Kawahara Y, Niiro M, Yokoyama S, Kuratsu J. Dural congestion accompanying meningioma invasion into vessels:
the dural tail sign. Neuroradiology. 2001 Jun;43(6):462-5.
12. Maiuri F et al: Intracranial meningiomas: correlations between MR imaging and histology. Eur J Radiol. 1999; 31:
69-75
13. Nagele T, Petersen D, Klose U, Grodd W, Opitz H, Voigt K. The "dural tail" adjacent to meningiomas studied by
dynamic contrast-enhanced MRI: a comparison with histopathology. Neuroradiology. 1994 May;36(4):303-7.
14. Nakasu S, Nakasu Y, Matsumura K, Matsuda M, Handa J. Interface between the meningioma and the brain on
magnetic resonance imaging. Surg Neurol. 1990 Feb;33(2):105-16.
15. Nakau H, Miyazawa T, Tamai S, Tsuchiya K, Shima K, Shirotani T, Chigasaki H. Pathologic significance of
meningeal enhancement ("flare sign") of meningiomas on MRI. Surg Neurol. 1997 Dec;48(6):584-90; discussion
590-1.
16. Quekel LG, Versteege CW. The "dural tail sign" in MRI of spinal meningiomas. J Comput Assist Tomogr. 1995
Nov-Dec;19(6):890-2.
17. Sakai K, Tada T, Fukasaku K, Kyoshima K, Kobayashi S. Histological examination of the gadolinium-enhanced
dura mater around meningiomas on magnetic resonance imaging. Neurol Med Chir (Tokyo). 1993 Jul;33(7):429-
33.
18. Sandhyamani, Rao, Nair, Radhakrishan: Atypical Meningioma: A Clinicopathological Analysis.Neurology India
2000; 48: 338-342
19. Sato M, Matsumoto M, Kodama N. Meningeal enhancement surrounding meningiomas on Gd-DTPA MRI.
Fukushima J Med Sci. 1998 Jun;44(1):1-11.
20. Sekiya T, Manabe H, Iwabuchi T, Narita T. [The dura mater adjacent to the attachment of meningiomas: its
enhanced MR imaging and histological findings] No Shinkei Geka. 1992 Oct;20(10):1063-8. Japanese.
21. Takeguchi T, Miki H, Shimizu T, Kikuchi K, Mochizuki T, Ohue S, Ohnishi T. The dural tail of intracranial
meningiomas on fluid-attenuated inversion-recovery images. Neuroradiology. 2004 Feb;46(2):130-5. Epub 2004
Jan 28.
22. Wilms G, Lammens M, Marchal G, Van Calenbergh F, Plets C, Van Fraeyenhoven L, Baert AL. Thickening of dura
surrounding meningiomas: MR features. J Comput Assist Tomogr. 1989 Sep-Oct;13(5):763-8.
23. Yamaguchi N, Kawase T, Sagoh M, Ohira T, Shiga H, Toya S. Prediction of consistency of meningiomas with
preoperative magnetic resonance imaging. Surg Neurol. 1997 Dec;48(6):579-83.
Biological Clock
• Day-Night Diurnal Rhythms
• Pineal Melatonin Suppresses GnRH
➢ Longer daylight decreases melatonin and leads
to increased Gonadotropin Releasing Hormone
➢ GnRH => LH and FSH
➢ Increased sexual drive and activity in the Spring
… and I thought it was the Pollen … Pineal gland and surrounding region: Third
ventricle, quadrigeminal plate and cistern, bilateral
Normal Pineal [Figures 5-14-1 and 5-14-2] thalami
Neuroradiology 1173
1175 “PINEALOMAS” and, other Pineal Region Masses
Parinaud Syndrome: Aqueduct/Tectal Syndrome
• Failure of conjugate vertical eye movement
➢ Upward >> downward
• Mydriasis, fixed pupils
• Failed ocular convergence
➢ Lateral midbrain tegmentum
• Blepharospasm
➢ Eyelid spasm
Intracranial Germinoma
• Central:
➢ pineal (para-pineal)
➢ Suprasellar cistern
• Homogeneous Solid
• Hyperdense on NCT
• Isointense on T1W
• “Hormonally silent”
➢ no AFP/HCG but PLAP+
Surgical Planning
• Find the Internal Cerebral Veins and the VOG
• If Tumor is BELOW these veins
➢ Suboccipital Infratentorial Approach
• If Tumor is ABOVE these veins
➢ Interhemispheric Approach
➢ Sub Temporal Approach
➢ Various other techniques Pineal region germinoma
Neuroradiology 1175
1177 “PINEALOMAS” and, other Pineal Region Masses
Pineal Region Neoplasms Figure 5-14-8
• Germinoma:
➢ Iso on T1W
➢ slightly Hyper on T2W
• Choriocarcinoma:
➢ Hyper on T1W (blood)
• Dermoid, Teratoma:
➢ Hyper on T1W (lipid)
MR AJNR 11:557–565,1990
Figure 5-14-9
Famous Quote
Aunt Voula:
“You family now, so I tell you a story. All my life ... I have this lump on the back of
my neck. When I reach the menopause, the lump get bigger. I go to the doctor,
and he performs a...bo-bobopsy. And inside the lump, he finds teeth, and a spinal
column.”
Figure 5-14-12
Germinoma
CSF Dissemination
Neuroradiology 1177
1179 “PINEALOMAS” and, other Pineal Region Masses
Pineal Parenchyma Figure 5-14-14
• Pineoblastoma (PNET)
➢ Young Patients (1st two decades)
➢ Tumor ITSELF Calcifies
➢ ”Exploded” Pineal Ca++
• Pineocytoma (Mature pineal cells)
➢ Young or Old
• Trilateral Retinoblastoma
➢ Inherited Rb (chromosome 13)
➢ 1/3 inherited but 2/3 heritable
➢ Look at ORBITS for signs of Tx
Figure 5-14-16
Pineoblastoma
Figure 5-14-17
Figure 5-14-18
Pineal Cysts
• Autopsy
➢ ~ 5% of Adults
➢ < 2 mm in a Normal Size Gland
• MR Visible
➢ 2%-8% of Adults
➢ 2-7 mm common
➢ 14-25 mm cysts are not rare
➢ May expand the gland
➢ Ring enhancement should be smooth and thin 1-2 mm
• Why do they grow? – Unknown
Hydrocephalus
• Mechanical
➢ Aqueductal Obstruction
• Impaired CSF Resorption
➢ Venous Hypertension
Neuroradiology 1179
1181 “PINEALOMAS” and, other Pineal Region Masses
Intracranial Lipoma [Figure 5-14-22] Figure 5-14-22
• Congenital, NOT a true neoplasm
• MIDLINE (usually)
• Usually around Corpus Callosum
• Occasional Tectal, Hypothalamic, CPA
• Abnormal Differentiation
➢ Meninx Primativa Into Fat
Figure 5-14-23
Figure 5-14-24
Figure 5-14-25
Figure 5-14-26
Mass in the splenium of the corpus callosum –
Glioblastoma multiforme
Astrocytoma of Tectum
References
1. Barboriak DP, Lee L, Provenzale JM. Serial MR imaging of pineal cysts: implications for natural history and
follow-up. AJR Am J Roentgenol. 2001 Mar;176(3):737-43.
2. Barbouriak DP, Lee L, Provenzale JM: Serial MR Imaging of Pineal Cysts: Implications for Natural History and
Follow-Up.AJR 2001; 1737-743.
3. Fain JS, Tomlinson FH, Scheithauer BW, Parisi JE, Fletcher GP, Kelly PJ, Miller GM. Symptomatic glial cysts of
the pineal gland. J Neurosurg. 1994 Mar;80(3):454-60.
4. Fleege MA, Miller GM, Fletcher GP, Fain JS, Scheithauer BW. Benign glial cysts of the pineal gland: unusual
imaging characteristics with histologic correlation. AJNR Am J Neuroradiol. 1994 Jan;15(1):161-6.
5. Fujimaki T, Matsutani M, Funada N, Kirino T, Takakura K, Nakamura O, Tamura A, Sano K.J Neurooncol. CT and
MRI features of intracranial germ cell tumors. 1994;19(3):217-26.
6. Hayashida Y, Hirai T, Korogi Y, Kochi M, Maruyama N, Yamura M, Yamashita Y. Pineal cystic germinoma with
syncytiotrophoblastic giant cells mimicking MR imaging findings of a pineal cyst. AJNR Am J Neuroradiol. 2004
Oct;25(9):1538-40.
7. Jinkins JR, Xiong L, Reiter RJ. The midline pineal "eye": MR and CT characteristics of the pineal gland with and
without benign cyst formation. J Pineal Res. 1995 Sep;19(2):64-71.
8. Koenigsberg RA, Faro S, Marino R, Turz A, Goldman W. Imaging of pineal apoplexy. Clin Imaging. 1996 Apr-
Jun;20(2):91-4.
9. Korogi Y, Takahashi M, Ushio Y. MRI of pineal region tumors. J Neurooncol. 2001 Sep;54(3):251-61.
10. Lee DH, Norman D, Newton TH. MR imaging of pineal cysts. J Comput Assist Tomogr. 1987 Jul-Aug;11(4):586-
90.
11. Mamourian A, Towfighi J. MR of pineal cysts. AJNR Am J Neuroradiol. 1994 Oct;15(9):1796-7.
12. Mamourian AC, Towfighi J. Pineal cysts: MR imaging. AJNR Am J Neuroradiol. 1986 Nov-Dec;7(6):1081-6.
13. Mamourian AC, Yarnell T. Enhancement of pineal cysts on MR images. AJNR Am J Neuroradiol. 1991 Jul-
Aug;12(4):773-4. No abstract available.
14. Osborn RE, Deen HG, Kerber CW, Glass RF. A case of hemorrhagic pineal cyst: MR/CT correlation.
Neuroradiology. 1989;31(2):187-9.
15. Reis F, Faria AV, Zanardi VA, Menezes JR, Cendes F, Queiroz LS. Neuroimaging in pineal tumors. J
Neuroimaging. 2006 Jan;16(1):52-8.
16. Sener RN. The pineal gland: a comparative MR imaging study in children and adults with respect to normal
anatomical variations and pineal cysts. Pediatr Radiol. 1995;25(4):245-8.
17. Welton PL, Reicher MA, Kellerhouse LE, Ott KH. MR of benign pineal cyst. AJNR Am J Neuroradiol. 1988 May-
Jun;9(3):612. No abstract available.
Neuroradiology 1181
1183 “PINEALOMAS” and, other Pineal Region Masses
The Phakomatoses
James G. Smirniotopoulos, MD
The Phakomatoses
• Neuro-ectodermal
or
• Nerves and Skin
Phakomatoses – Plan
• Demographics
• Diagnostic Criteria
• Ocular/Orbit Lesions
• Skin
• Brain
• Visceral Manifestations
• Complications of Disease
Neurofibromatosis
• NF-1, von Recklinghausen (“peripheral” – bad term)
• NF-2, Bilateral Acoustic (“central” – bad term)
• NF-3, Overlap of 1 and 2
• NF-5, Segmental (e.g. a quadrant)
• NF-6, Cafe-au-lait, w/o CNS/PNS
• NF-7, Late Onset
• NF-8, Other
Neurofibromatosis – Types
• Neurofibromatosis Type 1 (NF-1)
➢ von Recklinghausen Disease
➢ “True” Neurofibromatosis
➢ Prominent Cutaneous Signs
➢ Chromosome 17q
• Neurofibromatosis Type 2 (NF -2)
➢ Bilateral Acoustic Schwannoma
➢ “Central Neurofibromatosis”
➢ Minimal Skin Manifestations
➢ Chromosome 22q
Neurofibromatosis
• 1768 MARK AKENSIDE (New York)
• 1793 TILESIUS (Leipzig)
• 1849 R.W. SMITH (England)
• 1822 WISHART (Edinburg) NF-2
• 1882 von RECKLINGHAUSEN (Germany)
Neurofibromatosis - 1
• Clinical
➢ Incidence: 1/2,500 births
➢ Inheritance: Autosomal Dominant
➢ Age at Presentation: Birth to Death
➢ Sx at Presentation: Spots, NFB
➢ Diagnostic Criteria: Cutaneous, PNS
➢ Chromosome Abnl.: 17
➢ Ocular Findings: Myelinated retina
➢ Cutaneous Findings: cafe-au-lait, neurofibroma
➢ CNS Findings: Optic N. Glioma, Hamartoma, Heterotopia, macrocephaly,
mentation problems
Neuroradiology 1183
1185 The Phakomatoses
• Axillary (Intertriginous) Freckling-1 Figure 5-15-2
• Optic Glioma
• Lisch Nodules (Iris) – 2 or more
• “Distinctive Bone Lesions”
• 1st degree relative with NF-1
Neurofibromatosis – 1
• Clinical
• Chromosome Abnl.: 17
• Ocular: Myelinated retina
• Cutaneous: cafe-au-lait, neurofibroma
• CNS: Optic N. Glioma, Hamartoma, Heterotopia,
Macrocephaly, Mentation
Neurofibromatosis – 1
• Cutaneous Manifestations
➢ Cafe-au-Lait spots [Figure 5-15-4]
➢ Intertriginous Freckling
➢ Neurofibromas (Skin and SubQ)
➢ Fibroma Molluscum (TNTC NFB)
➢ Elephantiasis Neuromatosa
❖ diffuse skin thickening/plexiform NFB –
❖ or focal gigantism
Neurofibromatosis – 1
• Bone Dysplasia and Remodeling
➢ Macrocephaly Optic Nerve Glioma
➢ Craniofacial dysplasia
❖ especially sphenoid
➢ Vertebrae (scalloping, scoliosis)
➢ Pseudoarthrosis
❖ especially congenital
➢ Genu Valgum/Varum Figure 5-15-4
➢ Twisted “Ribbon Ribs”
Figure 5-15-7
Sphenoid Dysplasia
Figure 5-15-8
Progressive Pseudoarthrosis
Neuroradiology 1185
1187 The Phakomatoses
Figure 5-15-9 Figure 5-15-10
Schwannoma – a focal mass, even at the Neurofibroma – a diffuse lesion, even at the
microscopic level microscopic level
Intraspinal Neoplasms
• 68 Pts.
• 86 Spinal Nerve Sheath neoplasms
• Sporadic: 42 pts. (65%)
➢ 40 Schwannoma and 2 neurofibroma
• NF-1: 12 Pts. (18%)
➢ All were Neurofibroma
• NF-2: 7 Pts (11%)
➢ 6 Schwannoma/1 “mixed” tumor
• Unknown - 5 Pts. Acute Cervical Kyphoscoliosis – one of the
characteristic lesions of NF-1
Neurofibromatosis : Spine [Figure 5-15-11]
• Scoliosis (NF-1, only?)
➢ Simple ("idiopathic")
➢ Acute Cervical Kyphosis
• Dural Ectasia (NF-1, only?)
➢ Vertebral Scalloping
➢ Arachnoid "cysts"
➢ Lateral Thoracic meningocele
Figure 5-15-15
Neuroradiology 1187
1189 The Phakomatoses
Plexiform NF [Figure 5-15-16 ] Figure 5-15-16
Plexiform neurofibromas
Neurofibromatosis - 1: Spine Figure 5-15-17
[Figures 5-15-17 and 5-15-18]
• Scoliosis (Acute Cx Kyphoscoliosis)
• Vertebral Scalloping
• Enlarged Neural Foramina
• Lateral Thoracic Meningocele
Figure 5-15-19
Neurofibromatosis
• Malignant Nerve Sheath
➢ Tumor (malignant PNST, neurofibrosarcoma,...)
• Embryonal Malignancies:Wilms,
Rhabdomyosarcoma
• Leukemia (CML)
• Melanoma, Medullary Thyroid Ca.
• Low Incidence of Lung Cancer”
Neurofibromatosis Deep Bright Objects – DBO’s
Malignant Peripheral Nerve Sheath Tumor
Neurofibromatosis – Type 2
• Incidence: 1/50,000
• Inheritance: Autosomal Dominant
• Age at Presentation: Birth to 40’s (peak in 20’s)
• Sx at Presentation: Hearing loss from VS
• Diagnostic Criteria: VIII masses
• Chromosome Abnl.: 22
• Cutaneous Findings: minimal (skin tags)
• CNS Findings: Schwannoma, Meningioma, Ependymoma (intramedullary
spinal cord)
Neuroradiology 1189
1191 The Phakomatoses
CNS Neoplasms – Chromosome Loss of Figure 5-15-21
Heterozygosity
• NF-2
➢ SCHWANNOMA – 22q
➢ MENINGIOMA – 22q (long arm)
➢ EPENDYMOMA – 22
• NOT Neurofibroma
• NOT Astrocytoma
• NOT Optic Glioma
STURGE-WEBER: Manifestations
• Seizures, Mental Decline Trigeminal Angiomatosis in SWS
➢ Usually begins in first 24 months
• Facial Angioma
➢ At birth Figure 5-15-26
• Angiomatous Overgrowth of soft-tissue and bone
• Leptomeningeal Angioma
• Cortical Atrophy w/Ca++
STURGE-WEBER: Variants
• Facial and Intracranial w/o Eye
• Intracranial and Eye w/o Face
• Intracranial Alone
➢ (Cerebral and Leptomeningeal)
• Klippel-Trenaunay (KT Weber)
➢ Extracranial soft-tissue angiomas)
STURGE-WEBER SYNDROME:
Port Wine Stain (PWS) [Figures 5-15-25 and 5-15-26]
• Facial Neveus Flammeus
• Blanches w/ pressure
• Trigeminal Dermatome
➢ V1 – Ophthalmic
➢ V2 – Maxillary
➢ V3 – Mandibular
Neuroradiology 1191
1193 The Phakomatoses
Association of PWS with SWS Figure 5-15-27
• All 3 >> 1+2 >> 1 or 2 alone >> other
• medial aspect of eyelid (V1 or V2)
STURGE-WEBER: Vascular
• Absence of cortical veins
• Poor filling of sagittal sinus
• Persistent Primitive Plexus (SAS)
• Recruitment of Medullary Veins
• Prominent Choroid Plexus
STURGE-WEBER: Etiology
• Abnormal Development of Capillaries
➢ Poor cortical venous drainage
➢ Absent cortical veins T1W MR with contrast. Prominent
➢ Prominent veins in SAS medullary veins in SWS. Also note
➢ Prominent deep (medullary) veins the widened diploic space of the
➢ Enlarged choroidal vessels frontal bone and gyriform surface
➢ Persistence of Primitive Plexus enhancement posteriorly
STURGE-WEBER: Manifestations
• Seizures, Mental Decline
• Facial Angioma
• Angiomatous Overgrowth
• Leptomeningeal Angioma
• Cortical Atrophy w/Ca++
Buphthalmos or “Ox eye”. Congenital
glaucoma, caused by a choroidal
angioma, has led to enlargement
of the ocular globe
Figure 5-15-31
Figure 5-15-33
Neuroradiology 1193
1195 The Phakomatoses
Progression in SWS [Figure 5-15-34] Figure 5-15-34
STURGE-WEBER: Treatment
• Symptomatic (anticonvulsants)
• Cosmetic Tattooing
• Laser Treatment of Skin Lesions
• Hemispherectomy
• Aspirin (mild antiplatelet)?
Figure 5-15-38
Tuberous Sclerosis
• Original “VOGT TRIAD”
➢ FACIAL NEVUS (ADENOMA SEBACEUM)
➢ SEIZURES
➢ MENTAL DEFICIENCY
Tuberous Sclerosis
• AUTOSOMAL DOMINANT
• No Racial/Sexual
• High Spontaneous Mutation
• High Penetrance
➢ “SPORADIC” over-reported
• Multiple Genes
➢ TSC1 – 9q
➢ TSC2 – 16p
Tuberous Sclerosis
• Definitive (need 1)
➢ (1) facial angiofibroma
➢ (2) ungual fibroma
➢ (3) retinal hamartoma
➢ (4) cortical tubers
➢ (5) subependymal nodules
➢ (6) multiple renal AML
Neuroradiology 1195
1197 The Phakomatoses
• Presumptive (need 2)
➢ (1) hypomelanotic nodules
➢ (2) shagreen patch
➢ (3) single renal AML
➢ (4) multicystic kidney
➢ (5) cardiac rhabdomyoma
➢ (6) pulmonary lymphangiomyomatosis
➢ (7) radiographic “honeycomb” lung
➢ (8) first degree relative with TS
Tuberous Sclerosis:
• Seizures 90%
• Adenoma Sebaceum 60%-90%
• Retardation 40%-60%
• Retinal Phakoma 50%
• Xr: Intracranial Ca++ 50%
• Ungual Fibromata 17%
• Giant Cell Astrocytoma 15%
Tuberous Sclerosis
• “Hamartomas”
➢ CNS (Cortical Ventricular)
➢ Retina (Phakoma)
➢ Kidney (Angio Myo Lipoma – AML)
• Angiofibromas
➢ Face (“Adenoma Sebaceum”)
➢ Nail Bed (“Fibromas”)
Tuberous Sclerosis:
• Rhabdomyomas – Heart
➢ “Hamartomas”
• Angiomyomatosis – Lung
➢ smooth muscle proliferation
Adenoma Sebaceum
• AKA PRINGLE’S DISEASE
• NOT present at birth
• develop before puberty
• nasolabial fold ->bi-malar
• papules of angiofibroma
Figure 5-15-40
Depigmentation:
• Ash-Leaf Spots
➢ (Lance- Ovate Shape)
Figure 5-15-41
• Confetti – Like Hypopigmentation
➢ (Inverse Freckle)
Neuroradiology 1197
1199 The Phakomatoses
• SUBEPENDYMAL NODULES (almost 100%) Figure 5-15-42
➢ “hamartomas” vs. neoplasia
➢ Caudothalamic groove
➢ Polypoid “Candle Gutterings”
• DILATED VENTRICLES
➢ variable
➢ obstructive, atrophic vs. “idiopathic”
• TUMORS 15%
• Sub-ependymal Giant Cell Astrocytoma
➢ True neoplasm, Benign WHO Grade I
Cortical Tubers
[Figure 5-15-42]
Subependymal Nodules
[Figures 5-15-43 and 5-15-44]
Figure 5-15-43
Figure 5-15-44
Tuberous Sclerosis is a
disorder of neuronal
migration and maturation
Figure 5-15-49
Multiple renal angiomyolipomas in
Tuberous Sclerosis
Neuroradiology 1199
1201 The Phakomatoses
Angiomyomatosis vs. Lymphangiomyomatosis Figure 5-15-50
[Figure 5-15-50]
• “sporadic” cases, all are female
➢ 50% chylothorax
➢ Perilymphatic smooth mm.
➢ May have abdominal LN involvement
• In TS, males can be affected
➢ chylothorax is rare
➢ Periarterial smooth mm around pulmonary aa
von Hippel-Lindau
• 1. CNS and Retinal hemangioblastoma
• 2. Hemangioblastoma and one:
➢ a. renal, pancreatic, hepatic, epididymal cyst
➢ b. pheochromocytoma
➢ c. renal cancer
• 3. Family history and one:
➢ a. hemangioblastoma
➢ b. viscera
➢ c. pheochromocytoma
➢ d. renal cancer
Hemangioblastoma:
• True Neoplasm Endothelial Origin
• Hypervascular
➢ capillary to sinusoidal
➢ dilated feeding artery
➢ dilated draining vein
➢ slow flow
• Stromal Cells
➢ foamy, lipid -laden
Hemangioblastoma – the classic
von Hippel-Lindau: Hemangioblastoma “cyst with nodule” morphology
• Cerebellum 66%
• Retina (“angiomas”) 58%
• Spinal Cord / Roots 28%
Figure 5-15-54
• Medulla 14%
Figure 5-15-55
Figure 5-15-58
Figure 5-15-59
Figure 5-15-60
Erythropoietin
• in cyst fluid
• Elevated ESR
• Elevated Hct
Von Hippel-Lindau
• Hemangioblastoma
➢ Cerebellum
➢ Retina
➢ Medulla, Cord
• Cysts/Neoplasms
➢ Kidney
➢ Liver
➢ Pancreas
➢ Epididymis
➢ Endolymphatic sac
• Pheochromocytoma -Adrenal Endolymphatic Sac Tumor
Neuroradiology 1203
1205 The Phakomatoses
VHL - Multiple hemangioblastomas [Figure 5-15-64] Figure 5-15-64
Educational Objectives
• Describe why NF-1 is truly “Neurofibromatosis”
• Describe three neoplasms caused by the chromosome 22 mutation in NF-2
• Describe the vascular abnormalities of Sturge Weber Syndrome
• Explain why Tuberous Sclerosis is a disorder of neuronal migration
• Distinguish von Hippel-Lindau from the ‘neurocutaneous’ phakomatoses
References Part 1
1. Aizpuru RN, Quencer RM, Norenberg M, Altman N, Smirniotopoulos JG. Meningioangiomatosis: clinical,
radiologic, and histopathologic correlation. Radiology 1991; 179:819-821.
2. American Journal of Neuroradiology 8[6], 1031-1036. 1987
3. Aoki S, Barkovic AJ, Nishimura K, Kjos B, Brown EW, Riccardi VM et al. Neurofibromatosis Types-1 and Type-
2: Cranial MR Findings. Radiology 1989; 172(2):527-534.
4. Baldwin D, King TT, Chevretton E, Morrison AW. Bilateral cerebellopontine angle tumors in neurofibromatosis
type 2. J Neurosurg 1991; 74:910-915.
5. Barker D, Wright E, Nguyen K, Cannon P. Gene for von Recklinghausen Neurofibromatosis is in the
Pericentromeric Region of Chromosome 17. Science 1987; 236:1100-1102.
6. Brown EW, Riccardi VM, Mawad M, Handel S, Goldman A, Bryan RN. MR Imaging of Optic Pathways in
Patients with Neurofibromatosis.
7. Brzowski AE, Bazan III C, Mumma JV, Ryan SG. "Spontaneous regression of optic glioma in a patient with
neurofibromatosis.". Neurology 1992; 42(3):679-681.
8. Chui MC, Bird BL, Rogers J. Extracranial and Extraspinal Nerve Sheath Tumors: Computed Tomographic
Evaluation. Neuroradiology 1988; 30:47-53.
9. Cohen MM. Invited Historical Comment: Further Diagnostic Thoughts About the Elephant Man. Am J Med
Genetics 1988;777-782.
Neuroradiology 1205
1207 The Phakomatoses
References Part 2
1. Afra D, Muller W, Slowik F, Firsching R. Supratentorial lobar pilocytic astrocytomas: report of 45 operated cases,
including 9 recurrences. Acta Neurochir (Wien ) 1986; 81(3-4):90-93.
2. Alexander GL. Sturge-Weber Syndrome. Chap 7 in The Phakomatoses Vinken PJ, Bruyn GW Eds., Vol. 14 of
Handbook of Clinical Neurology. Elsevier Publishing Co , New York, 1972.
3. Bachmann K, Markwalder R, Seiler RW. Supratentorial hemangioblastoma: Case Report. Acta Neurochirurgica
1978; 44:173-177.
4. Barath B, Voros E, Bak Z, Bodosi M. Cerebral venous drainage via the ophthalmic veins in the Sturge-Weber
syndrome. Neuroradiology 1994; 36(4):318-320.
5. Bender BL, Yunis EJ. The Pathology of Tuberous Sclerosis. Path Annu 1982; 17:339-382.
6. Choyke PL, Glenn GM, McClellan WM, Patronas NJ, Linehan WM, Zbar B. von Hippel-Lindau Disease:
Genetic, Clinical, and Imaging Features. Radiology 1995; 194:629-642.
7. Choyke PL, Glenn GM, Walther MM, Zbar B, Weiss GH, Alexander RB et al. "The Natural History of Renal
Lesions in von Hippel-Lindau Disease: A Serial CT Study in 28 Patients.". AJR 1992; 159:1229-1234.
8. Dahlen RT, Harnsberger HR, Gray SD, Shelton C, Allen R, Parkin JL et al. Overlapping thin-section fast spin-echo
MR of the large vestibular aqueduct syndrome. AJNR Am J Neuroradiol 1997; 18:67-75.
9. Dyke DG, Davidoff LM, Masson CB. Cerebral Hemiatrophy with Homolateral Hypertrophy of the Skull and
Sinuses. Surgery, Gynecology and Obstetrics 1933; 57:588-600.
10. Feghali JG, Levin RJ, Llena J, Bradley MK, Kantrowitz AB. Aggressive Papillary Tumors of the Endolymphatic
Sac: Clinical and Tissue Culture Characteristics. Am J Otology 16[6], 778-782. 1995.
11. Fetner CD, Barilla DE, Scott T, et al. Bilateral renal cell carcinoma in von Hippel-Lindau syndrome: Treatment
with staged bilateral nephrectomy and hemodialysis. J Urol 17, 534-536. 1977.
12. Filing-Katz MR, Choyke PL, Oldfield E, Charnas L, Patronas NJ, Glenn GM et al. Central nervous system
involvement in Von Hippel-Lindau disease. Neurology 1991; 41:41-46.
13. Filling-Katz MR, Choyke PL, Patronas NJ, et al. Radiologic scrreening for von Hippel-Lindau disease: The role of
Gd-DTPA-enhanced MR imaging of the CNS. Journal of Computer Assisted Tomography 13, 745-755. 1989.
14. Hirose T, Scheithauer BW, Lopes MB, Gerber HA, Altermatt HJ, Hukee MJ et al. Tuber and subependymal giant
cell astrocytoma associated with tuberous sclerosis: an immunohistochemical, ultrastructural, and immunoelectron
and microscopic study. Acta Neuropathol (Berl) 1995; 90:387-399.
15. Ho VB, Smirniotopoulos JG, Murphy FM, Rushing EJ. Radiologic-pathologic correlation: hemangioblastoma.
AJNR 1992; 13:1343-1352.
16. Hoang MP, Amirkhan RH. Inhibin alpha distinguishes hemangioblastoma from clear cell renal cell carcinoma. Am
J Surg Pathol 2003; 27(8):1152-1156.
17. Huson SM, Harper PS, Hourihan MD, Cole G, Weeks RD, Compston DAS. Cerebellar Haemangioblastoma and
von Hippel-Lindau Disease. Brain 1986; 109:1297-1310.
18. Jelinek J, Smirniotopoulos JG, Parisi JE, Kanzer M. Lateral ventricular neoplasms of the brain: differential
diagnosis based on clinical, CT, and MR findings. AJR 1990; 155:365-372.
19. Koeller KK, Sandberg GD. From the archives of the AFIP. Cerebral intraventricular neoplasms: radiologic-
pathologic correlation. Radiographics 2002; 22(6):1473-1505.
20. Levine E, Weigel JW, Collins DL. Diagnosis and management of asympptomatic renal cell carcinomas in von
Hippel-Lindau syndrome. Urology 21, 146-150. 1983.
21. Lonser RR, Glenn GM, Walther M, Chew EY, Libutti SK, Linehan WM et al. von Hippel-Lindau disease. Lancet
2003; 361(9374):2059-2067.
22. Megerian CA, McKenna MJ, Nuss RC, Maniglia AJ, Ojemann RG, Pilch BZ et al. Endolymphatic Sac Tumors:
Histopathologic Confirmation, Clinical Characterization, and Implication in von Hippel-Lindau Disease.
Laryngoscope 105, 801-808. 1995.
23. Mukherji SK, Albernaz VS, Lo WW, Gaffey MJ, Mergerian CA, Feghali JG et al. Papillary endolymphatic sac
tumours: CT, MR imaging, and angiographic findings in 20 patients. Radiology 202[3], 801-808. 1997.
24. Murphy FM, Smirniotopoulos JG. Hemangioblastoma: Radiologic-Pathologic Correlation. Paper Presented at the
87th Annual Meeting of the Roentgen Ray Society . 1987.
25. Neumann H. Basic criteria for clinical diagnosis and genetic couselling in von Hippel-Lindau Syndrome. VASA
1987; 16:220-226.
26. Nixon JR, Houser OW, Gomez MR, Okazaki H. Cerebral Tuberous Sclerosis: MR Imaging. Radiology 170:869-
873, 1989.
27. Nixon JR, Houser OW, Gomez MR, Okazaki H. Cerebral Tuberous Sclerosis: MR Imaging. Radiology 1994;
170:869-873.
28. Ouallet JC, Marsot-Dupuch K, Van Effenterre R, Kujas M, Tubiana JM. Papillary adenoma of endolymphatic sac
origin: a temporal bone tumor in von Hippel-Lindau disease. Case report. J Neurosurg 1997; 87:445-449.
29. Ozek MM, Ozek E, Pamir MN, Ozer AF, Erzen C. Subependymal giant cell astrocytomas in tuberous sclerosis.
Turk J Pediatr 1993; 35:145-150.
Neuroradiology 1207
1209 The Phakomatoses
Subarachnoid Hemorrhage and
Intracranial Aneurysms
Mary E. Jensen, MD
Epidemiology
• Most common cause of non-traumatic SAH is aneurysmal rupture
• Annual incidence of aneurysmal SAH: 1:10,000
➢ Higher than primary brain tumors, MS
➢ Remained stable over last 30 yrs
➢ Females 1.6 x over males
➢ Blacks 2.1 x over whites
➢ Higher in Japan and Finland
• Accounts for 2-5% of all new strokes each yr
➢ 21,000 – 33,000 Americans
➢ Average age much lower than other strokes
❖ Peaks in 6th decade
Types of Aneurysms
[Figures 5-16-1 and 5-16-2]
• Saccular (“berry”)
➢ 90% of all aneurysms
• Fusiform
➢ Serpentine: Partially thrombosed
aneurysm containing tortuous
vascular channels
➢ Cirsoid: Dilated, elongated and
tortuous Saccular, paraophthalmic (left) Fusiform, vertebral (center)
• Dissecting Serpentine, MCA (right)
• Blister/bleb
Figure 5-16-2
Non-Modifiable Risk Factors
• Personal history of SAH
➢ Risk of developing a new aneurysm: 2%
❖ Annual incidence of SAH: 6:10,000
• Family history of SAH
➢ 5%-20% of patients with SAH have a positive
family history
❖ First-degree relatives of pts with SAH have 3-
7X increased risk
➢ Second-degree relatives have same risk as
general population
➢ Probably an autosomal transmission that does
not follow a specific mendelian model
• Female gender Dissecting, PICA (left) Blister-bleb, AComA (right)
➢ Before the 5th decade, the risk is higher in men
➢ Risk is greater in post-menopausal women than men
❖ Supplemental low-estrogen hormones may impart some protection
Neuroradiology 1209
1211 Subarachnoid Hemorrhage-Intracranial Aneurysms
Pathogenesis: Saccular Aneurysms
• Congenital defect in tunica media no longer considered the cause of aneurysm
formation
➢ Gaps in muscles layers are also seen in unaffected individuals
➢ In aneurysms, the gap is not at the neck but in the sac
• Acquired changes due to environmental factors (HTN, smoking, EtOH abuse)
are more likely
➢ Formation of intimal thickening proximal and distal to branch points
❖ May cause increased strain in the more elastic portion of the wall
➢ Structural abnormalities in structure proteins of the extracellular matrix
Figure 5-16-6
Pathogenesis: Saccular Aneurysms
Hemodynamic factors
• Wall shear stress
➢ Frictional force of viscous blood
❖ High WSS fragments the internal elastic lamina
- Initiation of aneurysm formation
❖ Low WSS degenerates endothelial cells via apoptosis
- Responsible for aneurysm growth/rupture
• Increased flow
➢ 10%-20% of patients with brain AVMs have aneurysms
Clinical Presentation
• Subarachnoid hemorrhage
➢ Unique headache
➢ Nausea/vomiting
➢ Meningeal irritation
➢ Photophobia
➢ Focal or global neurological deficits
➢ Subhyaloid hemorrhages
Clinical Presentation
• Mass effect
➢ Headache
➢ Cranial nerve palsies
➢ Focal neurological findings
➢ Seizures
➢ Risk of rupture of unruptured aneurysm causing
mass effect is 6%/yr
• Cerebral ischemia
➢ Distal embolization from intra-aneurysmal
thrombus
Outcomes of SAH
• 12% die before reaching hospital
• 40% of hospitalized patients die within first month
• >1/3 of survivors have major neurological deficits
➢ Unable to live independently
• Many “good outcomes” have persistent cognitive
AComA pattern (left images) - Basilar tip pattern
deficits
(right images)
Outcomes of SAH - Major factors associated with poor outcome
• Patient’s level of consciousness on
admission
Figure 5-16-9
➢ Based on the sum score of the
Glasgow Coma Scale
❖ Eye opening (4 pts), best motor
response (6 pts), best verbal
response (5 pts)
➢ Age
➢ Amount of blood on CT
➢ Predicts risk of delayed cerebral
ischemia using two parameters
❖ Amount of subarachnoid clot 59 y.o. female evaluated for headache and cognitive
❖ Ventricular hemorrhage dysfunction
➢ Risk is additive
Neuroradiology 1211
1213 Subarachnoid Hemorrhage-Intracranial Aneurysms
SAH-induced Vasospasm Figure 5-16-12
• Occurs angiographically in 30%-70% of patients
• Clinical symptoms seen in 20%-45% of patients
• Adds 10%-20% significant morbidity/mortality
• Smooth muscle constriction and vessel wall edema,
infiltration and fibrosis leads to luminal narrowing
and decreased compliance
• Time course
➢ Range: 4-14 days
➢ Peak: 7-10 days
• Treatment
➢ Fluid status, blood pressure, calcium channel Severe vasospasm of the supraclinoid ICA and M1
blockers segment leading to poor perfusion of the right MCA
➢ Induced hypertension territory
➢ Angioplasty, intra-arterial infusion of vasodilators
CT of Subarachnoid Hemorrhage
[Figure 5-16-14]
CT Findings of Ruptured
Aneurysm [Figure 5-16-15]
Diagnostic Testing:
Lumbar puncture
Usually done when CT is negative or Acute SAH (left image)-SAH 5 days post bleed with CTA
equivocal showing PComA aneurysm (right two images)
• Should be done 6-12 hours after event
➢ Time it takes for xanthochromia to Figure 5-16-15
occur
➢ Xanthochromia is diagnostic
❖ Detectable in all patients
between 12 hrs and 2 wks
• Findings
➢ Elevated opening pressure
➢ Elevated RBCs that do not clear
❖ Unreliable way to r/o traumatic
tap
➢ Xanthochromia
NCCT shows extensive SAH, intraparenchymal hematoma with
fluid-fluid level, uncal and subfalcine herniation, small amount
of intraventricular blood, and an MCA aneurysm (arrow)
CTA with Active Extravasation CTA shows the location, size and relationship of the aneurysm
[Figure 5-16-17] to the surrounding branches, and active extravasation into the
hematoma
CTA of Small Aneurysms
[Figure 5-16-18] Figure 5-16-18
Neuroradiology 1213
1215 Subarachnoid Hemorrhage-Intracranial Aneurysms
DSA: Evaluation of Aneurysm Figure 5-16-20
• Location and number
• Size and configuration
• Characteristics of aneurysm neck
➢ neck to dome ratio; absolute size of neck
➢ slit, oval, round, wide
➢ relationship to adjacent vessels
• Suspected rupture site (“tits”)
• Collateral circulation distal to aneurysm
• Hemodynamics
• Calcification
• Intraluminal thrombus
Location
• Anterior circulation (80%-85%)
➢ ICA/PComA junction
➢ AComA complex
➢ MCA trifurcation
• Posterior circulation (15%-20%)
➢ Basilar terminus (5%)
➢ PICA
➢ SCA
Common locations for aneurysms on the anterior
Aneurysm Locations: Anterior Circulation circulation
[Figure 5-16-20]
Figure 5-16-21
Aneurysm Locations: Posterior Circulation
[Figure 5-16-21]
Aneurysm Measurements
• Aneurysm
➢ Small: less than 10 mm
➢ Large: 10-25 mm
➢ Giant: > 25 mm
• Aneurysm neck
➢ Absolute size
❖ Small: 4mm or less
➢ Dome to neck ratio Common locations for aneurysms on the posterior circulation
❖ Small: 2:1 or greater
Treatment Outcomes
• ISAT trial Permanent occlusion of the left ICA with detachable balloons
➢ Comparative study of coiling vs. results in flow perpendicular to the neck of the aneurysm and
clipping clotting of the dome
❖ 23.9% relative/7.4% absolute
risk reduction for coiling vs. clipping
➢ Controversial study Figure 5-16-28
• Should patients be offered the option of
coiling vs. clipping in the acute setting?
Deconstructive Therapy
[Figures 5-16-27 and 5-16-28]
1. Aryan H, Giannotta SL, Fukushima T, et al. Aneurysms in children: review of 15 years experience. J Clin
Neurosci 2006;13(2):188-92.
2. Claassen J, Bernardini GL, Kreiter K, et al. Effect of cisternal and ventricular blood on risk of delayed cerebral
ischemia after subarachnoid hemorrhage: the Fischer scale revisited. Stroke 2001; 32:2012-20.
3. Hamada Y, Mannoji H, Kaneko Y. A ruptured dissecting aneurysm of the vertebral artery: comparison of the
angiographic and histological findings. Neuroradiology 2001; 375-8.
4. Hoh BL, Cheung AC, Rabinov JD, et al. Results of a prospective protocol of computed tomographic angiography
in place of catheter angiography as the only diagnostic and pretreatment planning study for cerebral aneurysms by
a combined neurovascular team. Neurosurgery 2004; 54(6):1329-40.
5. Molyneux A, Kerr RS, Yu LM, et al. International subarachnoid aneurysm trial (ISAT) of neurosurgical clipping
versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised comparison of
effects on survival, dependency, seizures, rebleeding, subgroups, and aneurysm occlusion. Lancet 2005;
366(9488):809-17.
6. Nakatomi H, Segawa H, Kurata A, et al. Clinicopathological study of intracranial fusiform and dolichoectatic
aneurysms: insight on the mechanism of growth. Stroke 200; 31:896-900.
7. Schievink W. Intracranial aneurysms. [Review] NEJM 1997; 336(1):28-40.
8. Shojima M, Oshima M, Takagi K, et al. Magnitude and role of wall shear stress on cerebral aneurysm:
computation fluid dynamic study of 20 middle cerebral artery aneurysms. Stroke 2004; 35:2500-05.
9. Suarez JI, Tarr RW, Selman WI. Aneurysmal subarachnoid hemorrhage. Review NEJM 2006; 354:387-96.
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2001; 124:249-78.
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evaluation with CT angiography. Radiology 1998; 208: 423-430.
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Neuroradiology 1217
1219 Subarachnoid Hemorrhage-Intracranial Aneurysms
Intracranial Vascular Malformations
Mary E. Jensen, MD
Classification of IVMs
• Traditional (path-based)
➢ Arteriovenous malformations
❖ Pial
❖ Dural
➢ Venous vascular malformations
❖ Venous angioma
➢ Capillary telangectasias
➢ Cavernous angiomas
• Functional (flow-based)
➢ AV Shunting
❖ Pial AVM
❖ Cerebral AVF
❖ Dural AVF
➢ Non-shunting
❖ Capillary malformations
❖ Venous malformations
❖ Cavernous malformations
Epidemiology
• Detection rate of AVM
➢ 1.1:100,000 (excluding autopsy cases)
➢ 2.1:100,000 (including autopsy cases)
➢ 1.2:100,000 person-years (symptomatic)
• Prevalence
➢ 0.1% of US population (300,000 people)
➢ Point prevalence 18:100,000 adults
• Account for
➢ 1%-2% of all strokes
➢ 3% of strokes in young adults
➢ 9% of subarachnoid hemorrhage
➢ 4% of all intraparenchymal hemorrhages
❖ 1/3 of young adult hemorrhages
Etiology
• Congenital
➢ Sporadic
• Genetic
➢ Hereditary hemorrhagic telangectasia
❖ 4%-13% with cerebral AVMs
❖ ?ENG, ACVR1 gene mutations
❖ Encode proteins in TGFB1 receptor complexes
➢ Neurocutaneous disorders
Pathogenesis
• Wedge-shaped abnormal tangle of arteries and veins
➢ Arteries and veins linked by fistulae
➢ No normal capillary bed
➢ Deficient muscularis in small arteries
• Hemodynamic effects
➢ Fistulous effects
❖ High flow, rapid shunting
❖ Induced hypotension in feeders and adjacent areas (“arterial steal”)
➢ Opening of collateral pathways, “angiomatous change”
➢ Dysplastic appearance of feeding pedicles, “flow-induced angiopathy”
❖ Luminal dilatation or stenosis
❖ Aneurysms
Intracranial Vascular Malformations 1218
1220 Neuroradiology
Clinical Presentation
• Usually present before 40 years of age
➢ Men and women equally affected
• Hemorrhage is #1 complication (>50%)
➢ 2%-4% yearly rupture rate
❖ 6%-18% annual rate after first bleed
- Increased rate for the first year reported but not consistently noted
➢ 10%-18% mortality from hemorrhage
❖ 1.0%-1.5% annual rate
Clinical Presentation
• Seizures: 20%-25%
➢ Generalized more common than focal
• Headache: 15%
• Focal neurologic deficit: <5%
➢ Steal phenomenon is uncommon
• Pulsatile tinnitus
• Children (< 2 yr)
➢ Congestive heart failure
➢ Large head from hydrocephalus
➢ seizures
Location
• Supratentorial (85%), infratentorial (15%)
➢ Cortical AVMs (72%)
❖ Gyral, sulcal, mixed
➢ Subcortical AVMs (1%) Figure 5-17-1
➢ Deep AVMs (27%)
❖ Subarachnoid, parenchymal,
plexal, mixed
Hemorrhage Predictors
• Many are not consistent
➢ Radiologic findings
➢ Prior hemorrhage
➢ Small AVM in diameter or volume
➢ Increased feeding artery pressures
➢ Periventricular/intraventricular
location
An enlarged lenticulostriate running through the ventricle is the
Radiologic Predictors presumed source of hemorrhage
• Features that may result in a higher risk
of bleeding
➢ Arterial aneurysms (10%) Figure 5-17-2
➢ Intranidal aneurysms (20%-58%)
➢ Arterial supply from perforators
➢ Location
❖ Intraventricular/periventricular
❖ Basal ganglia, thalamus
➢ Deep venous drainage
➢ Single venous drainage outlet
➢ Venous stenosis
Intraventricular Hemorrhage
[Figure 5-17-1] CTA, MRA and DSA all show intranidal aneurysm within a
small AVM
Intraparenchymal Hemorrhage
[Figure 5-17-2]
Neuroradiology 1219
1221 Intracranial Vascular Malformations
Hemorrhage Risk: Summary
• Lowest-risk group (1%)
➢ No history of prior hemorrhage
➢ >1 draining vein
• Highest-risk group (8.9%)
➢ History of prior hemorrhage
➢ Single draining vein
➢ Diffuse nidus
AVM Grading
• There are many grading systems
• The most commonly used is the Spetzler-Martin system
➢ Size (<3 cm = 1, 3-6 cm = 2, >6 cm = 3)
➢ Eloquence of surrounding brain
(non-eloquent = 0, eloquent = 1)
➢ Pattern of venous drainage (superficial = 0, deep = 1)
Radiographic Evaluation
• CT
➢ Usual first study
➢ Hemorrhage, calcifications,
parenchymal changes, iso- or
hyperdense serpentine structures
➢ Contrast study outlines boundaries
• CTA
➢ Vascular elements NCCT shows enlarged MCA trunk and sylvian arteries,
❖ Location of feeding intraventricular hemorrhage, focal atrophy and hyperdense
arteries/draining veins vessels
❖ Associated aneurysms
➢ Volumetric determination Figure 5-17-4
Radiographic Evaluation
• Angiography
➢ Arterial supply, regional and individual
➢ High flow arteriopathy
❖ stenosis
❖ dolichoectasia
❖ flow related aneurysms (10%)
➢ Arterial supply to the brain
T1 images without and with Gd (left images)
❖ Pial
T2 and FLAIR images (right images)
❖ Dural
➢ Assessment of nidus
❖ plexiform vs. fistulous Figure 5-17-6
❖ intra-nidal aneurysms and ectasias
❖ true nidus vs. angiomatous change
Figure 5-17-8
Figure 5-17-7
Superselective
injections of a
temporal lobe AVM
(A) show different
nidal components
including a
macrofistula (B) and a
racemose nidus (C)
Neuroradiology 1221
1223 Intracranial Vascular Malformations
Radiographic Evaluation Figure 5-17-9
• Angiography
➢ Venous drainage, regional and individual
➢ High-flow venopathy
❖ dural sinus high-flow
❖ venous thrombosis
❖ venous enlargement, stenoses, varix
➢ Normal drainage of the brain
Treatment
• Controversial
➢ Observation
➢ Microsurgery Superselective study (right) of temporal AVM
➢ Embolization shows multiple “en passage” feeders with distal
➢ Stereotactic radiosurgery arterial supply to normal brain
➢ Combination therapy
Figure 5-17-10
Figure 5-17-11
Figure 5-17-12
Intracranial AVFs
• Dural
➢ Most common type of cerebral AV fistula
➢ Shunt occurs primarily from dural arteries to
dural sinuses or cortical veins
• Cerebral
➢ Rare
➢ Pediatric population
❖ Vein of Galen malformation
❖ Pial
Pre- and post-embolization of distal pericallosal
artery with coils and NBCA
Etiology/Pathogenesis
• Adults (Dural AVF)
➢ Acquired lesions
❖ Present in later life (40s-60s) Figure 5-17-14
❖ Shunting within dural/venous wall
❖ Sinus thrombosis
- Environment conducive to the
development of DAVF
- Triggered by factors which stimulate
angiogenesis
• Children (Pial AVF)
➢ Congenital lesions
❖ ?vascular remodeling of the venous
endothelial cells in the capillary bed caused
by a trigger such as hypoxia
Newborn with congestive heart failure and cranial
Pial A-V Fistula [Figure 5-17-14] bruit
Location of DAVFs
• Transverse - sigmoid sinus: 62.6 %
• Cavernous sinus: 11.9 %
• Tentorial - incisural: 8.4 %
• Convexity - sagittal sinus: 7.4 %
• Orbital - anterior falx area: 5.8 %
• Sylvian - middle fossa area: 3.7 %
• Others: marginal sinus, etc
Classification of DAVFs
• Borden, Djindjian and Merland, Cognard
➢ Venous drainage
❖ Sinus vs. cortical veins
➢ Direction of flow
❖ Antegrade, retrograde, both
➢ Involvement of cortical venous drainage
❖ Benign vs. aggressive
❖ Determines risk
Borden Classification
Neuroradiology 1223
1225 Intracranial Vascular Malformations
Benign: All Classifications [Figure 5-17-15] Figure 5-17-15
Clinical Presentation
• Symptoms and signs vary with location
• Tinnitus, bruit
➢ Cranial nerve palsies
➢ Orbital congestion
➢ Focal neurological deficits
➢ Global neurological deficits
➢ Hemorrhage Benign transverse sinus DAVF with fistulous flow
❖ ICH: 35%-42% overall; only to sinus
75%-95% in tentorial, ACF
Figure 5-17-16
Hemorrhage Associated with DAVF
[Figure 5-17-17]
Clinical Outcomes
• Without cortical venous involvement
➢ Symptom improvement or resolution
❖ No treatment: 81%
❖ Treatment: 86%
• With cortical venous involvement
➢ non-hemorrhagic neurological deficit: 6.9%/yr
➢ Hemorrhage: 8.1%/yr Aggressive transverse sinus DAVF with all fistulous
➢ Mortality: 10.4%/yr flow into the cortical veins
• Malignant transformation of benign lesion: <1%
Figure 5-17-17
Radiographic Evaluation
• Acute symptoms
➢ CT to rule out hemorrhage
➢ MRI/A, CTA to show prominent vessels
❖ Not adequate for demonstration of shunt
➢ DSA
❖ Confirm diagnosis
❖ Identify angioarchitecture
❖ Evaluate hemodynamics
• Chronic symptoms
➢ Contrast CT/MR
➢ DSA
Tentorial DAVF with SAH (left) and transverse
Aggressive DAVF [Figure 5-17-18] sinus DAVF with ICH (right)
Figure 5-17-18
Treatment
• Benign
➢ Observation
• Aggressive
➢ Endovascular therapy
❖ Transvenous, transarterial,
combined
➢ Surgery
❖ Failed endovascular therapy
❖ Isolated sinus that required
direct puncture/exposure
Diffusion study shows temporal lobe edema and old
Developmental Venous Anomaly hemorrhage; Gd MRI shows marked venous congestion and a
• Most common type of vascular multi-channel left transverse sinus; DSA confirmed
malformation development of a DAVF
Pathology
• Veins are closely aggregated and dilated
➢ lack muscular and elastic fibers
➢ abnormally hyalinized
• Normal adjacent arteries
• Adjacent parenchyma
➢ Normal
➢ Gliosis, neuronal degeneration, demyelination
➢ May be associated with focal neuronal migrational abnormalities
Clinical Presentation
• Incidental finding in most cases
➢ Associated with H/N vascular malformations
• Rarely cause neurologic symptoms
➢ Posterior fossa
❖ Dizziness, ataxia, diplopia
➢ Cerebrum
❖ Seizures, headaches, focal deficits
• Hemorrhage
➢ Not the DVA that hemorrhages, but the associated cavernoma
• Treatment
➢ Surgery may be required to remove hemorrhage/cavernoma
➢ Leave DVA
Imaging Findings
• NCCT
➢ Normal
➢ Ill-defined hyperdense area without edema or mass effect
• CECT
➢ Diffuse enhancement of linear vessels adjacent to the ventricle
❖ Stellate pattern
❖ Converge on collector vein
❖ Well-visualized on CTA
• MR
➢ Variable degrees of T2 and T1 prolongation in the adjacent parenchyma
❖ Due to increased blood pool
➢ Signal intensity void in draining vein on T2
➢ Occasionally gliosis
➢ Associated with cavernomas in 8%-33% of DVAs
➢ CE MR
❖ Dilated deep veins converge on a collector vein
❖ Follows a transhemispheric course to a normal vein
• Angiography
➢ Pathognomonic
➢ Normal arterial phase
➢ Radially oriented dilated medullary veins converge on an enlarged
transcortical draining vein
❖ Caput medusa opacifies at the same time as normal veins
❖ Collector vein seen on late venous phase
➢ Location
❖ In the deep white matter near the margin of an adjacent ventricle
❖ Frontal>parietal>brachium pontis/dentate
❖ Frontal lobes may opacify earlier and show a capillary blush
Neuroradiology 1225
1227 Intracranial Vascular Malformations
Developmental Venous Anomaly [Figure 5-17-19]
Cavernous Angioma
• Prevalence: 0.5%-0.7% on MR/autopsy
• Account for 5%-13% of cerebral VMs
• Sporadic
• Familial form
➢ Autosomal dominant, Hispanic
➢ Multiple lesions
➢ Increased number of lesions with aging
➢ Correlation of symptoms with the presence of high signal intensity lesions
on MR
Figure 5-17-19
Pathology
• Gross findings
➢ Small, reddish-purple (“mulberry”)
lesions
➢ Few mms to several cms
➢ Multiple or single
➢ Often encapsulated and multilobar
➢ Occasionally calcified
➢ Often associated with DVA
➢ Found throughout the CNS
Pathology
• Histologic findings
➢ Thin-walled vascular sinusoids
➢ Endothelium lacks smooth muscle,
elastin, and intervening parenchyma
➢ Lacks blood brain barrier
➢ Surrounded by hemosiderin
deposits and gliosis
➢ May or may not be thrombosed
NCCT and T1 and T2 weighted MRI shows dystrophic
Clinical Presentation microcalcifications and/or hemosiderin staining in the right
• Usually present between age 30-50 basal gangliar region
years
• Symptoms
➢ Seizures
❖ Lesions usually in frontal or temporal lobe
➢ Focal neurologic deficits Figure 5-17-20
➢ Acute hemorrhage
❖ Risk is 0.25%-6% per year
❖ Increased risk with previous hemorrhage,
pregnancy
➢ Headache
Imaging Findings
• CT
➢ Variable density
❖ Hemorrhage
❖ Calcification
- Rim, coarse, stippled, granular DSA shows “caput medusa” in early venous phase
• DSA followed by filling of the collector vein
➢ Cavernous angioma not visualized
➢ Associated DVA
Treatment
• Stereotactic microsurgery
➢ Reasons for surgery
❖ Repeat hemorrhage
T1, T2 and GRE images show a Type 2 lesion in the right
❖ Mass effect from enlarging
frontal lobe and a Type 4 lesion in the left occipital lobe
lesion
❖ Seizure focus
• Radiosurgery
➢ Controversial
➢ Associated with hemorrhage and
radiation-induced mass effect
• Follow
➢ Deep lesions
➢ Familial lesions
Figure 5-17-23
Capillary Telangiectasia
• Represents 16%-20% of all CVMs
• Incidental finding
➢ Nearly always asymptomatic
➢ Sx: headache, vertigo, ataxia, hearing loss
• Congenital vs. acquired lesions
➢ Obstructed venous drainage; radiation
• May be associated with VA, CM, AVM
➢ “Transitional malformations”
Neuroradiology 1227
1229 Intracranial Vascular Malformations
Pathology
• Location
➢ Pons, cerebral/cerebellar hemispheres, spinal cord
• Histology
➢ Thin-walled, “capillary-type,” ectatic blood vessels
➢ Interspersed with normal brain
• Size
➢ Few millimeters to 2 cm
• Hemorrhage
➢ Rare
➢ Usually from an associated vascular malformation
Figure 5-17-24
Imaging [Figure 5-17-23]
• CT
➢ Usually normal
• MR
➢ T1: hypo- or isointense
➢ T2: iso- or slightly hyperintense
➢ GRE: hypointense
❖ Most consistent finding
❖ Due to intravascular
deoxyhemoglobin
➢ CE-MR
❖ Faintly enhance in a “stippled”
or “brushlike” pattern
❖ 2/3d with enlarged vessel
Typical MR findings in a capillary telangiectasia
References
1. Al-Shani R, Warlow C. A systematic review of the frequency and prognosis of arteriovenous malformations of the
brain in adults. Brain 2001; 124:1900-26.
2. Augustyn GT, Scott JA, Olson E, et al. Cerebral venous angiomas: MR imaging. Radiology 1985; 156:391–395
3. Camacho DL, Smith JK, Grimme JD, et al. Atypical MR imaging perfusion in developmental venous anomalies.
AJNR Am J Neuroradiol 2004; 25(9):549-52.
4. Gault J, Sarin H, Awadallah N, et al. Pathobiology of human cerebrovascular malformations: basic mechanisms
and clinical relevance. Neurosurgery 2004; 55(1):1-17.
5. Lai CW, Agid R, van den Berg R, ter Brugge K. Cerebral arteriovenous fistulas induced by dural arteriovenous
shunts. AJNR J Neuroradiol 2005; 26:1259-62.
6. Lawton MT, UCSF Brain Arteriovenous Malformation Study Project. Spetzler-Martin Grade II arteriovenous
malformations: surgical results and a modification of the grading scale. Neurosurgery 2003; 52(4):740-8.
7. Mast H, Young WL, Koennecke HC, et al. Risk of spontaneous haemorrhage after diagnosis of cerebral
arteriovenous malformation. Lancet 1997; 350:1065-8.
8. Ogilvy C, Steig P, Awad I, et al. Recommendations for the management of intracranial arteriovenous
malformations. A statement for health care professionals from a special writing group of the Stroke Council,
American Stroke Association. Circulation 2001; 103:2644-57.
9. Peebles TR, Vieco PT. Intracranial developmental venous anomalies: diagnosis using CT angiography. J Comput
Assist Tomogr 1997; 21(4): 582-6.
10. Sakata N, Takebayashi S, Kojima M, et al. Different roles of arteriosclerosis in the rupture of intracranial
dissecting aneurysms. Histopathology 2001; 38(4):325-37.
11. Stapf C, Mohn JP, Choi JH et al. Invasive treatment of unruptured brain arteriovenous malformations is
experimental therapy. Current Opinion in Neurology 2006; 19(1):63-8.
12. The Arteriovenous Malformation Study Group. Arteriovenous malformations of the brain in adults. NEJM 1999;
340(23):1812-18.
13. The Scottish Intracranial Vascular Malformation Group. Prospective, population-based detection of intracranial
vascular malformations in adults. Stroke 2003; 34:1163-69.
Summary
• Meningeal Disease
➢ Epidural abscess
➢ Subdural empyema
➢ Meningitis
• Parenchymal Infection
➢ Cerebritis to abscess
➢ Encephalitis – HSV, CJD, ADEM
➢ Parasitic – Cysticercosis, Lyme disease
➢ Tuberculosis
➢ Mycotic
➢ AIDS related infections
Intracranial Infection
• Location
➢ Intra-axial – Parenchymal Figure 5-18-1
➢ Extra-axial – Epidural, subdural, leptomeningeal
• Response to infection
➢ Edema and swelling
➢ Mass and mass effect
➢ Abnormal enhancement
➢ Chronic – Atrophy
Blood-brain barrier
• Tight junctions (no gaps) exist between normal endothelial cells
• Little communication between capillary & extracellular space or
neurons
• Infection results in loss of tight junctions, with increased
permeability of endothelial membranes = LOSS OF BBB
• Loss of BBB + increased local blood volume = ABNORMAL
ENHANCEMENT
Subdural empyema
Intracranial infection – Location Meninges (courtesy of Amirsys, Inc.)
• Dura mater –
➢ 2 layers
➢ Outer layer is calvarial periosteum
➢ Inner layer is separation between dura mater and arachnoid
• Collection between inner table of skull & dura is EPIDURAL
Figure 5-18-2
Intracranial infection – Location Meninges [Figure 5-18-1]
• Arachnoid Mater
➢ Thin connective tissue
➢ Parallels dura mater
• Collection between dura & arachnoid is SUBDURAL
• Subdural space is potential space w/ bridging veins
Neuroradiology 1229
1231 Imaging of Intracranial Infections
Extra-axial Infection Epidural [Figures 5-18-3 and 5-18-4] Figure 5-18-3
• Usually starts in paranasal sinuses or mastoids
• Low density on CT
• Enhancing periphery
• ? SI on T1
• ? SI on T2, FLAIR
• Enhancing dura
• Check for osteomyelitis of calvarium
Meningitis, complications
• Hydrocephalus
• Ependymitis
➢ Subependymal enhancement
➢ In HIV disease, diff dx is lymphoma
Meningitis, complications
• Infarction
• May be arterial or venous
• Well-demarcated – best way to differentiate from cerebritis
• Typical CT/MR features with restricted diffusion on DWI
Neuroradiology 1231
1233 Imaging of Intracranial Infections
Cerebritis to brain abscess Figure 5-18-10
• Early cerebritis
➢ 3-5 days after infection
➢ Unencapsulated – white cells, edema, necrosis,
petechial hemorrhage
• Late cerebritis
➢ 4-14 days after infection
➢ Poorly delineated rim, necrotic core, white
cells/inflammatory cells, granulation tissue
Herpes encephalitis
• Adults - HSV-1 (oral) Frontal sinusitis resulting in frontal abscess, with
• Neonates – HSV-2 (genital) low signal rim on T2, and enhancement
• Confusion, progressing to coma
• 50%-70% mortality, especially when delay to diagnosis (most common cause
of fatal encephalitis)
• Necrotizing hemorrhagic encephalitis, often resulting in diffuse atrophy
• Axonal spread from reactivation in trigeminal ganglion
Herpes encephalitis
• Imaging may be normal early in disease course
• MR > CT, especially early
• MR
➢ Inc. SI on T2 & FLAIR
➢ Mass effect
➢ +/- enhancement Herpes encephalitis of left temporal lobe
➢ 60% bilateral
➢ May have small punctate hemorrhage Figure 5-18-14
Herpes encephalitis [Figure 5-18-14]
• Subtle, gyral enhancement
• Unilateral early, then bilateral
• Temporal lobes, insular cortex, inferior frontal lobes,
cingulate gyri
Creutzfeldt-Jakob Disease
• Transmissible spongiform encephalopathy (TSE)
• Prion: proteinaceous infectious particle
• Sporadic – most common (85%-90%)
• Genetic (10%-15%)
• Infectious (rare)
Creutzfeldt-Jakob Disease
CLASSIC CJD VARIANT CJD
• Older (mean 68 yrs) Younger (mean 28 yrs)
• Sporadic BSE contaminated food
• Shorter duration Longer duration Herpes encephalitis, with high SI in temporal
• Dementia Behavior changes lobes and patchy enhancement
• Rare “pulvinar sign” “Pulvinar sign” on MR >
75%
• Variable amounts of PrPres Lots of PrPres
CNS Tuberculosis
• Increasing incidence – homeless, prisoners (2%-5% of pts. w/ TB)
• AIDS population
• Hematogenous dissemination from lungs
• Most have pulmonary TB
• Drug resistance increasing & ominous
• Either meningitic or tuberculoma, rarely both forms found together
Neuroradiology 1233
1235 Imaging of Intracranial Infections
CNS Tuberculosis Cerebritis [Figure 5-18-15] Figure 5-18-15
CNS TuberculosisTuberculoma
• Most common parenchymal form(may
be extra-axial)
• Supratentorial > infra
• Dense fibrous capsule with caseous
necrotic core
CNS Tuberculosis Tuberculoma TB cerebritis with typical pattern of right temporal edema and
[Figure 5-18-16] enhancement
• Small or coalesced larger nodules
• Edema, mass effect
• Wall may have increased SI on T1, decreased SI on T2 Figure 5-18-16
• Old/treated lesions may Ca+
Neurocysticercosis
• Taenia solium (Pork tapeworm)
• Worldwide, most common CNS infection
• Worldwide, most common cause of epilepsy
• Central/South America; East/SE Asia; India; Africa
• CNS disease: 60%-90%
• Seizures, intracranial hypertension, focal deficit
• Four variants
➢ 1. Parenchymal
➢ 2. Intraventricular
➢ 3. Cisternal Multiple tuberculomas, with low signal intensity rim
➢ 4. Spinal on T2 and enhancement
Parenchymal Cysticercosis
• Vesicular stage
➢ Eccentric nodule (scolex), no edema or enhancement
• Colloidal stage
➢ Dying scolex, capsule thickens, extensive edema & enhancement
• Granular nodular stage
➢ Cyst ? in size, small enhancing nodules, no edema
• Nodular calcified stage
➢ Cyst involutes, calcifies, no edema or enhancement Figure 5-18-17
Parenchymal Cysticercosis
Vesicular stage
• Larva is fully grown,with thin intact capsule
surrounding distended bladder
• Fluid in bladder is clear, no surrounding inflammatory
reaction.
• Well-defined cyst, scolex enhances (mural nodule)
• Wall does not enhance, no edema
Parenchymal Cysticercosis
Colloidal stage [Figure 5-18-17] Colloidal stage of CNS cysticercosis, with thick
• Larva degenerates, cyst fluid turbid capsule, edema, and mass effect
• Cyst wall thickens
• Vasogenic edema
• Cyst fluid ? SI on T1WI
• Cyst wall ? SI on T2WI
• Vasogenic edema & enhancement
Cisternal Cysticercosis
• Basilar cisterns or sylvian fissures Intraventricular and subarachnoid
• MRI more sensitive than CT cysticercosis, with hydrocephalus
• Can incite leptomeningeal inflammatory response
• Hydrocephalus, infarctions
Human Retroviruses
• HIV (HIV-1 and HIV-2) and HTLV-1
• HIV-1 found in CNS in AIDS (neurotrophic) Patchy symmetric abnormal signal
• Encephalopathy, myelopathy, peripheral neuropathy, myopathy intensity in patient with HIV
• HIV replicates in multinucleated giant cells & macrophages in encephalitis
CNS
• Oligodendrocytes, astrocytes, neurons less frequently directly infected
Neuroradiology 1235
1237 Imaging of Intracranial Infections
HIV Leukoencephalopathy Figure 5-18-20
• Disease on MR parallels clinical progression
• NAA/Cho & NAA/Cr ratios reduced due to neuronal
loss
Toxoplasmosis
• Necrotic debris, inflammatory cells, organisms Figure 5-18-22
• Vasogenic edema
• Robust enhancement
• 15% are solitary
• Pyrimethamine + sulfa or clindamycin
• Life-long maintenance abs
Cryptococcus neoformans
• Ubiquitous fungi within contaminated soil
• Inhaled, then hematogenous spread immuno- compromised hosts
• Most common fungus in AIDS (6%-7%)
• Subacute meningitis, HA, AMS, fever
• DX – India ink preparation, antigen in CSF, fungal culture of CSF Figure 5-18-23
• Perivascular spaces distended with mucoid material and fungus
Cryptococcus meningitis
• Basal ganglia,often bilateral
• CT may be normal
• Non-enhancing low density lesions in Virchow-Robin
spaces “gelatinous pseudocysts”
HAART
• Ability to mount immune response may change imaging findings, especially enhancement patterns
• Enhancement in crypto. meningitis
Summary
• Meningeal Disease
➢ Epidural empyema
➢ Subdural empyema
➢ Meningitis
• Parenchymal Infection
➢ Cerebritis to abscess
➢ Encephalitis – HSV, CJD, ADEM
➢ Parasitic – Cysticercosis, Lyme disease
➢ Tuberculosis
➢ Mycotic
➢ AIDS related infections
References
1. Chang L, Ernst T. MR spectroscopy and diffusion-weighted MR imaging in focal brain lesions in AIDS.
Neuroimaging Clin N Am. 1997 Aug;7:409-26.
2. Collie DA, Summers DM, Sellar RJ, et al. Diagnosing variant Creutzfeldt-Jakob disease with the pulvinar sign:
MR imaging findings in 86 neuropathologically confirmed cases. AJNR Am J Neuroradiol. 2003l 24:1560-9.
3. Enzman DR, Britt RH, Obana WG, et al. Experimental staphylococcus aureus brain abscess. AJNR 7:395-402,
1986
4. Fernandez RE, Rothbert M, Ferencz G, et al. Lyme disease of the CNS: MR imaging findings in 14 cases. AJNR
1990;11:479-481
5. Filippi CG, Sze G, Farber SJ, et al. Regression of HIV encephalopathy and basal ganglia signal intensity
abnormality at MR imaging in patients with AIDS after the initiation of protease inhibitor therapy. Radiology
1998;206:491-498
6. Galassi W, Phuttharak W, Hesselink JR, et al. Intracranial meningeal disease: comparison of contrast-enhanced
MR imaging with fluid-attenuated inversion recovery and fat-suppressed T1 weighted sequences. AJNR 2005; 26:
553-9
7. Gaviani P, Schwartz RB, Hedley-Whyte ET, et al. Diffusion-weighted imaging of fungal cerebral infection. AJNR
Am J Neuroradiol. 2005 May;26(5):1115-21.
8. Han XY, Weinberg JS, Prabhu SS, et al. Fusobacterial brain abscess: a review of five cases and an analysis of
possible pathogenesis. J Neurosurg 2003; 99: 693-700
9. Kramer LD, Locke GE, Byrd SE, et al. Cerebral cysticercosis: documentation of natural history with CT.
Radiology 1989;171:459-462
10. Lai PH, Li KT, Hsu SS, et al. Pyogenic brain abscess: findings from in vivo 1.5 T and 11.7 T in vitro proton MR
spectroscopy. AJNR 2005; 26:279-88
11. Murata T, Shiga Y, Higano S, et al. Conspicuity and evolution of lesions in Creutzfeldt-Jakob disease at diffusion-
weighted imaging. AJNR Am J Neuroradiol. 2002; 23:1164-72
12. Nadal Desbarats L, Herlidou S, de Marco G, et al. Differential MRI diagnosis between brain abscess and necrotic
or cystic brain tumors using the apparent diffusion coefficient and normalized diffusion-weighted images. Magn
Reson Imaging 2003; 21: 645-650
13. Post MJD, Tate LG, Quencer RM, et al. CT, MR, and pathology in HIV encephalitis and meningitis. AJNR 1988;
9:469-476
14. Prusiner SB. Prions and neurodegenerative diseases. N Engl J Med. 1987; 317:1571-81.
15. Sze G, Zimmerman RD. The magnetic resonance imaging of infections and inflammatory diseases. Radiol Clin
North Am. 1988: 26:839-59.
16. Tien RD, Felsberg GJ, Osumi AK. Herpesvirus infections of the CNS: MR findings. AJR Am J Roentgenol. 1993
Jul;161:167-76.
17. Wehm SM, Heinz ER, Burger PC, et al. Dilated Virchow-Robin spaces in cryptococcal meningitis associated with
AIDS: CT and MR findings. J Comput Assist Tomogr 1989;13:756-762
Neuroradiology 1237
1239 Imaging of Intracranial Infections
The Paranasal Sinuses
Patricia A. Hudgins, MD
Ethmoid sinus
• Bilateral
• Groups of cells formed by septa and lamella
• Anterior ethmoids
➢ Multiple small cells
➢ Middle turbinate
• Posterior ethmoids Pneumatized agger nasi cell on left
➢ Fewer but larger cells on coronal CT
• Basal lamella
➢ Lateral insertion of middle turbinate Figure 5-19-3
➢ Separates ant from post ethmoids
Maxillary sinus
• Drainage
➢ Ostium is at superomedial portion
➢ Drains into infundibulum Maxillary sinus cilia beat secretions
• Uncinate process up and medial, drain via maxillary
➢ Medial wall of ostium sinus ostium into infundibulum
➢ Located at insertion of inferior turb on lateral nasal wall Figure 5-19-5
➢ Contiguous with lacrimal bone anteriorly
Ostiomeatal complex
(courtesy of Amirsys, Inc.)
Neuroradiology 1239
1241 Paranasal Sinuses
Normal OMU [Figure 5-19-8] Figure 5-19-8
• 3 turbinates/meati
• Frontal recess
• Infundibulum and middle meatus
Ostiomeatal complex
(Courtsey of Amirsys, Inc)
Neuroradiology 1241
1243 Paranasal Sinuses
• Lymphoma of maxillary antrum Figure 5-19-14
• SCCa maxillary sinus
• Adenoid cystic ca
Sinusitis - Fungal
• Two distinct forms
• Acute, fulminant invasive fungal sinusitis
• Allergic fungal sinusitis with sino-nasal polyps
• Imaging appearance variable for both
Figure 5-19-17
Figure 5-19-19
Fungal sinusitis
• Acute invasive Figure 5-19-20
➢ Immunesuppressed
➢ Acute
➢ Pain, fever, local invasion
➢ May be fulminant, rapidly progress
➢ Often treated surgically local resection, orbital
exenteration
➢ High mortality
• Allergic fungal
➢ Clinically well
➢ Aspirin intolerance
➢ Chronic
➢ Presents with nasal obstruction
➢ Txed with endoscopic polyp resection
➢ High rate of recurrence
Neuroradiology 1243
1245 Paranasal Sinuses
Mucocele [Figure 5-19-21] Figure 5-19-21
• Airless, expanded sinus
• Sinus walls thinned, may appear dehiscent
• Frontal, ethmoid, maxillary, sphenoid in order of
frequency
• CT/MR signal intensity variable, depending on age of
secretions
• Check sinus ostium for obstructing lesion
Figure 5-19-23
Neuroradiology 1245
1247 Paranasal Sinuses
SCCa Staging – critical findings Figure 5-19-27
• Primary site
➢ Size
➢ Bone - maxillary or orbit walls, skull base
➢ Local - cheek, nasal cavity, nasopharynx, orbit
Neuroradiology 1247
1249 Paranasal Sinuses
The Sella and Parasellar Region
Patricia A. Hudgins, MD
Neuroradiology 1249
1251 Sella and Parasellar Region
Pituitary Microadenoma Figure 5-20-6
Sella: Pathology
• Pituitary Microadenoma
• Dynamic Imaging
➢ Increases sensitivity (10% seen only on dynamic
MR)
➢ Enhances slower than normal gland
Physiologic Hypertrophy
• Maximum normal height
➢ 6 mm infants and children Pituitary hypertrophy in a patient with
➢ 8 mm males, postmenopausal females hypothyroidism
➢ 10 mm young women (convex superiorly)
➢ 12 mm late pregnancy, postpartum females (convex superiorly)
• Abnormal hypertrophy
➢ End-organ failure (esp. hypothyroid) Figure 5-20-7
➢ Neuroendocrine tumor (rare)
Lymphocytic hypophysitis
• During pregnancy or shortly after delivery
• F >>> M
• Pituitary insufficiency
• H/A & visual changes
• Amenorrhea or inability to lactate
• Diffuse enlargement of adenohypophysis
• May mimic hyperplasia or adenoma
Lymphocytic hypophysitis
Suprasellar: Pathology
• Macroadenoma
➢ > 10mm
➢ Enlarged sella turcica
➢ Sellar/suprasellar
➢ MR test of choice
➢ Robust enhancement
➢ ? Cav. sinus invasion, mass effect on chiasm
Pituitary Adenoma
• Prolactinoma
➢ 30% of adenomas
➢ Female >> Males
➢ Galactorrhea
➢ Amenorrhea
➢ Serum PRL > 150ng/mL
➢ If > 1000ng/mL, cavernous sinus invasion
Neuroradiology 1251
1253 Sella and Parasellar Region
Pituitary Macroadenoma: CT
• CECT
➢ Enlarged sella turcica
➢ Moderate to strong enhancement
➢ May be heterogeneous (cysts, hemorrhage)
Pituitary Macroadenoma: MR
Figure 5-20-10
Invasive macroadenoma
(courtesy of Amirsys, Inc.)
Pituitary Apoplexy
1. Hemorrhage into tumor
2. Pituitary gland infarction
• Acute onset Figure 5-20-11
• Headache, visual changes, vomiting
• Usually hemorrhagic, may be non-hem
• May be life threatening
Suprasellar: Pathology
• Meningioma
➢ 2nd most common (adults)
➢ 15% of meningiomas Pituitary apoplexy can be hemorrhagic or not
❖ Tuberculum sellae
❖ Clinoid processes
❖ Cavernous sinus
➢ Look for pituitary gland distinct from mass
➢ Sag images helpful
Suprasellar: Aneurysm
• Third most common lesion in adults
• Noncalcified suprasellar mass
• Must differentiate from other suprasellar masses
➢ Macroadenoma
➢ Meningioma
Suprasellar: Aneurysm - CT
• Noncalcified central suprasellar mass
• Can be difficult to distinguish from adenoma, Suprasellar meningioma on T2 and post-contrast
meningioma T1 coronal images
Figure 5-20-14
Figure 5-20-15
Suprasellar: Aneurysm
Craniopharyngioma: CT
• NECT scan
➢ Adamantinomatous
❖ 90% Ca++ (rim)
❖ 90% Cystic
➢ May enlarge sella
➢ Papillary type
❖ 50% Ca++
❖ Majority solid
• CECT scan
➢ 90% enhance
➢ Solid Complex multiloculated sellar and suprasellar
➢ Nodular craniopharyngioma
➢ Rim
Craniopharyngioma: MR
• Variable signal
• Often heterogeneous
• Ca++ difficult to detect
• Nodular & rim enhancement
• Occasionally optic tract hyperintensity on T2WI – mass effect
Chiasmatic-hypothalamic glioma
• Clinical
➢ Second most common suprasellar mass in children
➢ Often large at presentation
➢ H/A, visual, endocrine abnormalities common
➢ M=F
➢ 15%-30% have NF-I
Chiasmatic-hypothalamic glioma
• Pathology
➢ 30% of all pilocytic astrocytomas occur in chiasm or hypothalamus
➢ 75% Pilocytic astrocytoma
➢ 25% Low-grade fibrillary
➢ Long-term survival (90% at 5 yrs, 75% at 10 yrs)
Figure 5-20-18
Chiasmatic-hypothalamic glioma - MR
• Variable signal
• Iso-, hypointense on T1WI
• Hyperintense on T2WI
• Variable enhancement
• Spread along optic tracts common
Hypothalamic Hamartoma
Comparison of suprasellar pediatric lesions
Suprasellar Mass: Child [Figure 5-20-20]
• Cranio
➢ Complex mass
➢ 90% cystic
➢ 90% calcified
• Astrocytoma
➢ Chiasm/Hypoth
➢ T2 hyperintense
➢ Variable C+
• Hamartoma
➢ Hypothalamus
➢ GM signal
➢ No C+
Germinoma: Imaging
• CT & MR
➢ Combined lesion typical but may affect only infundibular stalk
➢ May be hyperdense (CT)
➢ Isointense T1WI
➢ Hyper- to isointense T2WI
➢ Enhances homogeneously
➢ CSF dissemination common
Germinoma: MR
Sarcoid
• Clinical
➢ Chronic, multisystem, inflammatory disease
➢ Noncaseating granulomas
➢ Neurologic findings 5%
➢ Diabetes insipidus or hormone deficiency
➢ Steroid responsive
Lymphoma
• Imaging
➢ Pituitary gland, hypothalamus, stalk
➢ Hyperdense on CT
➢ T1 Iso- to hypointense
➢ T2 hypointense Lymphoma
➢ Homogeneous enhancement
Metastasis:Infundibulum
Presentation Summary
• Intrasellar Mass
➢ Microadenoma, Rathke cleft cyst
• Suprasellar Mass
➢ Craniopharyngioma, Macroadenoma, Meningioma, Aneurysm
• Infundibular Lesion
➢ Germinoma, LCH
➢ Granulomatous disease, LH
References
1. Bonneville JF, Cattin A, Racle A, et al: Dynamic CT of the laterosellar extradural venous spaces. AJNR 1989; 10:
535-542
2. Cottier J-P, Destrieux C, Brunereau L, Bertrand P, Moreau L, Jan M, Herbreteau D. Cavernous sinus invasion by
pituitary adenoma: MR imaging. Radiology 2000; 215:463-469
3. Elster AD, Chen MYM, Williams DW III, et al: Pituitary gland: MR imaging of physiologic hypertrophy in
adolescence. Radiology 1990;174: 681-685
4. Elster AD, Sanders TG, Vines FS, et al: Size and shape of the pituitary gland during pregnancy and post partum:
measurement with MR imaging. Radiology 1991; 181 :531-535
5. Elster AD. Modern imaging of the pituitary. Radiology 1993; 187: 1-14
6. FitzPatrick M, Tartaglino LM, Hollander MD, Zimmerman RA, Flanders AE. Imaging of sellar and parasellar
pathology. Radiol Clin North Am 1999;37:101-121
7. Sato N, Tanaka S, Tateno M, Ohya N, Takata K, Endo K. Origin of posterior pituitary high intensity on T1-
weighted magnetic resonance imaging: immunohistochemical, electron microscopic, and magnetic resonance
studies of posterior pituitary lobe of dehydrated rabbits. Invest Radiol 1995; 30:567-571
Neuroradiology 1257
1259 Sella and Parasellar Region
Congenital Spinal Anomalies
Erin Simon Schwartz, MD
Figure 5-21-1
Spinal Dysraphism [Figure 5-21-1]
• Defect of closure of neural tube
• For defects of primary neurulation
➢ Involving tubulation of neural plate, separation
from ectoderm, disjunction of superficial from
neural ectoderm
Axial schematic of
lumbar MMC with
placode forming dorsal
wall of expanded CSF
space
HemiMMC/Hemimyelocele
• Canal split, only one hemicord affected
• Rare, crucial to recognize as septum can tether cord --> decline
in function after repair
• Present with markedly asymmetrical neurological abnormalities
Neuroradiology 1259
1261 Congenital Spinal Anomalies
Meningocele [Figure 5-21-8] Figure 5-21-8
• Meningeal-lined CSF sac protruding through defect
• Cord does not enter sac, may be assoc with hypertrophy of filum
or cord tethering
• ? From CSF pulsations
• Lateral assoc with NF 1, also post-trauma, connective tissue
disorders
Figure 5-21-9
Thoracic meningocele
Figure 5-21-10
Schematic of terminal
myelocystocele. The expanded CSF
spaces are separate from the
markedly dilated terminal ventricle.
Neuroradiology 1261
1263 Congenital Spinal Anomalies
Neurenteric Cyst [Figure 5-21-16] Figure 5-21-15
• From partial regression of neurenteric canal
• Lined by secretory epith, contents iso to CSF or proteinaceous
• Intraspinal, ventral to T cord, anywhere
• Assoc with dysplastic vert > GI, resp anom
• Present late teens, compressive signs & sx
Figure 5-21-18
Axial lumbar myelocele with placode Scoliosis and hairy patches indicating
at level of skin defect underlying split cord malformation
References
1. Barkovich AJ. Pediatric Neuroimaging. 4th Ed. Lippincott, Williams & Wilkins, Philadelphia 2000.
2. Dias MS, Partington M. Embryology of myelomeningocele and anencephaly. Neurosurg Focus 2004; 16:E1.
3. Ellison D, Love S, Chimelli L, Harding BN, Lowe J, Vinters HV. Neuropathology: A Reference Text of CNS
Pathology. 1st ed. Mosby International Ltd, London 1998.
4. Tortori-Donati P, Rossi A, Cama A. Spinal dysraphism: a review of neuroradiological features with embryological
correlations and proposal for a new classification. Neuroradiology 2000; 42:471-491.
Neuroradiology 1263
1265 Congenital Spinal Anomalies
Imaging of the Suprahyoid Neck:
Superficial, Parapaharyngeal and Carotid Spaces
Wendy R. K. Smoker MS, MD, FACR
Figure 5-22-1
Cervical Fascia [Figure 5-6-1]
• Superficial Cervical Fascia
➢ Fat-filled layer of connective tissue that completely surrounds
the neck and permits the skin to glide easily over deeper
structures
• Deep Cervical Fascia
➢ Superficial Layer (Investing Fascia)
➢ Middle Layer (Visceral or Pre-tracheal Fascia)
➢ Deep Layer (Perivertebral Fascia)
Superficial Space-Contents
• Sternocleidomastoid muscle
• Trapezius muscle
• Platysma muscle
• Lymph nodes
• Blood vessels/EJV Hemangioma
• Hair follicles Figure 5-22-2
• Fat
Superficial Space-Pathology
• Hair follicles
➢ Sebacceous cyst
• Blood vessels:
➢ EJV thrombosis
➢ Hemangiomas/vascular malformations
• Lymph nodes
➢ Reactive/suppurative adenopathy;
➢ Nodal metastases
• Fat
➢ Lipoma/liposarcoma
• Pseudomass
➢ Fibromatosis coli
Madelung’s Disease
• Almost exclusively a disease of middle aged
alcoholic males
• 50 years of age
• Appearance of lesions is preceded by 10 years of
heavy drinking A large lymphatic malformation with multiple
• Non encapsulated fatty masses septations
• SIGHT DIAGNOSIS
Liposarcoma
• Slowly enlarging, painless, non-ulcerated mass
• Middle-aged onset
• Most arise de novo; frequently arise from the stroma rather than the
submucosal or subcutaneous fat Figure 5-22-4
• WHO classification recognizes 5 categories of
liposarcomas:
➢ Well differentiated (adipocytic, sclerosing, and
inflammatory subtypes)
➢ Dedifferentiated
➢ Myxoid
➢ Round cell
➢ Pleomorphic
Fibromatosis coli
Figure 5-22-9
Figure 5-22-8
Small PPS
lymphangioma
(arrows) is iso-
intense on T1WIs
and demonstrates a
fluid-fluid level on
the T2WI
Figure 5-22-17
Large vagal paraganglioma
displaces the ICA
anteriorly with the ECA
(arrows). Large flow
voids are seen. The
MRA optimally
demonstrates the
anterior vascular
displacements (arrows)
Figure 5-22-19
Figure 5-22-20
1. Ablin DS, et al. Ultrasound and MR imaging of fibromatosis colli (sternomastoid tumor of infancy). Pediatr
Radiol. 28(4):230-233, 1998.
2. Ahuja A, et al. Madelung disease: Distribution of cervical fat and preoperative findings at sonography. MR, and
CT. AJNR Am J Neuroradiol. 19(4):707-710, 1998.
3. Alkadhi H, et al. Evaluation of topography and vascularization of cervical paragangliomas by magnetic resonance
imaging and color duplex sonography. Neuroradiology. 44(1):83-90, 2002.
4. Bancroft LW, et al. Imaging characteristics of spindle cell lipoma. AJR Am J Roentgenol. 181(5):1251-1254,
2003.
5. Bousson V, et al. Dissections of the internal carotid artery: Three-dimensional time-of-flight MR angiography and
MR imaging features. AJR Am J Roentgenol. 173(1):139-143, 1999.
6. Eldevik OP, et al. Imaging findings in schwannomas of the jugular foramen. AJNR Am J Neuroradiol.
21(6):1139-1144, 2000.
7. Fruin ME, et al. The carotid space in the suprahyoid neck. Seminars Ultrasound CT MR 11:504-510, 1990.
8. Gilbert MR, et al. Meningioma of the jugular foramen: Glomus jugulare mimic and surgical challenge.
Laryngoscope. 114(1):25-32, 2004.
9. Gilmer-Hill HS, et al. Neurogenic tumors of the cervical vagus nerve: Report of four cases and review of the
literature. Neurosurgery. 46(6):1498-1503, 2000.
10. Harnsberger et al. Diagnostic Imaging: Head and Neck. Amirsys Publishers, 2005.
11. Heis HA, et al. Carotid body tumors. Int Surg. 88(4):226-230, 2003.
12. Koeller KK, et al. Congenital cystic masses of the neck: Radiologic-pathologic correlation. RadioGraphics.
19(1):121-146, 1999.
13. Macdonald AJ, et al. Primary jugular foramen meningiomas: Imaging appearance and differentiating features.
AJR Am J Roentgenol. 182(2):373-377, 2004.
14. Mafee MF, et al. Glomus faciale, glomus jugulare, glomus tympanicum, glomus vagale, carotid body tumors, and
simulating lesions: Role of MR Imaging. Radiol Clin North Am. 38(5):1059-1076, 2000.
15. Nadgir RN, et al. Simultaneous bilateral internal carotid and vertebral artery dissection following chiropractic
manipulation: Case report and review of the literature. Neuroradiology. 45(5):311-314, 2003.
16. Noujaim SE, et al. Paraganglioma of the temporal bone: Role of magnetic resonance imaging versus computed
tomography. Top Magn Reson Imaging. 11(2):108-122, 2000.
17. Rao AB, et al. From the archives of the AFIP. Paragangliomas of the head and neck: Radiologic-pathologic
correlation. Armed Forces Institute of Pathology. RadioGraphics. 19(6):1605-1632, 1999.
18. Sharma S, et al. Fibromatosis colli in infants: A cytologic study of eight cases. Acta Cytol. 47(3):359-362, 2003.
19. Snitzer EL, et al. Magnetic resonance imaging appearance of fibromatosis colli. Magn Reson Imaging.
15(7):869-871, 1997.
Masticator Space
Normal Anatomy Coronal Plane
[Figure 5-22-22]
Figure 5-22-22
Figure 5-22-27
Benign Neoplasms
[Figure 5-22-28]
• Neurogenic Tumors
• Aggressive Fibromatosis (Extraabdominal Desmoid)
• Lipomas
Figure 5-22-29
Massive enlargement of
the right foramen ovale
(arrows) produced by a
large V3 schwannoma
traversing the foramen
Non-Hodgkin lymphoma. There is loss of the fat planes within the masticator space, including
enlargement and infiltration of the temporalis muscle in the suprazygomatic masticator space
(arrow). The right pterygopalatine fossa is enlarged indicating V2 perineural extension.
Involvement of the extraconal orbit and extra-axial middle cranial fossa are evident. Involvement
of the lateral pterygoid and temporalis muscles are evident (arrows) and extension along V2 and
V3 is noted (open arrows)
Figure 5-22-31 Figure 5-22-32
T1 WI
Figure 5-22-35
A well-circumscribed, first
branchial cleft cyst involves the
parotid tail (arrows). Other cystic
lesions cannot be differentiated
Figure 5-22-37
Warthin Tumor:
Warthin’s Tumor Large cystic/solid right parotid superficial mass in a
(Papillary Cystadenoma Lymphomatosum) 65 year-old man. The heterogeneity would suggest
[Figure 5-22-41] a lesion other than a pleomorphic adenoma
• Second most common benign tumor of the parotid space Figure 5-22-42
• 80% male, greater than 50 years of age
• Usually slow-growing mass in region of parotid tail
• Arise from ectopic salivary gland rests within
intraparotid lymph nodes
• Limited to PAROTID GLAND ONLY
• Bilateral in 10%-15% of patients
• Imaging: Well-circumscribed, usually 3-4 cm
➢ Complex mixture of solid and cystic components
➢ Appears more complex than typical PA
Oncocytoma
• Occurs exclusively in adults over 50 years of age; No
sex predilection; about 1% of parotid tumors
• Oncocytes are large cells with granular eosinophilic
cytoplasm that may be found in groups, normally
within the parotid gland. Multiple facial nerve neurofibromas (arrows) in a
• An ONCOCYTOMA describes a solid tumor patient with NF2. Also note the ipsilateral V2
composed entirely of oncocytes neurofibroma in the right retromaxillary fat, bowing
• Imaging features are essentially identical to those of the posterolateral maxillary wall
a pleomorphic adenoma Figure 5-22-43
• May be multiple
Malignant Tumors
• The smaller the salivary gland, the higher
the chance a mass is malignant
• Sublingual mass-70% malignancy
• Submandibular mass-60% malignancy
• Parotid mass-20% malignancy
• Mucoepidermoid Carcinoma-more than 80%
occur in parotid glands; most common
malignant salivary gland tumor in most
series
• Adenoid Cystic Carcinoma-2%-6% of parotid
tumors
• Acinic Cell Carcinoma-10%-30% of parotid
tumors
• Adenocarcinoma-rare in major salivary Low-grade superficial parotid lobe mucoepidermoid
glands carcinoma. The lesion is somewhat complex and exhibits
indistinct margins laterally (arrows) leading away from the
diagnosis of a benign neoplasm
Figure 5-22-46
Suprahyoid Neck: Pharyngeal Mucosal Space and Oral Cavity 1282 Neuroradiology
Nasopharyngeal Carcinoma (NPSCCa) [Figures 5-22-47 and 5-22-48] Figure 5-22-47
• Centered in lateral pharyngeal recess
• Invasion of levator palatini results in eustachian tube
dysfunction and serous otitis media with CHL (check
mastoids!)
• Perivascular spread (via foramen lacerum) and
perineural extension (mainly V3) are common so
skull base must be carefully assessed
• Nodal metastases present in 90% at presentation
(retropharyngeal, level II, and level V-first)
• Distant metastases-uncommon at presentation
(<10%) (bone, lung, and liver)
• Strong relationship with Epstein-Barr virus (EBV)
48 year-old male
with bilateral IX-XII
Figure 5-22-49
palsies
Very large
NPSCCA replaces
the entire
basiocciput (distal
clivus), occipital
condyles, jugular
tubercles, and
portions of the C1
lateral masses
(seen on the
coronal images).
Coronal images
also demonstrate
extensive bilateral
This homogeneous, bulky, NHL mass fills the adenopathy
nasopharynx but exhibits no infiltrtion of adjacent
spaces and no skull base involvement
Neuroradiology 1283 Suprahyoid Neck: Pharyngeal Mucosal Space and Oral Cavity
Oropharynx Figure 5-22-50
[Figure 5-22-50]
Figure 5-22-52
Suprahyoid Neck: Pharyngeal Mucosal Space and Oral Cavity 1284 Neuroradiology
Lingual Thyroid Gland Figure 5-22-53
[Figure 5-22-53]
• Failure of thyroid descent from foramen cecum
• Accounts for 90% of ectopic thyroid
• High female predominance (7:1)
• Only functioning thyroid tissue in 70-80%
• CT: Hyperdense with avid enhancement
• MR: Iso-to hyperintense to muscle on both T1- and
T2WI with strong enhancement
• Look in lower neck to confirm lack of gland in normal
location
• Subject to typical “thyroid pathology”
Figure 5-22-54
Figure 5-22-55
Neuroradiology 1285 Suprahyoid Neck: Pharyngeal Mucosal Space and Oral Cavity
Oral Cavity Normal Anatomy Figure 5-22-57
[Figures 5-22-57 to 5-22-59]
Figure 5-22-58
T1 WI
A: Sagittal MR.
Black arrows=intrinsic muscles of the
tongue;
white arrows=genioglossus muscles;
dotted arrows=geniohyoid muscles
T1 WI
B. Coronal MR.
Vertical white arrows=sublingual
spaces;
horizontal black/white
arrows=submandibular spaces;
vertical black/white arrows=platysma
muscles
Suprahyoid Neck: Pharyngeal Mucosal Space and Oral Cavity 1286 Neuroradiology
Oral Cavity Pathology Figure 5-22-60
[Figure 5-22-60]
• Congenital Lesions
➢ Hemangiomas/vascular
malformations; dermoids/epidermoids
• Inflammatory Lesions
➢ Cellulitis/abscesses; sialoliths;
ranulas
• Benign Neoplasms
➢ Pleomorphic adenomas; aggressive
fibromatosis
• Malignant Neoplasms
➢ SCCa (floor of mouth, oral tongue…);
minor salivary gland neoplasms
(SMG, SLG)
Dermoid Cysts
[Figure 5-22-61]
• Refers to dermoid. epidermoid, and
teratoid lesions
• Most uncommon of the congenital lesions Multiple oral cavity venous malformations in a child with Blue
• Sublingual and submandibular locations Rubber Bleb Nevus Syndrome
• Low density/intensity, unilocular, well-circumscribed Figure 5-22-61
• Cyst wall enhances with contrast
• Individual fat globules=dermoid
• In absence of fat, cannot DDx epidermoid from
dermoid
Ranulas
[Figures 5-22-62 and 5-22-63]
• Mucoceles/mucous retention cysts of the floor of the
mouth
• Secondary to trauma or obstruction of sublingual
gland/ducts
• Thin-walled; unilocular; non-enhancing
• Two varieties:
• Simple ranula-in SLS (true)
• Plunging ranula-in SMS (pseudocyst)
Neuroradiology 1287 Suprahyoid Neck: Pharyngeal Mucosal Space and Oral Cavity
Pleomorphic Adenomas Figure 5-22-64
[Figure 5-22-64]
• Most common benign glandular tumor--majority in
parotid gland
• 8% in submandibular gland; 0.5% in sublingual gland
• Well demarcated; homogeneous when small
• Heterogeneous (cystic changes necrosis,
hemorrhage)
• Hypo-isointense on T1WI
• Hyperintense on T2WI
• Homo/heterogeneous enhancement
Exostoses
[Figure 5-22-65]
• Dense cortical bone w/ or w/o cancellous bone
• Incidental unless they preclude proper denture fitting
• Occasionally very large and interfere with swallowing
• Torus palatinus
• Torus mandibularis Sublingual gland pleomorphic adenoma
➢ interna / externa
• Torus maxillaris
➢ interna / externa
Figure 5-22-65
Figure 5-22-66
References
1. Fischbein NJ, et al. Clinical utility of positron emission tomography with 18F-fluorodeoxyglucose in detecting
residual/recurrent squamous cell carcinoma of the head and neck. AJNR Am J Neuroradiol. 19(7):1189-1196,
1998.
2. Harnsberger et al. Diagnostic Imaging: Head and Neck. Amirsys Publishers, 2005.
3. King AD, et al. In vivo proton MR spectroscopy of primary and nodal nasopharyngeal carcinoma. AJNR AM J
Neuroradiol. 25(3):484-490, 2004.
4. Mukherji SK, et al. Squamous cell carcinoma of the oropharynx and oral cavity: How imaging makes a
difference. Semin Ultrasound CT. 19:463-475, 1998.
5. Roh JL, et al. Nasopharyngeal carcinoma with skull base invasion: A necessity of staging subdivision. Am J
Otolaryngol. 25(1):26-32, 2004.
6. Sigal R, et al. CT and MR imaging of squamous cell carcinoma of the tongue and floor of the mouth.
RadioGraphics. 16:787-810, 1996.
7. Smoker WRK, et al. Computed tomography of the nasopharynx and related spaces. Seminars Ultrasound CT MR.
7:107-130, 1986.
7. Smoker WRK. The Oral Cavity in Head and Neck Imaging (4th ed) Som and Curtin, eds. Mosby Year Book
Publishers. pp 1377-1464, 2002.
8. Weber AL, et al. Malignant tumors of the oral cavity and oropharynx: Clinical, pathologic, and radiologic
evaluation. Neuroimaging Clin N Am. 13(3):443-464, 2003.
Neuroradiology 1289 Suprahyoid Neck: Pharyngeal Mucosal Space and Oral Cavity
Spine: Degenerative Disease and
Infections
Wendy R. K. Smoker MS, MD, FACR
Figure 5-23-1
Low Back Pain Annual Costs
• 250,000 operations/year
• 18-56 billion dollars/year
• 85% of costs are due to recurrent or chronic disability
Figure 5-23-2
Protrusion Extrusion
Extrusion with migration plus sequestered fragment
L4-5 Disc Extrusion with Migration [Figure 5-23-6]
Figure 5-23-6
Low T1WI
Type I Vascularized Marrow (edema) High T2WI
High T1WI
Type II Proliferation of endplate fatty marrow High T2WI
Low T1WI
Type III Dense bone devoid of marrow (sclerosis) Low T2WI
Neuroradiology 1289
1291 Spine: Degenerative Disease and Infections
Lumbar Spinal Canal and Foraminal Stenosis Figure 5-23-7
Figure 5-23-8
Facet Joint Synovial Cysts [Figure 5-23-9] Note the nerve root exits
• Intraspinal juxta-articular synovial cysts are uncommon; associated with facet superiorly within the
arthopathy neural foramen, just
• Most in lumbar spine, especially L4-5 under the pedicle
• Slight female preponderance; mean age 58 years (arrow). Note the normal
• Origin: DJD? Trauma?? “keyhole” configuration
• No specific symptom history; waxing and waning symptoms as these increase of the neural foramen
and decrease in size
• CT: Cystic lesion w/ or w/o calcified rim adjacent to degenerated facet
• MR: Iso- or slightly hyperintense on SE sequences
Figure 5-23-9
• DDx: Ganglion cyst (does not communicate with joint)
Figure 5-23-11
Figure 5-23-12
Figure 5-23-13
Neuroradiology 1291
1293 Spine: Degenerative Disease and Infections
Ossification of the Posterior Figure 5-23-14
Longitudinal Ligament (OPLL) C2
[Figures 5-23-15 and 5-23-16]
• Begins with calcification followed by
frank ossification of the posterior
longitudinal ligament in upper C-spine
and progresses into upper T-spine C4-5
• Can see on plain films in 0.12% of
asymptomatic North Americans and
20%-30% of symptomatic patients
• Most easily seen on CT
• On MR, thick band of decreased signal C5-6
on T1 and T2WI with mass effect on
thecal sac and cord
• Associated with DISH
T1WI
Figure 5-23-16
Pyogenic Osteomyelitis
[Figures 5-23-17]
• Ill-defined T1-hypointense vertebral
marrow with loss of adjacent endplate
definition on both sides of infected disc;
hyperintense on T2WI; enhances
• Lumbar-48%; Thoracic-35%; Cervical-
6.5%
• Paraspinal and/or epidural involvement
in 75%
• S aureus most common; E coli if gram
negative; salmonella in sickle cell
• Source: GU, GI, lung, cardiac,
cutaneous/mucous-seeds vascularized
subchondral bone
• Disc first site of involvement in children
(vascularity)
Pyogenic osteomyelitis. Note paraspinal and epidural
• Bimodal: Pediatric patients and 6th-70th
involvement (arrows).
decade; also IV drug abusers and those
with HIV
• Pain, tenderness, and fever Figure 5-23-18
Post Gd
Tuberculous Osteomyelitis
[Figure 5-23-18]
• AKA: Pott’s disease
• Typical: Gibbus vertebrae with relatively
intact disc and paraspinal abscess
• Abscesses dissect over considerable
length T2 WI
• Mid-thoracic or thoracolumbar most
common
• Inoculum in anterior vertebral body;
spreads under anterior longitudinal
ligament; spares discs due to absence
of proteolytic enzymes
• M=F; presents in 50s; fever infrequent Tuberculous osteomyelitis. Note gibbus deformity and
• Concomitant pulmonary TB in 10% extension under the anterior longitudinal ligament (arrows)
Neuroradiology 1293
1295 Spine: Degenerative Disease and Infections
Miscellaneous Figure 5-23-20
1. Akman S, et al. “Magnetic resonance imaging of tuberculous spondylitis”. Orthopedics. 26(1):69-73, 2003.
2. Ben Hamouda K, et al. “Thoracic myelopathy caused by ossification of the ligamentum flavum: A report of 18
cases”. J Neurosurg. 99(2 Suppl):157-161, 2003.
3. Boos N, et al. “Classification of age-related changes in lumbar intervertebral discs: 2002 Volvo Award in basic
science”. Spine. 27(23):2631-2644, 2002.
4. Carragee EJ. “The clinical use of magnetic resonance imaging in pyogenic vertebral osteomyelitis”. Spine.
22(7):780-785, 1997.
5. Cinotti G, et al. “Stenosis of lumbar intervertebral foramen: Anatomic study on predisposing factors”. Spine.
27(3):223-229, 2002.
6. Consensus statement on nomenclature and classification of lumbar disc pathology by NASS, ASSR, and ASNR.
2001.
7. Dix JE, et al. “Spontaneous thoracic spinal cord herniation through an anterior dural defect”. AJNR Am J
Neuroradiol. 19(7):1345-1348, 1998.
8. Doi K, et al. “Cervical nerve root avulsion in brachial plexus injuries: Magnetic resonance imaging classification
and comparison with myelography and computerized tomography myelography”. J Neurosurg. 96(3 Suppl):277-
284, 2002.
9. Eastwood JD, et al. “Diffusion-weighted imaging in a patient with vertebral and epidural abscesses”. AJNR Am J
Neuroradiol. 23(3):496-498, 2002.
10. Fassett DR, et al. “Spinal epidural lipomatosis: A review of its causes and recommendations for treatment”.
Neurosurg Focus. 16(4):Article 11, 2004.
11. Geers C, et al. “Polygonal deformation of the dural sac in lumbar epidural lipomatosis: Anatomic explanation by
the presence of meningovertebral ligaments”. AJNR Am J Neuroradiol. 24(7):1276-1282, 2003.
12. Modic MT, et al. “Degenerative disk disease: Assessment of changes in vertebral body marrow with MR
imaging”. Radiology. 166(1 Pt 1):193-199, 1988.
13. Munter FM, et al. “Serial MR imaging of annular tears in lumbar intervertebral disks”. AJNR Am J Neuroradiol.
23(7):1105-1109, 2002.
14. Ross JS, et al. “Assessment of extradural degenerative disease with Gd-DTPA-enhanced MR imaging:
Correlation with surgical and pathologic findings”. AJNR Am J Neuroradiol. 10(6):1243-1249, 1989.
15. Ross JS, et al. “Association between peridural scar and recurrent radicular pain after lumbar discectomy:
Magnetic resonance evaluation”. Neurosurgery. 38:855-861, 1996.
16. Ross JS, et al. “MR imaging of lumbar arachnoiditis”. AJR. 1987;149:1025-1032.
17. Sasaoka R, et al. “Idiopathic spinal cord herniation in the thoracic spine as a cause of intractable leg pain: Case
report and review of the literature”. J Spinal Disord Tech. 16(3):288-294, 2003.
18. Van Goethem JW, et al. “Review article: MRI of the postoperative lumbar spine”. Neuroradiology. 44(9):723-
239, 2002.
19. Wang MY, et al. “Intradural spinal arachnoid cysts in adults”. Surg Neurol. 60(1):49-55; discussion 55-56, 2003.
20. Watters MR, et al. “Transdural spinal cord herniation: Imaging and clinical spectra”. AJNR Am J Neuroradiol.
19(7):1337-1344, 1998.
Neuroradiology 1295
1297 Spine: Degenerative Disease and Infections
Spinal Tumors, Cysts, and Mimics
Wendy R. K. Smoker MS, MD, FACR
Uncommon Rare
• Non-neoplastic Lesions • Non-neoplastic Lesions
➢ Acute cord ischemia/stroke ➢ Vascular lesions (cavernomas, AVM, etc)
➢ Myelitis (Post viral ADEM, etc) ➢ Infections (sarcoid, TB, Lyme disease…)
• Neoplastic Lesions • Neoplastic Lesions
➢ Hemangioblastoma ➢ Metastases
➢ Astrocytoma (anaplastic and GBMs)) ➢ Lipoma
➢ Subependymoma
➢ Oligodendroglioma
➢ Ganglioma
➢ Paraganglioma
Neuroradiology 1297
1299 Spinal Tumors, Cysts, and Mimics
Intramedullary Metastases [Figure 5-24-5] Figure 5-24-4
• Intramedullary metastases are rare
• 1%-3% of all intramedullary tumors
• No specific imaging characteristics to
clearly distinguish from other
intramedullary lesions Breast and lung
most common
• Also lymphoma, leukemia, and
malignant melanoma
Non-Neoplastic Intramedullary
Pathology
Acute Disseminated
Encephalomyelitis [Figure 5-24-7]
Figure 5-24-6
Figure 5-24-7
Extramedullary-Intradural Lesions
Common Uncommon
Figure 5-24-10
T1WI T2WI Post Gd
Neuroradiology 1299
1301 Spinal Tumors, Cysts, and Mimics
Meningiomas [Figures 5-24-12 and 5-24-13] Figure 5-24-11
• Second most common spinal tumor (25%)
• 90% intradural; 10% extradural or dumbell
• Females > males at 4:1; Primarily 5th-6th decade
• Thoracic (80%) > Cervical (16%) > Lumbar (4%)
• More often anterior in cervical region
• Below C7, more common posterior to cord
• 85% intradural; usually single unless NF 2
• Iso on T1WI; iso or hyperintense on T2WI;
hypointense if Ca++
• Marked homogeneous enhancement
Figure 5-24-12
Figure 5-24-13
“Other” Extramedullary-Intradural
Neoplastic Lesions
Figure 5-24-16
Figure 5-24-17
Neuroradiology 1301
1303 Spinal Tumors, Cysts, and Mimics
Figure 5-24-18 Figure 5-24-19
T1WI
Epidural Lipomatosis
[Figures 5-24-23 and 5-24-24]
• Most often associated with chronic steroid use (exogenous or endogenous
Cushing’s syndrome)
• Also associated with rapid weight gain and obesity
• Thoracic spine most common
• Myelopathic symptoms predominate Figure 5-24-22
Figure 5-24-23
Figure 5-24-24
Anencephaly
• Symmetric absence of calvaria, cerebral hemispheres,
diencephalon
• Replaced by flat amorphous vascular- neural mass
• Facial structures and orbits present
• Most common CNS malf (1:1000)
• Invariably fatal (aborted/stillborn)
• Implications for future pregnancies:
➢ 1 in 50 (2%) risk in next child
➢ if 2 prior pg with CNS mal, risk is 1 in 10)
Cephaloceles
• Skull base (enchondral bone)
➢ Failure of neural tube closure or failure of ossification centers
to unite Large cephalocele containing brain,
• Calvarium (membraneous bone) ventricles, and midline fat. Note
➢ Defective bone induction, pressure erosion, or failure of neural absence of the corpus callosum and
tube closure an open-lip schizencephalic cleft
• Occipital (Arrow)
➢ 80%-90%; F>M; assoc with neural tube defects; most
common in Caucasian NAs and Europeans
• Frontal
• Sincipital
➢ Nasofrontal
➢ Nasoethmoidal-Most common in SE Asia; M>F
➢ Nasoorbital
• Basal
➢ Transethmoidal, transsphenoidal, sphenomaxillary, sphenoorbital
Neuroradiology 1305
1307 Congenital Abnormalities of the Brain
Chiari I Malformation Figure 5-25-2
• Probably due to occipital bone dysplasia and small posterior
fossa
• Caudal displacement of “pegged” cerebellar tonsils into upper
cervical spinal canal
• Associated with:
➢ Syringohydromyelia (25%-50%)
➢ CVJ anomalies in up to 50%
➢ Associated with many brainstem/lower cranial nerve sxs
(hearing loss, vertigo, abnormal gag/swallowing, etc.)
Chiari II Malformation-sagittal.
Note tectal beaking,
caudal displacement of cerebellar tonsils to C4, slit-like,
caudally-elongated fourth ventricle,
vertical straight sinus (small posterior fossa),
and concavity of the clivus
Neuroradiology 1307
1309 Congenital Abnormalities of the Brain
Disorders of Ventral Induction Figure 5-25-8
(Insult at 5-10 weeks)
• Holoprosencephaly
➢ Alobar, semilobar, lobar
➢ Septo-optic dysplasia (DeMorsier’s syndrome)
• Cerebral hemiatrophy (Dyke-Davidoff-Masson syndrome)
• Posterior fossa malformations
➢ Dandy Walker malformation and variants
➢ Joubert’s syndrome
➢ Rhombencephalosynapsis
Lobar holoprosencephaly
Figure 5-25-12
Semilobar holoprosencephaly
Septo-optic dysplasia
Neuroradiology 1309
1311 Congenital Abnormalities of the Brain
Cerebral Hemiatrophy Figure 5-25-13
(Dyke-Davidoff-Masson Syndrome) [Figure 5-25-13]
• Clinical: Hemiparesis, mental retardation, seizures
• Small cerebral hemisphere from in utero ischemia or infarction
after infection or trauma
• Compensatory ipsilateral:
➢ Lateral ventricular enlargement
➢ Calvarial thickening
➢ Enlarged paranasal sinuses
➢ Enlarged mastoid air cells
Note hydrocephalus,
torcular-lambdoid inversion
with large posterior fossa
cyst, and severe vermian
hypoplasia
Unilateral Megalencephaly
(Hemimegalencephaly) [Figure 5-25-17]
• Clinical: Intractable siezures, mental retardation, hemiplegia,
developmental delay
• Cerebral hemisphere may appear so anomalous as to appear
unrecognizable
• Association with Linear Sebaceous Nevus syndrome
• Multiple migration and sulcation anomalies
➢ Polymicrogyria/Agyria
➢ Grey matter heterotopias
Figure 5-25-17
Rhombencephalosynapsis
2 year-old male with ataxia and
developmental delay
Neuroradiology 1311
1313 Congenital Abnormalities of the Brain
Disorders of Neuronal Proliferation Figure 5-25-18
(Insult at 2-5 months)
• Lissencephaly (agyria, pachygyria)
• Non-lissencephalic cortical dysplasias (microgyria and
polymicrogyria)
• Schizencephaly
➢ Type I (closed-lip); Type II (open-lip)
• Grey matter heterotopias
• Callosal abnormalities
➢ Complete/partial agenesis
➢ Pericallosal lipomas
Lissencephaly Type I
• Arrested neuronal migration
• Also termed agyria-pachygyria complex
• Thick gray and thin white matter
➢ Agyria: Parietal-occipital
➢ Pachygyria (“incomplete lissencephaly”): frontal and
temporal
• “Figure 8” or hourglass configuration
• Assoc with Miller-Dieker syndrome
➢ Large deletion gene on chromosome 17p13.3
Lissencephaly Type II
• Also termed “Cobblestone” lissencephaly Classic lissencephaly
• Due to neuronal overmigration
• Associations include: Figure 5-25-19
➢ Walker-Warburg Syndrome
➢ Fukuyama congenital muscular dystrophy
Figure 5-25-22 Bilateral subcortical nodular heterotopia (A and C-arrows) with complete callosal
dysgenesis noted in B. Also note closed-lip schizencephaly in A (open arrow)
A B C
Neuroradiology 1313
1315 Congenital Abnormalities of the Brain
Callosal Dysgenesis [Figures 5-25-24 and 5-25-25] Figure 5-25-24
• Corpus callosum forms anterior to posterior:
➢ Genu ---> Body ---> Splenium --->Rostrum
• Complete Agenesis
➢ Clinical: Siezures, developmental delay, microcephaly
➢ Imaging:
❖ Absent corpus callosum
❖ Elevated third ventricle
❖ Separated lateral ventricles
❖ Colpocephaly
• Partial Dysgenesis
➢ Acquired: Anterior CC is affected
➢ Developmental: Posterior CC is affected A
• Lipomas
➢ Associated with ACC in 40%
➢ Located in interhemispheric fissure
➢ Often encase the pericallosal arteries
Figure 5-25-25
B
Partial callosal dysgenesis: (A) The
splenium is absent. (B) Note gyri
separating the occipital horns in a
position normally occupied by the
splenium on the axial image
1. Altman NR, Naidich TP, Braffman BH. Posteri or fossa malformations. AJNR Am J Neuroradiol 13:691-724,
1992
2. Barkovich AJ, Chung SH, Norman D. MR of neuronal migration anomalies. AJNR Am J Neuroradiol 8:1009-
1017, 1987
3. Barkovich AJ, Chung SH. Unilateral megalencephaly: Correlation of MR imaging and pathologic characteristics.
AJNR Am J Neuroradiol 11:523-531, 1990
4. Barkovich AJ, Jackson DE, Jr., Boyer RS. Band heterotopias: A newly recognized neuronal migration anomaly.
AJNR Am J Neuroradiol 171:455-458, 1989
5. Barkovich AJ, Kjos BO, Norman D, Edwards MS. Revised classification of posterior fossa cysts and cystlike
malformations based on the results of multiplanar MR imaging. AJNR Am J Neuroradiol 10:997-988, 1989
6. Barkovich AJ, Kjos BO. Grey matter heterotopias: MR characteristics and correlation with developmental and
neurological manifestations. Radiology 182:493-499, 1992
7. Barkovich AJ, Kjos BO. Non-lissencephalic cortical dysplasia: Correlation of imaging findings with clinical
deficits. AJNR Am J Neuroradiol 13:95-103, 1992
8. Barkovich AJ, Kjos BO. Schizencephaly: Correlation of clinical findings with MR characteristics. AJNR Am J
Neuroradiol 13:85-94, 1992
9. Barkovich AJ, Norman D. MR imaging of schizencephaly. AJNR Am J Neuroradiol 9:297-302, 1988
10. Barkovich AJ, Norman D. Anomalies of the corpus callosum. AJNR Am J Neuroradiol 9:493-501, 1988
11. Barkovich AJ. Subcortical heterotopia: A distinct clinicoradiologic entity. AJNR Am J Neuroradiol 17:1315-1322,
1996
12. Byrd S, Osborn R, Bohan T, Naidich T. The CT and MR evaluation of migration disorders of the brain, II:
Scizencephaly, heterotopia, and polymicrogyria. Pediatr Radiol 19:219-222, 1989
13. Catilo M. Bouldin TW, Scatliff JH, Suzuki K. Radiologic-pathologic correlation: Alobar holoprosencephaly.
AJNR Am J Neuroradiol 14:1151-1156, 1993
14. Fitz CR. Holoprosencephaly and related entities. Neuroradiol 25:225-238, 1983
15. Naidich TP, Altman NR, Braffman BH, McLone DG, Zimmerman RA. Cephaloceles and related malformations.
AJNR Am J Neuroradiol 13:655-690, 1992
16. Osenbach RK, Menezes AH. Diagnosis and management of the Dandy-Walker malformation: 30 years of
experience. Pediatr Neurosurg 18:179-189, 1992
17. Truit CL, Barkovich AJ, Shanahan R, Marlado TV. MR imaging of rhombencephalosynapsis: Report of three cases
and review of the literature. AJNR Am J Neuroradiol 12:957-965, 1991
Neuroradiology 1315
1317 Congenital Abnormalities of the Brain
Neuroradiology Seminar 1:
Discussion of Unknown Cases
Kelly K. Koeller, MD, FACR
History
• 6-year-old girl with 10 days of vomiting
Medulloblastoma or JPA?
• Use non-contrast CT
• Medulloblastoma: hyperdense
• JPA: iso- or hypodense
• Most reliable imaging feature to distinguish between these tumors
Medulloblastoma
• Most common (?) childhood brain tumor
• Childhood: 75% < 15 y/o, 50% < 10 y/o
➢ Peak 4-8 y/o; second peak 15-35 y/o
• Vermis into fourth ventricle
• Cysts, calcification, hemorrhage rare
• CT: 90-95% homogeneous, slightly hyperdense on NCCT, uniform
enhancement
Medulloblastoma
• MR
➢ Hypointense on T1WI
➢ Hyperintense on T2WI
• Cerebellopontine angle involvement rare
• CSF spread: 20-25% at time of diagnosis
➢ Check spine post-gad after brain MRI
Craniopharyngioma
• Arises from squamous epithelial remnants
• 50% <20 y/o; second peak: middle age
• Location
➢ 70%: both intrasellar and suprasellar
➢ 20%: intrasellar only
➢ 10%: purely suprasellar
Craniopharyngioma
• CT: “typical” = cystic with enhancing rim
➢ Partially calcified enhancing mural nodule
• MR: hyper or hypointense on T1WI; hyperintense on T2WI
➢ Appearance does not correlate well with chemical composition of contents
• Enhancement of rim: more common than in Rathke’s cleft cyst
History
• 30-year-old woman (12 weeks pregnant) with headaches, nausea, and
vomiting. Her obstetrician saw papilledema on fundoscopic exam and asked
for an imaging study.
History
• 62-year-old female with increasingly severe headaches
Tentorial Meningioma
• Most common primary non-glial intracranial neoplasm (16% of all brain
tumors)
• Females > males (2:1)
• Multiple 6-9%
• Rare in children unless neurofibromatosis
• Arise from meningothelial arachnoid villi and possibly dural fibroblasts or pial
cells
History
• 35 year-old African-American male with ataxia and headaches
Sarcoidosis
• Etiology: unknown
• Worldwide prevalence
• United States: more common in African-Americans and women
• Peak age: 20-40 years old
• Multi-organ disease
➢ CNS: 5% of cases
Sarcoidosis – Clinical
• Adenopathy
• Skin rash
• Ocular abnormalities
• Elevated angiotensin converting enzyme
• Diagnosis: biopsy of skin or nodes
Sarcoidosis – Imaging
• 4 forms
➢ Parenchymal mass
➢ Periventricular
➢ Leptomeningeal
➢ Mixed
• Enhances intensely
➢ Combination of parenchymal and leptomeningeal enhancement: clue to
diagnosis
Sarcoidosis – Imaging
• Hyperintense on T2-weighted images
• Parenchymal: may mimic glioma
• Dural: may mimic meningioma
• Hydrocephalus
• Lesions diminish with steroid therapy
History
• 11-year-old male with sudden onset of headache and vomiting at school,
followed 5 days later by onset of left hemiplegia and weakness
Ring-enhancing Masses
“MAGICAL DR”
• Metastasis
• Abscess
• Glioblastoma Multiforme
• Infarct (subacute)
• Contusion
• AIDS:
➢ Toxoplasmosis
➢ Lymphoma (usually immunocompromised)
• Demyelinating disease
• Resolving hematoma, Radiation necrosis
Glioblastoma Multiforme
• Most common primary CNS neoplasm overall
➢ 12-15% of all primary tumors
❖ 50% of all astrocytomas
➢ Most common supratentorial neoplasm in adults
• Peak age: 45-70 years old; children: 10%
• Shorter clinical duration (usually less than 3 months)
Glioblastoma Multiforme
• Heterogeneous hemispheric mass with abundant vasogenic edema
• Most develop from pre-existing astrocytomas
• Subcortical white matter: frontal-temporal predilection
Glioblastoma Multiforme
• Heterogeneous mass
➢ Necrosis and hemorrhage common
➢ Calcification: rare
• Enhancement: >90%
➢ Ring-enhancement: central necrosis
• “Butterfly” pattern: corpus callosum extension
History
• 70-year-old male with recurrent basal cell carcinoma and squamous cell
carcinoma. Had radiation therapy 18 months prior to this study.
History
• 42-year-old male with 2-day history of left upper extremity and shoulder
weakness.
Lymphoma
• Non-contrast CT: hyperdense mass
• Long TR images: hypointense
• Enhancement virtually always but may be heterogeneous
Lymphoma in AIDS
• Necrosis more common than in immunocompetent hosts
• CT: hypodense
• T2WI: hyperintense
• Ring enhancement
History
• 41-year-old male.
• History withheld.
Contusion
• Rough inner table of skull
➢ Anterior cranial fossa (frontal)
➢ Middle cranial fossa (temporal)
• “Bowl of Jell-O” model
• Spectrum: contusion —-> hematoma
➢ Perivascular space —-> parenchyma
• Variable clinical disability
Multiple Sclerosis
• Clinical diagnosis
• Etiology remains unknown
• Cooler climate predilection
• Children: very rare especially before puberty
• Optic neuritis
➢ Retrobulbar pain, central loss of vision, Marcus-Gunn pupil
➢ Strong affinity for females and MS
Multiple Sclerosis: MR
• T1WI: Hypointense
• T2WI: Hyperintense
➢ Frequently shows lesions that are clinically unsuspected
• Active plaques enhance
• Chronic plaques: no enhancement
• MR often shows more disease than predicted clinically
UTI
• E. coli responsible for vast majority of cases
• High recurrence rate
• Infants and young children are less likely to have specific symptoms
• Lower versus upper tract infection – fever, systemic illness
Imaging Studies
• Ultrasound
➢ Infant and young child kidneys versus adult
❖ Growth
❖ Fetal lobulation
❖ Increased cortical echogenicity <1 yo
❖ Hyopechoic pyramids
➢ Hydronephrosis vs. splaying of renal sinus fat
➢ Renal size
➢ Scarring, cortical thinning
➢ Anomalies
➢ Bladder – filling-defects, diverticula, wall thickening, PVR
➢ Lateral position of ureteral orifice
Ultrasound: Limitations
• US is NOT a screening exam
• Less sensitive than VCUG/RNC for diagnosis of VUR
• Less sensitive than CECT and DMSA for acute pyelonephritis
• Less sensitive than DMSA for renal scar
Congenital Anomalies
• Renal agenesis
Figure 6-1-1
• Renal ectopia
➢ Simple
➢ Crossed
• Renal fusion
➢ Horseshoe
➢ Lump or cake
Figure 6-1-3
Two cervices (arrows) and two widely separated Ultrasound of the kidneys shows ill-
uterine horns (arrow heads) associated with right defined lower poles on the
renal agenesis longitudinal images and a midline
parenchymal connection anterior to
the aorta on transverse imaging.
The midline parenchymal isthmus is
Renal Ectopia [Figures 6-1-5 and 6-1-6] well seen in babies and toddlers with
• Most are small and dysmorphic horseshoe kidney. The kidneys are
• Collecting system is superficial and renal sinus echo complex is abnormally echogenic in this patient
absent or eccentric with renal dysfunction
• May be mistaken for a mass
• Blood supply from iliac arteries
Imaging Studies
• Radionuclide cystogram
➢ Lower radiation dose
❖ Female gonads
➢ Continuous imaging
➢ Lack of spatial resolution
❖ Ureteral insertion
❖ Male urethra
❖ Grade I VUR Crossed fused renal ectopia on
excretory urogram. Note orthotopic
Imaging Studies insertions of left and right ureters
• Renal cortical scintigraphy
➢ DMSA or glucoheptonate
➢ More sensitive than ultrasound for renal scarring and pyelonephritis
➢ Indications
❖ Recurrent breakthrough infections
❖ Suspected acute pyelonephritis but equivocal laboratory or imaging
findings
Imaging Studies
• CT
➢ Disadvantage of ionizing radiation and need for intravenous contrast
compared with US
➢ More sensitive than US for acute pyelonephritis
Imaging Studies
• MR
➢ Gd-enhanced MR may be more sensitive than renal scintigraphy in acute
pyelo
➢ Sensitive for renal scarring
➢ Less available
➢ Costly
➢ Need for sedation
VUR
Vesicoureteric Reflux
• Primary abnormality related to length
and angle of submucosal course of
distal ureter
• Versus secondary – bladder outlet Internationally standardized VCUG reflux grading system.
obstruction, neurogenic bladder, Illustration by Heike Blum, MFA
bladder diverticulum
• Up to 50% of children with UTI
Figure 6-1-8
Vesicoureteric Reflux
• Normal US in 75%
• Hydronephrosis – especially if changing
• Mild pelviectasis does not predict VUR
• Renal scar, cortical thinning, or lack of growth
• Urothelial thickening
Figure 6-1-12
Figure 6-1-13
Intrarenal Reflux
• Important factor in the pathogenesis of renal scarring
• More commonly occurs at the poles
• Indication for surgery
Figure 6-1-16
US demonstrating focal enlargement with decrease flow mimicking a mass. The more
sensitive enhanced CT shows more diffuse triangular and striated areas of decreased
enhancement typical of acute pyelonephritis
Reflux Nephropathy
• Renal scarring – chronic pyelonephritis – post-infectious nephropathy
• Related to bacterial infection, VUR, and intrarenal reflux
• Usually at poles – especially upper
• Scarring can be prevented or limited if early diagnosis of upper tract infection
Bladder Augmentation
• Used to treat small, noncompliant bladders
• If small bowel is used, gut signature and peristalsis are seen on US
• Complication of bladder rupture
• Alternative - autologous bladder cells grown in tissue culture
Antenatal Pelvicaliectasis
• Prevalence of prenatal sonography has changed the natural history of some
causes of neonatal hydronephrosis
• Common causes
➢ VUR
➢ UPJO
➢ Obstructed upper pole of duplex system
➢ PUV
UPJO
• Associations
➢ Increased risk of abnormality of contralateral kidney – most
common is UPJO
➢ Renal dysplasia
➢ VUR
➢ UVJ obstruction
➢ Lower pole moiety of duplex kidney
➢ Horseshoe kidney
Radiograph of same patient showing
UPJO - Treatment flaccid abdominal wall musculature.
• Mild – mod obstruction is followed and treated if it worsens Also the infant is intubated with small
lungs, bell-shaped thorax and medial
• Severe obstruction in young children is treated with right pneumothorax due to associated
dysmembered pyeloplasty pulmonary hypoplasia
• In adults and adolescents alternative treatment is endopyelotomy
• Often remain dilated after repair
Congenital Megacalyces
• Nonobstructive enlargement of calyces and
hypoplasia of the medullary pyramids
• Benign nonprogressive condition
• Can coexist with megaureter
• Occasional stone formation, hematuria
Complications of endopyelotomy performed in a
Congenital Megacystis-Megaureter patient with UPJO due to crossing vessel. The
• Large bladder without obstruction upper left image shows the origin of the left main
• Large ureteral orifices with free reflux and voiding into renal artery. The lower right image shows the
markedly dilated ureters origin of an accessory renal artery to the lower
pole, which on the lower left image is seen to
cross the stent in the ureter (arrow). This artery
Summary was cut in the procedure causing the perirenal
• VUR may be primary or secondary to bladder outlet hematoma seen well in the lower two images.
obstruction/ neurogenic bladder or abnormal ureteral Note also the infarction of the anterior lower pole
insertion in the upper right image, due to spasm of the cut
artery
• Primary VUR is familial and resolves by age 6, but
secondary VUR requires surgical intervention
• In primary VUR the VCUG appears normal except for reflux Figure 6-1-28
• US is insensitive and is not a screening exam
• On US, look for scarring and lack of
growth
• RNC best for sibling screen, girls, and
follow-up
• VCUG best for symptomatic patients
and boys
• Surgical options are surgical
reimplantation or subureteric injection
• Bilateral hydro in an infant male is due
to PUV until proven otherwise
• Not all boys with valves have reflux and
hydronephrosis
• In utero obstruction causes renal
dysplasia
• UPJO is associated with abnormality of
Primary megaureter. Excretory urogram shows dilation of the
other kidney left ureter proximal to a short, fixed, relatively narrow segment
• UPJO diagnosed in utero or on of ureter near the UVJ
screening US is caused by intrinsic
abnormality in 85% of patients
• UPJO diagnosed due to symptoms is caused by extrinsic compression
(crossing vessel) in 50% of patients
• Extrinsic compression causes transient sx and findings
• Endopyelotomy is contraindicated in patients with crossing vessels
Texts
1. Kirks DR, ed. Practical Pediatric Imaging, 3rd ed. Philadelphia: Lippincott-Williams & Wilkins, 1998.
2. Siegel MJ, ed. Pediatric Sonography, 3rd ed. Philadelphia: Lippincott-Williams & Wilkins, 2002.
3. Swischuk LE. Imaging of the Newborn, Infant, and Young Child, 5th ed. Philadelphia: Lippincott-Williams & Wilkins,
2004.
Journal Articles
1. American Academy of Pediatrics Committee on Quality Improvement Subcomittee on Urinary Tract Infection. Practice
parameter: the diagnosis, treatment and evaluation of the initial urinary tract infection in febrile infant and young
children. Pediatrics 1999;103:842-852.
2. Berrocal T, Gaya F, Arjonilla A. Vesicoureteral reflux: diagnosis and grading with echo-enhanced cystosonography
versus voiding cystourethrography. Radiology 2001;221:359-365.
3. Blane CE, DiPietro MA, Strouse PJ, et al. Pediatric renal pelvic fullness: an ultrasonographic dilemma. J Urol
2003;170:201-203.
4. Blane CE, DiPietro MA, Zerin JM, et al. Renal sonography is not a reliable screening examination for vesicoureteral
reflux. J Urol 1993;150:752-755.
5. Brown T, Mandell J, Lebowitz RL. Neonatal hydronephrosis in the era of sonography. AJR Am J Roentgenol
1987;148:959-963
6. Daneman A, Alton DJ. Radiographic manifestations of renal anomalies. Radiol Clin North Am 1991;29:351-363.
7. Davey MS, Zerin JM, Reilly C, et al. Mild renal pelvic dilation is not predictive of vesicoureteral reflux in children.
Pediatr Radiol 1997;27:908-911.
8. Donnelly LF, Gylys-Morin VM, Wacksman J. Unilateral vesicoureteral reflux: association with protected renal function
in patients with posterior urethral valves. AJR Am J Roentgenol 1997;168:823-836.
9. Eggli KD, Eggli D. Color Doppler sonography in pyelonephritis. Pediatr Radiol 1992;22:422-425.
10. Elder JS, Peters CA, Arant BS Jr, et al. Pediatric vesicoureteral reflux guidelines panel summary report of primary
vesicoureteral reflux in children. J Urol 1997;157:1846-1851
11. Fernbach SK, Feinstein KA, Schmidt MB. Pediatric voiding cystourethrography: a pictoral guide. RadioGraphics
2000;20:155-168.
12. Gross GW, Lebowitz RL. Infection does not cause reflux. AJR Am J Roentgenol 1981;137:929.
13. Hoffer FA, Lebowitz RL. Intermittent hydronephrosis: a unique feature of ureteropelvic junction obstruction caused
by a crossing renal vessel. Radiology 1985;156:655-658.
14. Lavocat MP, Granjon D, Allard D, et al. Imaging of pyelonephritis. Pediatr Radiol 1997;27:159-165.
15. Lebowitz RL, Blickman JG. The coexistence of ureteropelvic junction obstruction and reflux AJR Am J Roentgenol
1983;140:231-238.
16. Lebowitz RL, Olbing H, Parkkulainen KV, et al. International system of radiographic grading of vesicoureteral reflux.
International Reflux Study in Children. Pediatr Radiol 1985;15:105-109.
17. Lonergan GJ, Pennington DJ, Morrison JC, et al. Childhood pyelonephritis: comparison of Gadolinium- enhanced
MR imaging and renal cortical scintigraphy for diagnosis. Radiology 1998; 207:377-384.
18. Mentzel JJ, Vogt S, Patzer L, et al. Contrast enhanced sonography of vesicoureterorenal reflux in children: preliminary
results. AJR Am J Roentgenol 1999;173:737-740.
19. Orellana P, Baquedano P, Rangarajan V. Relationship between acute pyelonephritis, renal scarring and vesicoureteral
reflux. Results of a coordinated research project. Pediatr Nephrol 2004;19:1122-1126.
20. Paltiel HJ, Mulkern RV, Perez-Atayde A. Effect of chronic low-pressure sterile vesicoureteric reflux on renal growth
and function in a porcine model: a radiologic and pathologic study. Radiology 2000;217:507-515.
21. Paltiel HJ, Rupich RC, Kiruluta HG. Enhanced detection of vesicoureteral reflux in infants and children with use of
cyclic voiding cystourethrography. Radiology 1992;184:753-755.
22. Rooks VJ, Lebowitz RL. Extrinsic ureteropelvic junction obstruction from a crossing renal vessel: demography and
imaging. Pediatr Radiol 2001;31:120-124.
23. Sargent MA. What is the normal prevalence of VUR? Pediatr Radiol 2000; 30:87-593.
24. Van den Abbeele AD, Treves ST, Lebowitz RL, et al. Vesicoureteral reflux in asymptomatic siblings of patients with
known reflux: radionuclide cystography. Pediatrics 1997;79:147-153.
25. Walsh G, Dubbins PA. Antenatal renal pelvis dilatation: a predictor of vesicoureteral reflux? AJR Am J Roentgenol
1996;167:887-890.
VACTERL
• Non-random association of anomalies
• No one patient has all
• High perinatal mortality > 60%
• 46% of patients with TEF
• Recurrence risk (offspring) 2-3%
• Recurrence risk (siblings)
➢ TEF or EA < 1%
➢ Other VACTERL lesions 1.2%
STOMACH
Malrotation/Malfixation - Pathogenesis
[Figures 6-2-6 and 6-2-7]
• All types referred to as malrotation
• Malfixation - short root of mesentery predisposes to midgut volvulus
• Ladd bands –
➢ Attempts to secure the bowel
➢ Most common site is from high medial cecum across 2nd-3rd portion of
duodenum to porta hepatis
➢ May cause obstruction Normal intestinal rotation
and fixation showing
long root of the
Figure 6-2-6 mesentery (line)
Figure 6-2-7
Figure 6-2-10
Malrotation - Treatment
• Ladd procedure
➢ Reduce midgut volvulus
➢ Lyse bands
➢ Place in orientation of nonrotation – all small bowel on the right and all
colon on the left
➢ Inversion appendectomy
➢ 95% have no recurrence
Duodenal Atresia/Stenosis/Web
• Atresia much more common than stenosis
• 3-6 weeks gestation – failure of canalization of solid tube of foregut
• Annular pancreas in 20%
• May have preduodenal portal vein
Figure 6-2-16
Figure 6-2-17
Figure 6-2-22
Figure 6-2-24
Berdon Syndrome
• Megacystis-microcolon-intestinal hypoperistalsis syndrome
• Functional small bowel obstruction
• Malrotation common
• Transient microcolon and dilated SB loops
• Large unobstructed bladder, also dilated ureters and pelvicalyceal
system
• 4:1 F:M
• Associated GU and cardiac anomalies
• Poor prognosis for long term survival
Meconium ileus. Contrast enema
shows a microcolon and pellet-like
COLON/RECTUM filling defects in the distal small bowel
Meconium plug
Hirschprung Disease
• Functional obstruction of colon due to absence of
intramural ganglion cells of myenteric plexus
• Failure of distal intestine to relax
• Etiology - ? arrest of craniocaudal migration of
neuroblasts in the distal colon in 12th week
• 1 in 5000 live births
Associated Anomalies
• 3%-5% Down syndrome
• Esophageal dysmotility syndromes
• Malrotation
• Ileal and colonic atresia Hirschprung disease. Lateral image
• Neurocristopathies from contrast enema showing
➢ Neuroblastoma abnormally low recto sigmoid ratio
➢ Ondine curse – central hypoventilation and congenital and saw tooth contractions in
neuroblastoma aganglionic segment
Imperforate Anus
• Anorectal malformation – abnormal separation of GU tract from hindgut Figure 6-2-32
• High vs. low - levator sling development
determines surgical approach and
prognosis
• Low – fistula to perineum
• High – fistula to
➢ Boys – post urethra, calcified
meconium, air in bladder
➢ Girls – vagina or vestibule
1. Buonomo C. Neonatal Gastrointestinal Emergencies. Radiologic Clinics of North America 1997;35: 845-864
2. Cohen MD. Choosing Contrast Media for the Evaluation of the Gastrointestinal Tract of Neonates and Infants.
Radiology 1987;162:447-56
3. Kao SC, et al. Nonoperative treatment of simple meconium ileus: a survey of the Society for Pediatric Radiology.
Pediatr Radiol 1995;25: 97-100
4. Kirks DR, et al. Practical Pediatric Imaging. 1998
5. Kirks DR. Emergency Pediatric Radiology. American Roentgen Ray Society. 95th Annual Meeting April, 1995
6. Long FR, Kramer SS, Markowitz RI, Taylor GE. Radiographic patterns of intestinal malrotation in children.
RadioGraphics 1996;16:547-556.
Figure 6-3-3
Figure 6-3-5
Figure 6-3-6
Figure 6-3-9
Figure 6-3-11
SMALL BOWEL
Duodenal Hematoma
• Etiology – blunt abdominal trauma
➢ Handlebar
➢ Seat belt
➢ Inflicted trauma
• Associated injury to other organs, especially
pancreas Embolic trichobezoar mimicking malrotation as
• Usually present with vomiting, pain, less commonly emboli connected to gastric bezoar by hair that
mass, jaundice straightened the bowel
NAT-Visceral Injury
• Seen at all ages
• Usually blunt
• Delay in seeking treatment
• 20%-50% mortality
• Proximal SB hematoma, distal SB perforation
Henoch-Schönlein Purpura
• Idiopathic anaphylactoid reaction with diffuse vasculitis
• In the small bowel it causes intramural hemorrhage
• Jejunum most frequently involved
• Enteroenteric intussusception common
Inguinal Hernia
• Most common cause of intestinal obstruction in
young infants
• Usually a clinical diagnosis
• Incarceration or strangulation can cause bowel Gross images showing the dilated markedly
obstruction thickened small bowel and classic purpuric rash
• Most male - 90%
• Bowel, fat, fluid, ovaries can herniate
Figure 6-3-18
Intussusception - Pathology
• 8-10% pathologic lead points
➢ Meckel diverticulum if younger
➢ Lymphoma if older
➢ Polyp
➢ Enteric duplication cyst
➢ Appendix
➢ Henoch-Schonlein purpura
Intussusception Reduction
• Air up to 120 mm Hg1 or Figure 6-3-21
• Water soluble contrast
• 3 attempts, 3 minutes each
• Largest tip possible
• Squeeze buttocks when at IC valve
• If losing air, apply forward pressure to tip
• Endpoint is reduction of soft tissue mass AND rush
of air into the SB
1Shiels WE, Maves CK, Hedlund G, Kirks DR. Air enema
for diagnosis and reduction of intussusception: clinical CT of colonic intussusception due to polyp. Note
experience and pressure correlates. Radiology fat and vessels inside the intussuscepiens
1991;181:169-172
Figure 6-3-24
Meckel diverticulum
Figure 6-3-25
Longitudinal (left) and transverse images showing Intraoperative image showing ileocolic
intussusception with large fluid-filled lead point, a intussusception and sectioned resected specimen
duplication cyst showing duplication cyst lead point
Enteric Duplication Cyst
• Developmental tubular or cystic structures adjacent to the GI tract
• Share wall and blood supply with adjacent bowel
• Usually round and do not communicate with bowel lumen
• Occasionally tubular, communicating with GI tract at one end and blind-ending at the other
Appendicitis
• Children more often have atypical presentation
• Children have a higher rate of negative laparotomy Duplication cyst (longitudinal and transverse)
and of perforation than adults showing round fluid-filled cavity surrounded by a
• Rare in infants wall with gut signature. Note echogenic rim of
mucosa
COLON/RECTUM
Neutropenic Enterocolitis
• AKA typhlitis
• Necrotizing enterocolitis often affecting the right colon in patients with neutropenia
• Pathologically similar to NEC in premature infants and pseudomembranous colitis
• Transmural – risk of perforation
Texts
1. Donnelly LF. Fundementals of Pediatric Radiology. Philadelphia: W.B. Saunders Company, 2001.
2. Kuhn JP, Slovis TL, Haller JO, eds. Caffey’s Pediatric Diagnostic Imaging. Philadelphia: Mosby, 2004
3. Stringer DA, Babyn PS, eds. Pediatric Gastrointestinal Imaging and Intervention. Hamilton: B.C. Decker Inc.,
2000
4. Stocker JT, Dehner LP, eds. Pediatric Pathology. Philadelphia: Lippincott Williams & Wilkins, 2002
5. Swischuk LE. Imaging of the Newborn, Infant, and Young Child. Philadelphia: Lippincott, 2004
Journal Articles
1. Berrocal T, Lamas M, Gutieerez J, et al. Congenital anomalies of the small intestine, colon and rectum.
RadioGraphics 1999:19:1219-1236
2. Blumhagen JD, Maclin L, Krauter D, et al. Sonographic diagnosis of hypertrophic pyloric stenosis. AJR
1988;150:1367-1370
3. Buonomo C. Neonatal Gastrointestinal Emergencies. Radiology Clinics of North America 1997; 35: 845-864
Viral Croup
[Figures 6-4-3 and 6-4-4]
• Laryngotracheobronchitis
• Characteristic barking, brassy cough w/
inspiratory stridor Figure 6-4-4
• Most frequent cause of
stridor 6 mo - 3 yo
• Self-limited disease-7
days
• Parainfluenza
• Subglottic edema 5-10
mm below cords
• Less than 1% need
intubation
Viral croup. Note the
hypopharyngeal overdistension and
subglottic tracheal narrowing and
indistinctness (block arrow). The
most important finding on this film is
the normal pinkie-like epiglottis
(arrow)
Epiglottitis DDX
• Caustic ingestion or thermal injury
• Angioneurotic edema
• Radiation
• Sarcoidosis
• Hemorrhage Epiglottitis with epiglottis shaped like
• Abscess a thumb, thickened aryepiglottic
• Epithelial cyst folds, and loss of the normal
concavity of the aryepiglottic folds
• Omega epiglottis (arrow)
Figure 6-4-6
Figure 6-4-8
Hydrocarbon aspiration
• Hydrocarbons – furniture polish, gasoline, kerosene, lighter fluid
• Aspirated due to low viscosity and surface tension
• Severe chemical pneumonitis with destruction of surfactant
• Radiographic abnormalities develop within 24h
• Pneumatoceles may develop
Nasal Dermoid
• Midline, usually round and cystic
• May have hypertelorism or nasal pit
• May occur anywhere along dermal sinus tract
• Tract may communicate with the cranial contents
Juvenile Angiofibroma
• Highly vascular, locally invasive, histologically benign
• Adolescent boys w/ nasal obstruction, sinusitis and epistaxis
• Originates in sphenopalatine foramen, nasopharynx or posterior nasal cavity Figure 6-4-15
• Spreads early into pterygopalatine fossa,
infratemporal fossa, middle cranial fossa, orbit or
sphenoid sinus
Rhabdomyosarcoma
• 3rd most common childhood primary malignancy of
the head and neck
• 40% arise in the head and neck Esthesioneuroblastoma on CT and coronal Gd-
enhanced T1W MRI showing mass in nasal cavity
• Orbit and nasopharynx most common with invasion of the right frontal lobe with
• Also paranasal sinuses and middle ear surrounding edema
• Usually embryonal cell subtype
• May spread intracranially via skull base foramina
• CT-iso to brain and enhances uniformly
• MR- T1 iso to muscle, T2 hyperintense and heterogeneous
• MR shows intracranial extension through fissures and foramina well
• CT shows bony erosion well
• Enhancement may make extracranial portions of the tumor less conspicuous
on MR
• Fat saturate post-gadolinium sequences of orbits and face
Nasal polyps
• Uncommon in children except those with cystic fibrosis
• Can also be associated with recurrent infection and allergies
• In CF can be so large and chronic as to widen the nasal passages
Macroglossia
• Down’s syndrome
• Hypothyroidism
• Beckwith-Wiedemann syndrome
• Storage diseases
Mandibular Hypoplasia
• Hemifacial microsomia – unilateral
➢ Ipsilateral TMJ hypoplasia
➢ Congenital ear defects
• “First arch” syndromes
➢ Pierre Robin sequence
➢ Goldenhar syndrome Left image is an IV contrast-enhanced CT
➢ Weyer mandibulofacial dysostosis showing left parotitis. Compared to the normal
➢ Treacher Collins mandibulofacial dysostosis right parotid gland, the left is enlarged, enhancing
and has small hypodense foci consistent with
➢ Trisomies intragland abscesses. The image on the right
➢ Airway obstruction by normal sized tongue shows a large calcification in the duct of the right
submandibular gland
Inflammatory disease of the salivary glands
[Figure 6-4-18]
• Acute infection is viral or bacterial
• Bacterial sialadenitis is most common in parotid gland Figure 6-4-19
• Bacterial infection usually due to decrease in flow of
secretions
• Predisposing conditions include sialolithiasis
• Can occur in dehydrated newborns
• On CT the affected gland is enlarged and
hyperdense
• Intragland abscess may be seen
• Most calcified duct stones are visible on noncontrast
CT
• US can be used to evaluate salivary glands
• Obstruction of a sublingual duct or accessory duct is
a ranula
Hypopharyngeal cyst
• Epiglottic or aryepiglottic folds
• Retention cysts or lymphatic malformations
• Inspiratory stridor or choking during feeding
• Present in infancy or early childhood Vallecular cyst (arrow). Bright on T2WI (top) and
• Treated with marsupialization nonenhancing on post-Gd T1WI (bottom)
Subglottic Hemangioma
• Rare cause of stridor in infants, but most common Lingual thyroid. Left CT image shows
subglottic soft tissue mass causing upper airway homogeneous intensely enhancing mass at base
obstruction of tongue. Lower right CT image shows no thyroid
gland in the base of the neck. Upper right image
• Noisy breathing at 6-12 months is a pertechnetate scan showing no uptake above
• 50% have cutaneous hemangiomas the sternal notch and most uptake at the base of
• Asymmetric narrowing of subglottic trachea tongue
• Ddx: subglottic cyst, papilloma, cervical ectopic
thymic tissue, tracheal granuloma
Hemangioma
• Benign vascular tumor of infancy – high flow lesion Figure 6-4-21
• Most common tumor of infancy
• Usually absent at birth and appears in first few
months
• Early proliferative phase, later involutional phase
• May involve skin and have characteristic appearance
Hemangioma
• PHACE syndrome
➢ Posterior fossa abnormalities
Figure 6-4-22
➢ Hemangioma of the face
➢ Arterial abnormalities
➢ Coarc/cardiac defects
➢ Eye abnormalities
• Kassabach-Merritt syndrome
➢ Thrombocytopenia and consumptive
coagulopathy associated with vascular tumor
Lymphoma
• Common malignant tumor in the neck
• Both Hodgkin's and NHL
• NHL more frequently involves extranodal sites, including tonsils and adenoids
• Immunodeficiency predisposes
• Enlarged lymph nodes and conglomerate masses of nodes
• On ultrasound the nodes may be sonolucent
Lymphoma
• On CT, isointense to muscle
• On MR, isointense to muscle on T1WI and hyperintense on T2WI
• Burkitt lymphoma – mass originating in jaw
Neuroblastoma
• Primary or metastatic in neck
• Neck or thoracic primary has better prognosis than intra-abdominal primary
• Calcification common
• US may show increased blood flow
• May involve skull or extend intracranially
Figure 6-4-23
Fibromatosis Colli [Figure 6-4-23]
• Focal thickening or mass of sternocleidomastoid muscle
associated with torticollis
• Noted at or shortly after birth
• Histologically – atrophy and partial replacement of muscle with
fibrous tissue
• US preferred – shows continuity of mass with SCM
• Resolves with physiotherapy
Laryngomalacia
• Most common laryngeal abnormality of the neonate
• Early inspiratory stridor US of sternocleidomastoid muscle
• Worsens at rest - unusual showing fusiform enlargement
• Laryngeal collapse during inspiration with hypopharyngeal characteristic of fibromatosis colli
overdistension seen on airway fluoroscopy
• Usually resolves by age 1 year
Laryngotracheal cleft
• AKA persistent esophagotrachea
• Extreme form of failure of separation of trachea from foregut
• Spectrum from posterior laryngeal cleft to common tube
• May have abnormal cry or mutism
• Symptoms mimic esophageal atresia
• Esophagram shows massive aspiration
Tracheomalacia
• Collapse of the trachea with expiration
• Delayed development of cartilage
• Focal or generalized
• Recurrent infections and stridor
• Compressed in AP diameter
• Associated with esophageal atresia and vascular ring
• Also common in Down’s syndrome
Tracheobronchomegaly
• AKA Mounier-Kuhn
• Dilation of airways in inspiration
• Due to congenital deficiency of elastic tissue
• 3rd-5th decade
• Dilated trachea and central bronchi with diverticulosis
of trachea Bronchogram showing long segment tracheal
• Perihilar bullae stenosis in a patient status post surgical
correction of pulmonary sling. Note that the
trachea is of smaller caliber than either mainstem
Tracheal bronchus [Figure 6-4-25] bronchus
• RUL bronchus arises directly from trachea
Figure 6-4-25
• 1% of the population
• May supply whole RUL or a supernumerary segment
• Persistent RUL pneumonia, atelectasis or air trapping
• Associated with TEF, tracheal stenosis, pulmonary
sling, Down syndrome
Laryngeal- Tracheopapillomatosis
• Most common laryngeal tumors in infancy Tracheal bronchus. Postmortem bronchogram
• Human papilloma virus implicated and specimen showing small bronchus to
supernumerary right upper lobe arising directly
• 2/3 pts less than 4 yo from the trachea
• Dx made on endoscopy with nodules on vocal cords
• Transbronchial spread < 5%, related to surgical procedures Figure 6-4-26
• Pulmonary solid lesions with cavitation
• Poor prognosis with pulmonary involvement
Texts
1. Ball WS Jr. Pediatric Neuroradiology. Philadelphia: Lippincott-Raven, 1997.
2. Barkovich AJ. Pediatric Neuroimaging. 3rd ed. Philadelphia: Lippincott-Raven, 2000.
3. Donnelly LF. Fundamentals of Pediatric Radiology. Philadelphia: W.B. Saunders Company, 2001.
4. Kirks DR, ed. Practical Pediatric Imaging. 3rd ed. Philadelphia: Lippincott-Williams & Wilkins, 1998.
Journal Articles
1. Capitanio MA and Kirkpatrick JA. Upper respiratory tract obstruction in infants and children. Radiol Clin North
Am 1968;6:265
2. Chinwuba C, Wallman J and Strand R. nasal obstruction: CT assessment. Radiology 1986;159:503
3. Dunbar JS. Upper respiratory tract obstruction in infants and children. AJR Am J Roentgenol 1970;109:227-246.
4. John SD, Swischuk LE. Stridor and upper airway obstruction in infants and children. RadioGraphics 1992;12:625-
643.
5. Panicek DM, et al. The continuum of pulmonary developmental abnormalities. RadioGraphics 1987;7:747.
Clinical Presentation
• Respiratory symptoms – tight complete rings
➢ Stridor
➢ Recurrent respiratory difficulties
➢ Apnea
• Feeding difficulties
Early in fetal development the
➢ Choking with feeds primitive aorta develops as a ventral
➢ Failure to thrive tube which separates into two ventral
➢ Solid food dysphagia aortae. Two dorsal aortae fuse to form
a single vessel supplying the lower
Evaluation of Stridor/Dysphagia body. As the pharyngeal pouches
develop at the rostrum of the embryo,
• PA and lateral chest and high kV airway films – determine side of so too do paired pharyngeal arterial
arch arches, numbering 6 (but no 5th arch
• Esophagram with airway fluoroscopy in humans) between the ventral and
➢ MRI/MRA or CTA if vascular ring suspected dorsal aortae. These arches go on to
➢ Otherwise, CT fuse, partially regress and fully
regress to form the pulmonary
arteries and the mature left-sided
Embryology of the Normal Left Aortic Arch aortic arch and its branches
[Figures 6-5-1 to 6-5-4]
• Arches 1 and 2 regress
• Arch 3 --> common and proximal internal carotid arteries
• Arch 4
➢ Right --> regresses (portion of right subclavian)
➢ Left --> persists as LEFT AORTIC ARCH
• Arch 5 – rudimentary in humans
• Arch 6 – pulmonary arteries and ducti arteriosi Figure 6-5-2
➢ Right regresses
➢ Left becomes ligamentum arteriosum
• Dorsal aortae
➢ Right regresses – part of RSCA
➢ Left becomes descending aorta
Diagram representing the normal regression In the development of the aberrant right
of the 8th segment of the right dorsal aorta subclavian artery, there is early obliteration of the
and right ductus arteriosus in development of right 4th arch, and the 8th segment of the right
the normal left arch. The right subclavian dorsal aorta persists, so the right subclavian artery
artery is separated from the descending maintains its connection to the descending aorta,
aorta and arises in common with the right becoming the last branch from the aortic arch
common carotid artery from the ascending (arrow). Thus, there are four, rather than the
aorta normal three, branches of the aortic arch and
there is no brachiocephalic (innominate) artery.
The descending aorta is on the left, so the
Aberrant RSCA [Figures 6-5-5 to 6-5-8] aberrant RSCA then crosses behind the
• Asymptomatic in children – normal variant esophagus to get to the right side
• Due to early complete obliteration of right 4th arch
and persistence of 8th segment of the right dorsal aorta
• Left arch
• RSCA originates distal to LSCA Figure 6-5-6
• Posterior impression on the esophagus
Figure 6-5-9
Figure 6-5-13
Figure 6-5-15
Esophagram in same
patient. The double arch
causes bilateral lateral
impressions on the
esophagus as seen on PA chest radiograph in a patient with
the AP view (left image). double aortic arch, showing a higher
On the lateral view (right larger right sided aortic impression
image), there is a on the trachea and a smaller, lower
prominent posterior left sided impression (arrow). The
impression caused by left impression is often difficult to
the joining arches. Thus, discern, so double aortic arch is in
there are 3 impressions the differential of right aortic arch
on the esophagus seen on plain film
Figure 6-5-22
3-D MRA of a double aortic arch,
viewed from posterior
Figure 6-5-23
Texts
1. Donnelly LF. Fundamentals of Pediatric Radiology. Philadelphia: W.B. Saunders Company, 2001.
2. Kirks DR, ed. Practical Pediatric Imaging. 3rd ed. Philadelphia: Lippincott-Williams & Wilkins, 1998.
3. Swischuk LE. Imaging of the Newborn, Infant, and Young Child, 5th ed. Philadelphia: Lippincott-Williams &
Wilkins, 2004.
Journal Articles
1. Berdon WE and Baker DH. Vascular anomalies and the infant lung: rings, slings and other things. Semin
Roentgenol 1972;7:39-63.
2. Berdon WE. Rings, slings and other things: vascular compression of the infant trachea updated from the
midcentury to the millennium—the legacy of Robert E. Gross, MD, and Edward B. D. Neuhauser, MD. Radiology
2000;216:624-632.
3. Bisset GS III et. Al. Vascular rings: MR imaging. AJR Am J Roentgenol 1987;149:251
4. Donnelly LF, Bisset GS 3rd , McDermott B. Anomalous midline location of the descending aorta: a cause of
compression of the carina and left mainstem bronchus in infants. AJR AM J Roentgenology 1995; 164:705-707.
5. Donnelly LF, Strife JL, Bisset GS III. The spectrum of extrinsic lower airway compression in children: MR
imaging. AJR Am J Roentgenol 1997;168:59-62
6. Kussman BD, Geva T, McGowan FX. Cardiovascular causes of airway compression. Paediatr Anaesth 2004;14:60-
72.
7. Newman R, Meza MP, Tobin RB, et al. Left pulmonary artery sling: diagnosis and delineation of associated
tracheobronchial anomalies with MR. Pediatr Radiol 1996;26:661-668
8. Pickhardt PJ, Siegel MJ, Gutierrez FR. Vascular rings in symptomatic children: frequency of chest radiographic
findings. Radiology 1997;205:581-582
9. Shuford WH, Sybers RG, Edwards FK. The three types of right aortic arch. AJR 1970;109:67-74
Terminology
• Cyst
• Polycystic kidney disease – ARPKD and ADPKD only
• Multicystic kidney
Old Classification1
• Type I, infantile polycystic kidney disease
• Type II, multicystic dysplastic kidney
• Type III, adult polycystic kidney
• Type IV, cortical cysts associated with massive hydronephrosis
1 Osthanondh V, Potter EL. Pathogenesis of polycystic kidneys: historical survey.
Arch Pathol 1964;77:459
Genetically-based Classification2
• Nongenetic
➢ Multicystic dysplasia
➢ Multilocular cyst (tumor)
➢ Simple cyst/calyceal diverticulum
➢ Medullary sponge kidney
➢ Acquired cystic disease
• Genetic
➢ Autosomal recessive polycystic kidneys
➢ Autosomal dominant polycystic kidneys
➢ Juvenile nephronophthisis (AR)-medullary cystic disease (AD) complex
➢ Cysts associated with multiple malformation syndromes
2Glassberg KI, Stephens FC, Lebowitz RL, et al. Renal dysgenesis and cystic
disease of the kidney: a report of the Committee on Terminology, Nomenclature
and Classification, Section on Urology, American Academy of Pediatrics. J Urol
1987, Oct; 138:1085
Calyceal Diverticulum
• Cyst that communicates with collecting system
• Need contrast study to distinguish from cyst
• Urine stasis leads to infection and stone formation
• Look for stone in tic on US, KUB, or non-con CT
• Delayed images show contrast-filling of the cyst and a neck
• Treatment – surgical ablation if symptomatic
MCDK - Presentation
• PNUS Figure 6-6-2
• Neonate with abdominal mass
• Incidentally in older child – mimics agenesis
Figure 6-6-3
Figure 6-6-5
Photomicrograph of
dysplastic kidney showing
primitive ducts surrounded
by mesenchymal collarettes
Figure 6-6-6
MCDK - DDx
• Multilocular cystic kidney
➢ A tumor
➢ Cysts within the intervening septa
• Severe hydronephrosis
➢ UPJO
➢ Nuclear renogram
➢ Contralateral kidney also affected Renal ultrasound showing normal right kidney and
left MCDK. Note noncommunicating cysts and
MCDK – Course and Prognosis lack of visible normal renal parenchyma
[Figures 6-6-7 and 6-6-8]
• Natural history of a true MCDK is to resolve
• Formerly these were all removed due to rare reports of nephroblastoma1 Figure 6-6-7
• Now followed to resolution
• If they do not resolve, surgical removal is indicated to prevent
complications of infection and neoplasm
1Strife JL, Souza AS, Kirks DR, Strife CF, Gelfand MJ, Wacksman J.
Multicystic dysplastic kidney in children: US follow-up. Radiology.
1993 Mar;186(3):785-8.
Figure 6-6-9
Figure 6-6-10
ARPKD Autopsy
Figure 6-6-13
Figure 6-6-14
ARPKD. High frequency linear transducer 12 yo diagnosed in infancy with ARPKD, now
ultrasound images show echogenic, markedly preop for liver transplant. Ultrasound on left shows
enlarged kidneys in which tiny cysts can be markedly dilated biliary ducts with hepatic artery
resolved and portal vein branches in the center, creating a
target appearance. CT shows same target
appearance of biliary ducts as well as cysts in the
renal medulla and splenomegaly due to portal
hypertension
Figure 6-6-17
ARPKD - Prognosis
• Infantile – poor prognosis due to renal insufficiency and
pulmonary hypoplasia Figure 6-6-19
• Outcome in childhood is better than previously thought
• Early recognition and management are important
Differential Diagnosis
Large Echogenic Kidneys in Neonate
• Glomerulocystic disease
• ADPKD
Glomerulocystic Disease
• Rare, sporadic or heritable (AD)
• May be found in some patients with malformative syndromes
• Occasionally found in children with family history of ADPKD
ADPKD - Presentation
• Present in 4th-5th decade with hypertension and renal failure
• Does not present in childhood but may be found incidentally or secondary to
flank pain due to bleeding into cyst
• Rarely presents in infancy – minimal cysts in enlarged, echogenic kidneys
ADPKD - Pathology
• Enlarged but reniform kidneys
• Cysts of varying size scattered throughout the kidney (cortex and medulla)
• Usually bilateral but may be asymmetric or even unilateral
• Abnormality of the ampullary and interstitial portions of the collecting tubules
and nephrons
• Hepatic fibrosis is rare
Figure 6-6-21
ADPKD - Ultrasound [Figure 6-6-21]
• Infantile presentation – small, spherical cysts on high resolution
US (vs. fan-like, tubular appearance in AR)
• Older children - cysts of varying size in cortex and medulla
• Can be unilateral at presentation
• Normal size or slightly enlarged
• Look for cysts in liver and pancreas
ADPKD - Prognosis
• Most develop renal failure in 4th-5th decade
• Presentation in infancy – more severe renal cystic disease, more
hypertension, more rapid progression to renal failure than adult
relatives
Summary
• ARPKD and MCKD are most common in perinatal period
• Classic MCDK is managed conservatively
• Renal dysplasia is caused by in utero obstruction
• VCUG indicated in MCDK to exclude contralateral VUR (solitary
functioning kidney)
• ARPKD is a spectrum of renal and hepatic disease
• ARPKD and ADPKD can both be diagnosed in infants as well as
adolescents/adults
Journals
1. Blane CE, Barr M, DiPietro MA, Sedman AB, Bloom DA.
2. Blickman JG, Bramson RT, Herrin JT. Autosomal recessive polycystic kidney disease: long-term sonographic
findings in patients surviving the neonatal period. AJR Am J Roentgenol. 1995 May;164(5):1247-50.
3. Corrales JG, Elder JS. Segmental multicystic kidney and ipsilateral duplication anomalies. J Urol. 1996
Apr;155(4):1398-401.
4. Diard F, Le Dosseur P, Cadier L, Calabet A, Bondonny JM. Multicystic dysplasia in the upper component of the
complete duplex kidney. Pediatr Radiol. 1984;14(5):310-3.
Objectives
• Describe a variety of renal masses in infants and children
• Recognize the imaging features of these masses
• Understand unique clinical and pathologic features of these tumors
Risk Factors
• Race: Afro-Americans > Caucasians > Asians
• Familial predisposition (1%)
➢ Autosomal dominant
• Aniridia
• Deletion of tumor suppressor genes on short arm of chromosome 11
➢ 11p13 locus (WT1 gene)
➢ 11p15 locus (WT2 gene)
Figure 6-7-3
Wilms’ Tumor
• Contrast enhanced CT
➢ low density, intrarenal mass
➢ rim of compressed parenchyma
• Little enhancement
• Central necrosis 75%
• May contain fat or calcifications
Wilms Tumor
• Exophytic mass, pseudocapsule Wilms tumor, CT. Transverse and coronal CT
reformation showing large mass extending
Wilms’ Tumor exophytically from lower pole of right kidney
Tumor Thrombus
Wilms’ Tumor
Figure 6-7-8
Wilms’ Tumor: Metastases
• About 10% have metastases at
diagnosis
➢ Lung: 85%-90% of all mets
➢ Liver: 10%-15%
• Plain radiographs have FN rate of 7-
29% when CT positive
• CT is study of choice for distant
staging
Bilateral Wilms tumor with caval invasion (arrow)
Wilms’ Tumor [Figure 6-7-9]
Nephroblastomatosis: Imaging
• Findings vary with “burden”
• Small lesions may be inapparent
• Larger lesions
➢ Multifocal cortical nodules & masses
➢ Nephromegaly with confluent solid peripheral rind Nephrogenic rests. Pathology. Small
cortical rests in peripheral cortex
Nephroblastomatosis: Imaging (arrowheads) and larger Wilms
• US: Hypo-, iso-, or hyperechoic masses or diffuse renal tumor in deep cortex
enlargement
• CT: Poorly enhancing low attenuation confluent subcortical rind or peripheral
nodules
• MRI: Low signal on T1, iso- or slightly increased signal on T2
Diffuse Nephroblastomatosis
• Clue is peripheral tissue rind
Diffuse Nephroblastomatosis
Rhabdoid Tumor
• Clue: peripheral low density collection
Figure 6-7-14
Bilateral Rhabdoid Tumors
[Figure 6-7-14]
Mesoblastic Nephroma
• Mimics Wilms tumor
• Clue: patient age
Cystic Masses
• < 5 years of age
➢ Multilocular cystic nephroma
➢ Multicystic dysplastic kidney Figure 6-7-21
• > 5 years of age
➢ Simple renal cysts (rare)
Multilocular Cystic Renal Tumor [Figure 6-7-21] Multilocular cystic renal tumor. Gross
• Composed of cysts & septa pathology showing multiple fluid-
• Encapsulated filled locules with surrounding
• Mean diameter 7 to 10 cm septations
Fat-containing
Masses:Angiomyolipoma
• Any age, but more often after 5 years
• Associated with tuberous sclerosis
• 80% of tuberous sclerosis patients have
angiomyolipomas Multicystic dysplastic kidney. Gross path and longitudinal
• Imaging: sonogram showing multiple cysts of variable size with no
➢ Bilateral fatty, renal masses normal renal tissue
➢ Solitary lesions, very rare
Figure 6-7-26
Angiomyolipoma: Imaging [Figure 6-7-26]
Lymphoma
• Secondary involvement from direct extension or hematogenous spread
• Non-Hodgkin >> Hodgkin disease
• Occurs late in course of disease Figure 6-7-28
• Usually asymptomatic
References
1. Siegel MJ. Urinary Tract. In: Siegel MJ, ed. Pediatric Sonography, 3rd ed. Lippincott Williams & Wilkins.
Philadelphia. 2002; 385-473.
2. Siegel MJ. The Kidney. In: Siegel MJ, ed. Pediatric Body CT. Philadelphia, Lippincott Williams & Wilkins,
1999; 226-252.
3. Siegel MJ. MRI of the pediatric abdomen. MRI Clin North Am 1995; 3:161-182.
4. Geller E, Smergel E, Lowry P. Renal neoplasms of childhood. Rad Clin North Am 1997; 35:1391-1413.
5. Green DM, Coppes MJ, Breslow NE, et al. Wilms tumor. In: Pizzo PA, Poplack DG, (eds). Principles and Practice
of Pediatric Oncology, 3rd ed. New York. Lippincott-Raven. 1997; 733-759.
6. Lowe LH, Isuani BH, Heller RM, et al. Pediatric renal masses: Wilms tumor and beyond. RadioGraphics 2000;
20:1585-1603.
7. Navoy JE, Royal SA, Vaid YN, Mroczek-Musulman EC. Wilms’ tumor: unusual manifestations. Pediatr Radiol
1995; 25:S76-S
8. DeBaun MR, Siegel MJ, Choyke PL. Nephromegaly in infancy and early childhood: a risk factor for Wilms
tumor in Beckwith-Wiedemann syndrome. J Pediatr 1998; 132:401-404.
Objectives
• Discuss differential diagnoses of adrenal masses in neonates and children
• Describe imaging features of common adrenal masses in a pediatric
population
• Describe pitfalls in diagnosis
Neuroblastoma: Epidemiology
• Most common extracranial solid neoplasm of childhood
• 2nd most common abdominal malignancy (after Wilms tumor)
• 10% of pediatric cancers
• 500-525 new cases/yr in the US
• Mean age ~ 2 yrs.
• 75% < 5 yrs.
Neuroblastoma: Symptoms
• Infant > 6 months
• Palpable abdominal mass
• 75% have systemic symptoms
➢ bone pain
➢ hepatomegaly
➢ paraplegia
➢ opsoclonus, ataxia
➢ diarrhea (VIP production)
Distribution of neuroblastoma
Neuroblastoma: Location [Figure 6-8-2]
• Abdomen: 75%
• Thorax: 20% Figure 6-8-3
• Neck: 1%-5%
• Pelvis: 2%-3%
• Unknown primary: 1%
➢ Present with mets
Neuroblastoma: Histology
• Small blue cell tumors with occasional cluster of cells arranged in
rosettes
Role of Imaging
• Identification of primary tumor
• Determination of extent of local disease
• Detection of distant metastases
Neuroblastoma: MRI
• T1-weighted images:
➢ low signal intensity (black)
• Fat-suppressed images:
➢ high signal intensity (bright)
• Contrast enhances
Figure 6-8-8
Figure 6-8-9
Neuroblastoma. Transverse CT
scan (top panel) and sagittal
STIR (bottom panel) images
showing intraspinal tumor
extension (arrows)
Thoracic Neuroblastoma
• Posterior mediastinum
• Fusiform shape
• Soft tissue density
• Calcifications (50%)
• Extends over several interspaces
• Osseous erosions (rib/vertebra)
Figure 6-8-13
Skeletal Metastases
• MRI
• FDG-PET
Neuroblastoma: Treatment
• Resectable disease: surgery
• Unresectable disease:
➢ chemotherapy
• Radiation therapy for tumor that does not regress with
chemotherapy
Differential Diagnosis
• Other neuroblastic tumors
➢ Ganglioneuroblastoma
➢ Ganglioneuroma Other neuroblastic tumors. Ganglioneuroblastoma (left panel).
• Pheochromocytoma Ganglioneuroma (right panel). The appearance overlaps
• Adrenocortical tumors that of neuroblastoma
• Metastases
Neurofibroma
Pheochromocytoma
• Mean age: 11 yr, (range 6-18 yr)
• 10% malignant
• Bilateral 20%: associated with:
➢ MEN-IIA & IIB
➢ von Hippel-Lindau syndrome
➢ von Recklinghausen syndrome (NF1)
• Clinical
➢ Paroxysmal hypertension, headaches, diaphoresis
Pheochromocytoma: Imaging
• Cystic changes, hemorrhage common
• US: Solid circumscribed mass with variable heterogeneity
• CT: Heterogenous mass (when large), enhances
• MR imaging: high signal T2-WT image
• MIBG avid
Adrenal Hematoma
• Clinical findings
➢ Abdominal mass
➢ Anemia
➢ Jaundice
Adrenal Hematoma: US
• Appearance varies with age of
hematoma
➢ Day1-2: echogenic or complex
mass (fibrin,debris)
➢ Day 3 to 2 wks: complex
(liquefaction)
➢ Later: cystic (hypo- or anechoic)
• Shrinkage within 1 to 2 weeks
• May calcify as early as 1 week
• Associated caval thrombus
Adrenal hematoma. Longitudinal sonograms on day 1 (left
Adrenal Hematoma upper panel), on day 12 (left lower panel), at 6 weeks
[Figures 6-8-24 and 6-8-25] (right upper panel) and at 2 months (right lower panel)
showing changes in echogenicity and near complete
resolution of a right adrenal hematoma
Adrenal Hematoma
• Calcified hematomas
Adrenal hematoma. Left panel. Day 3, complex suprarenal
Congenital Adrenal Hyperplasia mass. Right panel, day 10, nearly complete involution
• Autosomal recessive enzymatic
deficiency Figure 6-8-26
• 21-hydroxylase deficiency most common (>90%)
• Androgen overproduction
➢ virilism in girls
➢ premature masculization in boys
➢ advanced somatic development in both sexes
• Aldosterone underproduction
➢ salt wasting crisis
Adrenal Tumor-Neonate:
Hemorrhage or Neuroblastoma?
• Enlarged adrenal gland?
➢ Both
• Cystic and/or solid?
➢ Both
• Complete involution?
➢ Hemorrhage
• Liquefies?
➢ Hemorrhage Wolman disease. Plain radiographs (upper panels) showing
enlarged, calcified adrenal glands. Longitudinal sonogram
(left lower panel) showing a suprarenal mass with marked
shadowing. CT (right lower panel) showing bilateral
calcified adrenal glands.
1. Siegel MJ. Adrenal glands, pancreas and other retroperitoneal structures. In: Siegel MJ (ed), Pediatric Sonography,
3rd. Philadelphia. Lippincott Williams & Wilkins. 2002; 475-527.
2. Siegel MJ. Adrenal glands, pancreas and other retroperitoneal structures. In: Siegel MJ (ed), Pediatric Body CT.
Philadelphia. Lippincott-Williams & Wilkins. 1999; 253-286.
3. Westra SJ, Zaninovic AC, Hall TR, Kangarloo H, Boechat MI. Imaging of the adrenal gland in children.
RadioGraphics 1994; 14:1323-1340.
4. Abramson SJ. Adrenal neoplasms in children. Radiol Clin North Am 1997; 35:1415-1453.
5. Brodeur GM, Maris JM. Neuroblastoma. In: Devita VT, Hellman S, Rosenberg SA, eds. Cancer Principles and
Practice of Oncology. Lippincott Williams & Wilkins. Philadelphia. 2001; 895-933.
6. Lonnergan GJ, Schwab CM, Suarez ES, Carlson CL. Neuroblastoma, ganglioneuroblastoma and ganglioneuroma:
radiologic-pathologic correlation. Radiographics 2002; 22:911-934.
7. Berdon W, Ruzal-Shapiro C, Abramson S. The diagnosis of abdominal neuroblastoma: Relative roles of
ultrasonography, CT and MR. Urol Radiol 1992; 14:252-262
8. Cassady C, Winter WD. Bilateral cystic neuroblastoma: imaging features and differential diagnoses. Pediatr
Radiol 1997; 27:758-759.
9. Teoh SK, Whitman GJ, Chew FS. Neonatal neuroblastoma. AJR 1997; 168:54.
10. Meyer JA, Harty MP, Khademian Z. Imaging of neuroblastoma and Wilms’ tumor. Magn Reson Imaging Clin
2002; 10:275-302.
11. Siegel MJ. MR imaging of pediatric abdominal neoplasms. MRI Clin North Am 2000; 8:837-851
12. Gelfand M J. Meta-iodobenzylguanidine in children. Semin Nucl Med 1993; 23: 231-242
13. Shulkin BL, Wieland DM, Baro ME, et al. PET hydroxyephedrine imaging of neuroblastoma. J Nuc Med 1996;
37:16-21.
14. Argons GA, Lonergan GJ, Dickey GD, Perez-Monte JE. Adrenocortical neoplasms in children: radiologic-
pathologic correlation. Radiographics1999; 19:989-1008.
15. Riberio J, Ribeiro RC, Fletcher BD. Imaging findings in pediatric adrenocortical carcinoma. Pediatr Radiol 2000;
30:45-51.
16. Sivit CJ, Hung W, Taylor GA, Catena LM, Brown-Jones C, Kushner DC. Sonography in neonatal congenital
adrenal hyperplasia. AJR 1991; 156:141–143.
17. Özmen MN, Aygün N, Kiliç I, Kuran L, Yalçin B, Besim A. Wolman’s disease: ultrasonographic and computed
tomographic findings. Pediatr Radiol 1992; 22:541–542.
Pelvic Mass Lesions Normal uterine morphology. Left panel: Neonatal uterus.
• Anterior Pelvis
Longitudinal sonogram shows a tubular uterus (arrowheads)
➢ Ovarian
with prominence of the uterine fundus and a thin, hyperechoic
➢ Bladder and lower genital tract
endometrial stripe. Middle panel: A 2-year-old girl. The uterus
• Posterior Pelvis (Presacral)
is small and tubular with no differentiation between fundus and
➢ Neurogenic tumors
cervix and no recognizable endometrial stripe. Right panel.
➢ Teratomas
Sonogram showing a pear-shaped uterus with a fundus that is
larger than the cervix. The endometrial stripe (calipers) is again
Pelvic Masses: Imaging Approach visualized and varies in thickness with the phase of the
• US is screening examination of choice
menstrual cycle
for most clinically suspected masses
• CT is study of choice for evaluation of gynecologic, bladder and prostate
lesions shown on sonography
• MRI usually reserved for presacral masses
Ovarian Tumors: First Key Point Normal uterus. Left panel: CT scan of a 5-year-old girl. The
• Epithelial tumors are extremely rare in uterus (arrow) is seen as a small oval soft tissue structure.
the 1st two decades Middle panel: Normal pubertal uterus. CT scan of a 15-year-
➢ Put them low on the list old girl shows an oval uterine fundus that demonstrates zonal
• THINK SIMPLE CYSTS, GERM CELL differentiation-- higher attenuation myometrium and
TUMORS, OR STROMAL TUMORS endometrium and the lower attenuation endometrial canal.
Right panel: T2-weighted image from a 12-year-old girl shows
normal zonal anatomy--endometrial complex (e), junctional
zone (arrow), and outer myometrium (m)
Figure 6-9-8
Figure 6-9-9
Paraovarian Cysts
• Arise in broad ligament or fallopian tube
• Imaging:
➢ round or oval
➢ fluid-filled
• No cyclic changes
• Do not regress
• Can make diagnosis if cyst is separate
from ovary
Paraovarian cyst. Left panel: Longitudinal sonogram showing
Paraovarian Cysts (Fallopian a large cyst adjacent to a normal right ovary (arrow). BL =
Tube) bladder. Right panel: Fat-saturated T2-weighted axial MR
image showing a high signal intensity cyst separate from both
Paraovarian Cyst [Figure 6-9-10] ovaries
Teratoma
15 yo girl with abdominal
distention
Ovarian Cystadenoma
• Epithelial tumor Mature teratomas, US. Different patients. Left panel:
• < 5% neoplasms, benign Longitudinal sonogram showing a predominantly cystic mass
• Mucinous >> serous with a an echogenic mural nodule (dermoid plug) (arrow).
• 4 to 20 cm diameter B=bladder; UT=uterus. Right panel: Sonogram showing a
• Epithelial linings complex cystic mass containing large echogenic mural nodule
➢ Simple (serous type) anteriorly (arrow) with acoustic shadowing
➢ Columnar, mucinous (mucinous
type) Figure 6-9-13
Cystadenoma: Imaging [Figure 6-9-14]
• Usually large
• Cystic
• Multilocular with septations
• Sometimes unilocular
➢ Particularly serous type
Serous Cystadenoma
Ovarian Malignancies
• Germ cell tumors (85%)
• Stromal tumors (15%)
• Epithelial tumors
Figure 6-9-19
Uterine Masses
• Cystic
➢ hydrocolpos
• Solid
➢ rhabdomyosarcoma
Hydrocolpos
• Vaginal obstruction
➢ due to stenosis or membrane
• Result is pelvic/abdominal mass Hydrocolpos-hematocolpos, US. Left panel. Neonate.
• Imaging findings Longitudinal sonogram showing dilated fluid-filled vagina (V)
➢ Fluid-filled midline mass outlining the cervix (C). B = bladder. Right panel.
➢ Well defined walls Hematocolpos. Longitudinal sonogram showing a dilated
➢ Internal debris or blood vagina (V) with low level central echoes, representing blood.
❖ (hemato- or Uterus (U) is normal
hematometrocolpos)
Rhabdomyosarcoma
• Most common pelvic malignancy
• Bimodal age distribution: Figure 6-9-21
➢ 2 to 6 and 14 to 16 years
• Embryonal cell type
• Sites:
➢ Head/Neck 38%
➢ GU 21%
➢ Extremity 18%
Rhabdomyosarcoma: Prostate
Bladder Rhabdomyosarcoma
Sacrococcygeal Teratoma
• CA++: 60%
• Malignancy: 10% newborn
90 > 2 months
• Location: 45 % external
45% external & internal
10% presacral
• Bony defect: very low frequency
• Arise from coccyx
• Do not invade spinal canal
Sacrococcygeal Teratoma
Anterior Meningocele
• Herniation of spinal contents through a
congenital defect in a vertebral body
• Scimitar shaped sacrum Benign sacrococcygeal teratoma. T1-weighted MR (left panel)
• CT/MR showing a predominantly fat-containing mass with small fluid-
➢ absent sacral elements filled nodules. Fat-saturated T2-weighted MR (right panel).
➢ tethered cord The fatty tissue has decreased in signal intensity. Fluid
components are bright. The tumor arises from the coccyx
Anterior Meningocele (arrow)
Presacral Masses
• Cystic Figure 6-9-25
➢ benign teratoma
➢ meningocele
• Solid
➢ malignant teratoma
➢ neuroblastoma
Figure 6-9-26
Neurofibromas
• Nerve sheath tumors
• Often plexiform in the pelvis
➢ multiple or interlacing masses
• Affect about 5%-15% of people with NF1
• Imaging
➢ Multiple soft tissue masses
➢ Target sign T2 MR
➢ Enlarged sacral foramen
Plexiform Neurofibromatosis
• Clue: enlarged sacral foramen
Neurofibromatosis: T2 MR
Lymphadenopathy
References
1. Garel L, Dubois J, Grignon A, Filiatrault D, Van Vliet G. US of the pediatric female pelvis: a clinical perspective.
Radiographics 2001; 21:1393-1407.
2. Siegel MJ. Female pelvis. In: Siegel MJ, ed. Pediatric Sonography, 3rd ed. Philadelphia. Lippincott Wiliams &
Wilkins.
3. States LJ, Bellah RD. Imaging of the pediatric female pelvis. Semin Roentgenol 1996; 31:312-329.
4. Boechat IN. MR imaging of the pediatric pelvis. MRI Clin North Am. 1996; 4:679-697.
5. Rigsby CK, Siegel MJ. CT appearance of pediatric ovaries and uterus. J Comput Assist Tomogr 1994; 18:72-76.
6. Siegel MJ. Pelvic organs and soft tissues. In: Siegel MJ, ed. Pediatric Body CT. Philadelphia, Lippincott
Williams and Wilkins, 1999, pp 287-311.
7. Siegel MJ. Magnetic resonance imaging of the adolescent female pelvis. Mag Reson Imaging Clin North Am
2002; 10:303-324.
8. Baltarowich OH. Female pelvic organ measurements. In: Goldberg BB, Kurtz AB, eds. Atlas of Ultrasound
Measurements. Chicago. Year Book Medical Publishers. 1990; 190-242.
9. Cohen HL, Eisenberg P, Mandel F, Haller JO. Ovarian cysts are common in premenarchal girls: a sonographic
study of 101 children 2-12 years old. AJR 1992; 159:89-91.
10. Siegel MJ. Pelvic tumors. Radiol Clin North Am 1997; 35:1455-1475.
11. Fried AN, Kenney CM III, Stigers KB, Kacki MH, Buckley SL . Benign pelvic masses: sonographic spectrum.
RadioGraphics 1996; 16:321-334
12. Kim JS, Woo SK, Suh SJ, Morettin LB. Sonographic diagnosis of paraovarian cysts: value of detecting a separate
ipsilateral ovary. AJR 1995; 164:1441-1444
13. Jabra AA, Fishman EK, Taylor GA. Primary ovarian tumors in the pediatric patient: CT evaluation. Clin Imaging
1993;17:199-203.
Lecture Objectives
• Review normal bone marrow anatomy
• Discuss MRI marrow techniques
• Describe features of normal marrow on MRI
• Recognize causes of pathologic marrow on MRI
Marrow Components
• Osseous matrix
➢ (aka cancellous or spongy bone)
➢ Provides support for cellular components
Marrow Components
• Red Marrow
➢ Cellular, active or myeloid marrow
➢ Composed of red & white blood cells & platelets
Normal marrow constituents.
• Yellow Marrow
Histologic section showing
➢ Inactive or fatty marrow
hematopoietic and yellow marrow
➢ Composed of fat cells
Red Yellow
Water 40 15
Fat 40 80
Protein 20 5
• MRI appearance of marrow reflects the relative
fractions of red & yellow marrow
Whole-body MRI
• Technique
➢ Vertex to toes
➢ Coronal plane
❖ Sagittal plane
• Table moves 4-6 times
➢ Total imaging time
❖ ~ 7-20 minutes
Lauenstein, Radiology 2004;233:139
Normal Marrow: T1
• This is your “Fat Finder” sequence
• Yellow marrow will be bright due to abundant fat composition
• Red marrow contains much less fat, and will be intermediate in signal. (But
enough fat not to be dark!!!!)
Marrow Conversion
Appendicular to Axial Conversion
Custer. J Lab Clin Med 1932
Reconversion
• Axial skeleton responds first, followed by extremities
Marrow Reconversion
• Reverse order from normal conversion process! Vertebral marrow, red-yellow marrow
• Proximal to Distal!! distribution. Yellow marrow is
located near basivertebral vein in
neonates and young children
(upper right diagram). Other
patterns predominate in
adolescents and adults
Reconversion: Thalassemia
Marrow Replacement
• T1 WT: dark
• STIR/Fat sat: very bright
• Can be diffuse or focal
• Predominates in red marrow (axial
skeleton) Marrow reconversion. Two different patients. Coronal T1-
weighted image of the knees shows diffuse low signal
Diffuse Replacement Disorders: intensity red marrow in the distal femoral and proximal tibial
Leukemia [Figure 6-10-10] metaphyses. Scattered high signal intensity foci represent
islands of yellow marrow and/or infarcts
Figure 6-10-10
Figure 6-10-9
Pathologic Fracture
Osteoporotic Fracture
• Partial body involvement
➢ Usually involves end plate
• Signal of spared marrow is normal
• Thoracolumbar junction Vertebral fractures. Pathologic
• Clustering of abnormalities fracture (left panel). Gadolinium-
• Thin paraspinal soft tissue mass enhanced T1-weighted MR
• Improves in 6 to 8 weeks shows abnormal signal intensity
in entire vertebral body, convex
Compression fractures posterior cortex, and small
epidural mass. Osteoporotic
Pathologic and Osteoporotic Fractures [Figure 6-10-11] fracture (right panel). T1-
weighted MR shows partial body
Variations in Appearance of Metastases involvement (upper end plates),
• Blastic and fibrotic lesions normal marrow signal, and
• Low signal on T1 and fat -suppressed images clustering of abnormalities at
• Often heterogeneous thoracolumbar junction
Figure 6-10-13
Figure 6-10-14
Osteomyelitis: MR
Mimics of Fibrosis
• Gaucher disease
➢ Marrow replacement by glucocerebroside-laden
cells
• Hemosiderin deposition
➢ Marrow replacement by iron
➢ Usually from transfusion therapy
• Decreased T1 and T2-weighted signal
• Slightly increased signal on STIR
Gaucher Disease
• Due to deficiency of the enzyme acid beta- Primary myelofibrosis. Coronal T1-weighted (left
glucocerebrosidase, which helps to break down panel) and T2-weighted (right panel) MR
glucosyl ceramide images show low signal intensity marrow in
• Follows distribution of red marrow the ilia, femora and vertebral bodies
• Proximal to distal
Marrow Depletion
Fatty Replacement [Figure 6-10-18]
• Absence of red marrow
• Causes
➢ chemotherapy
➢ radiation therapy
➢ aplastic anemia
• Marrow has signal of fat
Figure 6-10-19
Figure 6-10-18
T1 STIR/FS
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8. Lauenstein TC, Goedhe SC, Herborn CU, et al. Whole-body MR imaging: evaluation of patients for metastases.
Radiology 2004; 233:139-148.
9. Mazumdar A, Siegel M, Narra V, Luchtman-Jones L. Whole-body fast inversion recovery MR imaging of small
cell neoplasms in pediatric patients: a pilot study. AJR 2002; 179:1261-1266.
10. O’Connell MJ, Hargaden G, Powell T, Eustace SJ. Whole-body short tau inversion recover MR imaging with a
moving table top. AJR 2002; 179: 866-868.
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bones with advancing years of life and their relative response to stimuli. J Lab Clin Med 1932; 17:960-962.
14. Moore DG, Dawson KL. Red and yellow marrow in the femur: age-related changes in the appearance at MR
imaging. Radiology 1990; 175:219-223.
15. Ricci C, Cova M, Kang YS et al. Normal age-related patterns of cellular and fatty bone marrow distribution in the
axial skeleton: MR imaging study. Radiology 1990; 177:83-88.
16. Taccone A, Oddone M, Dell’ Acqua A, Occhi M, Ciccone MA. MRI “road-map” of normal age-related bone
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17. Mirowitz SA. Hematopoietic bone marrow within the proximal humeral epiphysis in normal adults: investigation
with MR imaging. Radiology 1993; 188:689-93.
18. Fletcher BD, Wall JE, Hanna SL. Effect of hematopoietic growth factors on MR images of bone marrow in
children undergoing chemotherapy. Radiology 1993; 189:745-751.
19. Ryan SP, Weinberger E, White KS, et al. MR imaging of bone marrow in children with osteosarcoma: effect of
granulocyte colony-stimulating factor. AJR 1995; 165:915-920.
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images of the knee in asymptomatic marathon runners. AJR 1992; 335-338.
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conventional spin-echo, chemical shift, and STIR MR imaging. Radiology 1990; 174:495
22. Blomlie V, Rofstad EK, Skjonsberg A, Tverå, Lien HH. Female pelvic bone marrow: serial MR imaging before,
during, and after radiation therapy. Radiology 1995; 194:537-543.
23. Otake S, Mayr N, Ueda T et al. Radiation-induced changes in the MR signal and contrast enhancement of
lumbosacral vertebrae: do changes occur only inside the radiation therapy field? Radiology 2002; 222:179-183.
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1990; 154:745-750.
25. Hermann G, Shapiro RS, Abdelwahab IF, Grabowksi G. MR imaging in adults with Gaucher disease type I:
evaluation of marrow involvement and disease activity. Skeletal Radiol 1993; 22:247-251.
26. Levin TL, Sheth SS, Hurlet A, Comerci SC, Ruzal-Shapiro, Piomelli S, Berdon WE. MR marrow signs of iron
overload in transfusion-dependent patients with sickle cell disease. Pediatr Radiol 1995; 25:614-619.
Learning Objectives
• Review clinical & pathologic features of common lung anomalies
• Describe imaging appearances of the common congenital anomalies
• Emphasize imaging differential diagnosis
CCAM: Clinical
• 70%-90% symptomatic as neonates
➢ Cyanosis, grunting, tachypnea
• Rare in older children & adults
➢ Presents as pneumonia or recurrent infection
• May be antenatal diagnosis
CCAM: Imaging
• Air-filled mass, mediastinal shift
➢ Except may be opaque initially if fluid-filled
• Type I
➢ Multicystic lesion, with dominant cyst(s)
➢ Air fluid levels
• Type II
➢ Heterogeneous, uniform small cysts
• Type III
➢ Large, homogeneous, solid
➢ Resembles consolidation
Figure 6-11-6
Spectrum of CCAM
• 10% diagnosed in adolescents & adults
• Infection common
• May mimic infiltrate or mass on imaging studies
Infected CCAM
• Adolescent with cough
Figure 6-11-7
Infected CCAM [Figure 6-11-7]
Bronchogenic Cyst
• Failure of lung bud to incorporate into
primitive lung
• Lung (30%), mediastinum (70%)
• Asymptomatic & incidental finding
• Symptomatic from mass effect
Bronchogenic Cyst
• 7-day old girl, wheezing
Bronchogenic cyst, pathology. Gross
Bronchogenic Cyst [Figure 6-11-9] specimen showing a fluid-filled lung
• 7- year-old girl with cough mass. Histologic section showing
respiratory epithelium lining the cyst
Figure 6-11-9 wall
Figure 6-11-10
Differential Diagnosis: Enteric Cysts Enteric cyst. Transverse CT (left panel) showing a
[Figure 6-11-11]
water attenuation mass in the lower mediastinum.
Gross section (middle image) showing a cystic
mass. Histologic section (right panel) showing
gastrointestinal lining
Pulmonary Underdevelopment
• Agenesis: Complete absence of lung tissue, artery, & small or
absent bronchus
• Hypoplasia: Small lung & bronchus (artery may or may not
develop)
Figure 6-11-13
Pulmonary Hypoplasia
• Small lung & bronchus No PA
Pulmonary Sequestration
• No normal connection with bronchial tree or
pulmonary arteries
• Systemic blood supply
• 2 types
➢ Intralobar (acquired)
➢ Extralobar (congenital)
Hypogenetic lung syndrome. Transverse CT scan
Pulmonary Sequestration showing a small right lung and mediastinal shift
• ELS ILS towards the right. Also noted a left aortic arch with
➢ Own pleura Shared pleura anomalous right subclavian artery. Coronal
➢ Neonate Children & adults multiplanar (middle panel) and 3D volume
➢ 90% left 90% left rendered image (viewed posteriorly) showing an
➢ Solid Cystic or solid anomalous vein (arrow) draining the right lower
➢ Syst. arterial supply Syst. arterial supply lobe
➢ Syst.venous drainage Pulm. venous drainage
➢ Assoc. anomalies +/- assoc. anomalies Figure 6-11-16
Sequestration: US Features
• Gray-scale
Intralobar sequestration. Chest radiograph
➢ Echogenic mass
showing a left lobe air space opacity. Sonogram
❖ Supradiaphragmatic-likely ILS
showing a supradiaphragmatic echogenic mass
❖ Subdiaphragmatic (suprarenal)-likely ELS
with a feeding artery in the left lower lobe
• Doppler US
➢ Feeding artery off aorta Figure 6-11-20
➢ Draining vein usually not identified
Sequestration: CT Features
• Anomalous feeding artery
• Draining vein to pulmonary or systemic veins
• Parenchymal findings
➢ ILS:
❖ Infiltrate
❖ Abscess
❖ Focal emphysema
➢ ELS
❖ Triangular/round solid mass
Figure 6-11-19
Extralobar Sequestration:
Round Lower Lobe Mass [Figure 6-11-22]
Extralobar Sequestration:
Systemic Drainage
Extralobar Sequestration
• Solid, well-defined LLL mass
Extralobar sequestration. Chest radiograph
showing a triangular mass (arrow) at the left lung
Sequestration: MRI
base. Transverse sonogram showing an
heterogeneous mass (arrows) which was below
ELS with CCAM (40%)
the left hemidiaphragm
Summary
• ILS Figure 6-11-22
• ELS
Arteriovenous Malformation
• 80% Hereditary telangiectasia (OWR)
➢ 15% sporadic
➢ 5% cardiac surgeries (Glenn or Fontan)
• Symptomatic in older patients (cyanosis,
polycythemia, dyspnea)
• 80%-90% are simple AVMs
➢ single feeding and draining vessel
➢ commonly lower lobes
1. Siegel MJ. Lung, pleural and chest wall. In: Pediatric Body CT. Philadelphia, Lippincott Williams & Wilkins.
1999;101-.140
2. Kim WS, Lee KS, Kim IO, et al. Congenital cystic adenomatoid malformation of the lung: CT-pathologic
correlation. AJR 1997; 168:47-
3. Rosado-de-Christenson JL, Stocker JT. Congenital cystic adenomatoid malformation. J Comput Assist Tomogr
1989; 13:612-616
4. Shackelford GD, Siegel MJ. CT appearance of cystic adenomatoid malformation. J Comput Assist Tomogr 1989;
13:612-616.
5. Felker RE, Tonkin IL. Imaging of pulmonary sequestration. AJR 1990; 154:241-249
6. Frazier AA, Rosado de Christenson ML, Stocker JT et al. Intralobar sequestration: radiologic-pathologic
correlation. RadioGraphics 1997; 17:725-745.
7. Ko SF, Ng SH, Lee TY, et al. Noninvasive imaging of bronchopulmonary sequestration. AJR 2000; 175:1005-
1012
8. Lee E, Siegel MJ, Sierra LM, Foglia RP. Evaluation of angioarchitecture of pulmonary sequestration in pediatric
patients using multidetector CT angiography. AJR 2004; 183:183-188.
9. Rosado-de-Christenson ML, Frazier AA, Stocker JT, Templeton PA. Extralobar sequestration: radiologic-
pathologic correlation. From the archives of the AFIP. RadioGraphics 1993; 13:425-441.
10. Konen E, Raviv-Zilka L, Cohen RA, et al. Congenital pulmonary venolobar syndrome: Spectrum of helical CT
findings with emphasis on computerized reformatting. RadioGraphics 2003; 23:1175-1184
11. Woodring JH, Howard TA, Kanga JF. Congenital pulmonary venolobar syndrome revisited. RadioGraphics 1994;
14:349-369.
12. Remy J, Remy-Jardin M, Giraud F, et al. Angioarchitecture of pulmonary arteriovenous malformations: clinical
utility of three-dimensional helical CT. Radiology 1994; 191:657-664.
13. Hoffman LV, Kuszyk BS, Mitchell SE, et al. Angioarchitecture of pulmonary arteriovenous malformation:
characterization using volume-rendered 3D CT angiography. Cardiovasc Intervent Radiol 2000; 23: 165-170.
14. Rotondo A, Scialpi M, Scapati C. Pulmonary arteriovenous malformation: evaluation by MR angiography. AJR
1997; 168: 847-849.
Objectives
• Discuss lung diseases in preterm and term neonates
• Review treatment complications
• Understand important differential findings
Complications of Treatment
• Related to respirator Chest radiograph (left image) showing RDS,
➢ Air leaks pretreatment. Chest radiograph (right image)
➢ Bronchopulmonary dysplasia showing RDS, 24 hours after surfactant therapy
Air Leak: Pathogenesis
• Results from positive pressure ventilation of noncompliant lungs
• Rupture at bronchiolar-alveolar junction
• Gas dissects into interlobular septa and septal lymphatics (interstitial air)
• May enter pleural space, mediastinum, pericardium, peritoneum, venous
system
Pneumopericardium
Retained Fetal Lung Fluid: Radiographic Retained fetal lung fluid. Frontal chest radiograph
Findings showing reticular opacities and small right pleural
• Increased lung volumes effusion. Lateral radiograph showing fissural fluid
• Reticular opacities
• Fissural fluid
• Small pleural effusions Figure 6-12-16
• Clearing in 24 to 48 hours
Neonatal Pneumonia
• 0.5% of term infants
• Frequently associated with neonatal sepsis
• Clinical and radiographic challenging diagnosis
For Comparison
• Respiratory distress syndrome
➢ Decreased long volumes
➢ Granular lung disease
➢ NO effusions in uncomplicated disease!!
Chylothorax
• Rupture of thoracic duct
• Usually due to birth trauma
➢ Rarely congenital anomaly
• Full term infants
➢ 70% symptomatic in 1st week
• Right > left pleural effusions
➢ Rarely bilateral
Chylothorax
• Thoracentesis usually yields cloudy fluid because of the high lipid content of
chyle
• Treatment includes thoracentesis, chest tube drainage, and feedings of
medium-chain triglycerides
• Most lymphatic ruptures seal with combined chest tube and dietary treatment
Chylothorax
• Differential diagnosis includes causes of nonchylous pleural effusions
➢ Wet-lung disease
➢ Hydrops fetalis
➢ Turner’s syndrome
➢ Pulmonary vein obstruction
➢ Congestive heart failure
➢ Esophageal rupture
Alveolar Proteinosis
• Due to congenital surfactant protein B deficiency
• Autosomal recessive
• PAS-positive abnormal surfactant lipids & proteins accumulate in alveoli &
macrophages
• Diagnosis confirmed by alveolar lavage & peripheral blood DNA analysis Figure 6-12-22
• Treatment - lung transplantation
Pediatr Radiol 2001; 31: 327-331
Figure 6-12-24
References
1. Center for Disease Control and Prevention: National Center for Disease Statistics. National Vital Statistics
Reports, Vol. 52, No. 10, Dec 17, 2003. Web: www.cdc.gov/nchs
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neonates. AJR Am J Roentgenol 1988; 150:885-887.
Lecture Outline
• Review MRA and CTA techniques
• Discuss CT and MR appearances of common thoracic vascular anomalies
Double Arch
Infant with wheezing
Pulmonary Sling
• Created by anomalous course of left PA
➢ Arises from right pulmonary artery & crosses between trachea
& esophagus
• Usually symptomatic in children, dyspnea
Figure 6-13-6
Pulmonary Sling
Ductus
• Calcified ductus
Figure 6-13-8
Pulmonary sling. Chest radiograph
(upper panel) showing tracheal
compression. CTA (upper right panel)
showing the left pulmonary artery
(LPA) arising from the right pulmonary
artery (RPA) and crossing behind the
trachea to reach the left hilum. 3D
rendering of the airway (lower panel)
confirming right-sided tracheal
compression
Figure 6-13-9
RUL PAPVR
• 90% have venosum ASD
Scimitar syndrome
Figure 6-13-12
Right lower lobe anomalous
pulmonary venous return. Coronal
CT showing right lower lobe vein
draining into the inferior vena cava
Figure 6-13-16
Left superior vena cava. Transverse images
showing an enhancing left sided cava (arrow) and
a smaller right superior vena cava. The left
superior vena cava courses past the aortic arch
and left pulmonary hilum to enter into a dilated
coronary sinus
Differential diagnosis
Left paramediastinal structures
• Left superior intercostal vein
• Anomalous LUL venous return
Summary: Left Paramediastinal Structures Left superior intercostal vein. The vein (arrow)
• Left superior vena cava courses adjacent to the aortic arch and connects
➢ Subclavian vein to coronary sinus with the accessory hemiazygous vein inferiorly
• Anomalous LUL pulmonary vein
➢ Left pulmonary hilum to BCV
• Left superior intercostal vein Figure 6-13-19
➢ BCV to accessory hemiazygos vein
Differential diagnosis
Right paramediastinal structures
• Azygous vein
➢ joins hemiazygos
➢ ascends on right
➢ drains into SVC Summary: Left image, left superior vena cava.
• Superior intercostal vein Middle image, anomalous left upper lobe
➢ joins azygos vein pulmonary venous return. Right image, superior
➢ drains 2nd-4th intercostal veins left intercostal vein
Figure 6-13-21
Kawasaki Disease
• Aka Mucocutaneous lymph node syndrome
• Unknown etiology
• Clinical features Coronary artery aneurysm, Kawasaki disease. CT
➢ fever of a neonate (left panel) showing dilated left
➢ rash anterior descending and circumflex arteries
➢ conjunctivitis (arrows) . CT scan of an adolescent girl (right
➢ erythema of lips & buccal mucosa panel) showing calcified aneurysm (arrow) of the
➢ myocarditis left coronary artery
➢ coronary artery aneurysms
Marfan Disease
• Inherited connective tissue disorder transmitted as an autosomal dominant
trait
• Localized to a mutation in chromosome 15
• Cardinal features
➢ tall stature
➢ slender limbs and fingers
➢ ectopia lentis
➢ pectus excavatum
➢ scoliosis
1. Katz M, Konen E, Rozenman, et al. Spiral CT and 3D image reconstruction of vascular rings and associated
tracheobronchial anomalies J Comput Assist Tomogr 1995; 19:564-568.
2. Lee Ed, Siegel MJ, Hildebolt CF, Gutierrez FR, Bhalla S, Fallah JH. Multidetector CT Evaluation of Pediatric
Thoracic Aortic Anomalies: Comparison of Axial, Multiplanar, and Three-Dimensional Images. AJR 2004;
182:777-784
3. Lawler LP, Fishman EK. Multi-detector row CT of thoracic disease with emphasis on 3D volume rendering and
CT angiography. RadioGraphics 2001; 21: 1257-1273
4. Remy-Jardin M, Remy J, Mayo JR, Muller NL. Thoracic aorta. In: CT Angiography of the Chest. Lippincott
Williams & Wilkins. Philadelphia. 2001; 29-50.
5. Czum JM, Corse WR, Ho VB. MR angiography of the thoracic aorta. Magn Reson Clin N Am 2005; 13:41-64.
6. Choe YH, Kim YM, Han BK, Park KG, Lee HJ. MR Imaging In the morphologic diagnosis of congenital heart
disease. RadioGraphics 1997; 17:403-422.
7. Ho VS, Corse WR, Hood MN, Rowedder AM. MRA of the thoracic vessels. Semin Ultrasound CT MR 204:192-
216.
8. Gilkeson RC, Ciancibello L, Zahka K. Multidetector CT evaluation of congenital heart disease in pediatric and
adult patients. AJR 2003; 180:973-980.
9. Gup HW, Park I-S, Ko JK, et al. CT of congenital heart disease: normal anatomy and typical pathologic
conditions. Radiographics 2003; 23: S147-165.
10. Hopkins KL, Patrick LE, Simoneaux SF, et al. Pediatric great vessel anomalies: initial clinical experience with
spiral CT angiography. Radiology 1996; 200:811-815.
11. Stella VB, Toutouzas P. Patent arterial duct and aortopulmonary window. In: Gatzoulis MA, Wevbb GD,
Daubeney PEF. Adult Congenital Heart Disease. Churchill Livingstone. Edinburgh 2003; 247-252.
12. Morgan-Hughes GJ, Marshall AJ, Roobottom C. Morphologic assessment of patent ductus arteriosus in adults
using retrospectively ECG-gated multidetector CT. AJR 2003; 181:749-754.
13. Mahnken AH, Wildberger JE, Spuntrup E, et al. Unilateral absence of the left pulmonary artery associated with
coronary-to-bronchial artery anastomosis. J Thorac Imaging 2000; 15:187-190;
14. Gupta H, Mayo-Smith WW, Mainiero MB, Dupuy DE, Abbott GF. Helical CT of pulmonary vascular
abnormalities. AJR 2002; 178: 487-492.
15. Park HS, Im JG, Jung JW, et al. Anomalous left pulmonary artery with complete cartilaginous ring. J Comput
Assist Tomogr 1997; 21:478-480.
16. Zwetsch B, Wicky S, Meuli R et al. Three-dimensional image reconstruction of partial anomalous pulmonary
venous return to the superior vena cava. Chest 1995; 108:1743-1735,
17. Dillon EH, Camputaro C. Partial anomalous pulmonary venous drainage of the left upper lobe vs duplication of
the superior vena cava: distinction based on CT findings. AJR 1993;160: 375-379.
18. Van Praagh S, Carrera ME, Sanders S, Mayer JE, Van Praagh R. Partial or total direct pulmonary venous drainage
to the right atrium due to malposition of septum primum. Chest 1995; 107:1488-1498.
Lecture Outline
• Review CT & MRI techniques
• Describe CT and MR appearances of common congenital heart diseases
➢ Neonates and infants
➢ Older children & adolescents
• Discuss treatment options
Secundum ASD
• Large PAs
• Mid septal defect
Repaired ASD
• Occluder device for small secundum
ASD
Repaired ASD
• Septal patch for large secundum ASD & venosus &
primum ASD
Figure 6-14-8
Intramuscular VSD (arrow).
The defect is within the
interventricular septum
Figure 6-14-9
Subpulmonic VSD. MR
showing the septal defect Summary. Subaortic VSD (far left panel).
(arrow) at the level of the right Muscular VSD (middle left panel). Ostium
ventricular outlet in the primum (inlet) VSD (middle right
supracristal area panel).Subpulmonic VSD (far right panel)
Coarctation Repair
• Resection & end-to-end anastomosis
• Stents, angioplasty, patch aortoplasty
Stent Restenosis
Part III.
Common Cyanotic Diseases
SHUNTS OBSTRUCTIVE CYANOTIC HEART LESIONS
VSD Coarctation
ASD HLHS Tet of Fallot
PDA Tricuspid Atresia
AV Canal TGV
Truncus
TAPVR Figure 6-14-13
Cyanotic CHD
• Indicates that unoxygenated venous
blood is reaching aorta
• Causes:
➢ Right heart obstruction with Rt to Lt
shunting via a septation defect
❖ TOF, tricuspid atresia
➢ Mixing of pulmonary & systemic
blood due to incomplete separation Hypoplastic left heart syndrome. Transverse CT (left image)
of chambers showing small left ventricle (arrow). CT (right image) at a more
❖ TGV, Truncus, TAPVR proximal level shows small ascending aorta (arrow)
Tetralogy of Fallot-MR [Figure 6-14-14] Tetralogy of Fallot, MRI. Transverse MR (left panel) shows
perimembranous VSD (arrow) and right ventricular
Surgical Repair TOF [Figure 6-14-15] hypertrophy (RVH). Sagittal MR (middle panel) shows
• Initial surgery is palliative narrowed pulmonary outflow tract (arrow). (PA=normal size
➢ Blalock-taussig shunt main pulmonary artery). Sagittal MR (right panel) shows aorta
➢ Subclavian artery to PA (Ao) overriding right and left ventricles, VSD (arrow), and right
ventricular hypertrophy
Figure 6-14-15
Figure 6-14-18
Figure 6-14-19
Mustard Procedure
• Systemic venous baffle
• Pulmonary venous baffle
D-Transposition of great vessels. Sagittal MRA
Jantene Procedure (left panel) showing aorta arising from right
• Current procedure of choice ventricle (RV) and pulmonary artery from left
• Great artery switch ventricle (LV). Transverse MRI and CT showing
• Aorta and PA sectioned above valves & reconnected aorta (A) anterior and to right of pulmonary artery
to proper ventricles (PA)
• Coronary arteries reimplanted
Figure 6-14-21
Arterial Switch: Jatene Procedure [Figure 6-14-22]
Truncus Arteriosus
• I. Single PA arises from truncus (80%)
• II. R and L PA arise from posterior truncus
• III. R and L PA arise from sides of truncus. Atrial switch, mustard
• IV. R and L PA arise from descending aorta procedure. Coronal CT
(upper image) shows
systemic baffle
directing blood from
right heart to left heart
Figure 6-14-22 where it exits into
pulmonary arteries.
Transverse CT (lower
image) shows systemic
baffle and also
pulmonary venous (PV)
baffle which directs
blood from pulmonary
veins into right ventricle
where it exits into aorta
Additional Lesions: Older Children & Truncus arteriosus. Type I A single pulmonary
Adolescents artery arises from the truncus (T)
• Aortic stenosis
• Pulmonic stenosis
Figure 6-14-24
Aortic Stenosis
• Valvular >> sub- or supravalvular
• Usually due to bicuspid valve
• CT/MR: dilated ascending aorta
➢ Bicuspid valve
Summary
• Diagnosis of CHD depends on knowledge of the anatomic abnormality, the clinical findings &
understanding of imaging findings
References
1. Amplatz K, Moller JH Radiology of Congenital Heart Disease Mosby –Year Book Inc 1993
2. Boxt LM. MR imaging of congenital heart disease. Magn Reson Imaging Clin North America;1996:4:327-359
3. Choe YH, Kim Ym, Han BK, Park KG, Lee HJ. MR imaging in the morphologic diagnosis of congenital heart
disease. RadioGraphics 1997; 17:403-422.
4. Poustchi-Amin M, Gutierrez FR, Brown JJ, et al. How to plan and perform a cardiac MR imaging examination.
Radiol Clin North Am 2004; 42:497-514
5. Gilkeson RC, Ciancibello L, Zahka K. Multidetector CT evaluation of congenital heart disease in pediatric and
adult patients. AJR 2003; 180:973-980.
6. Goo HW, Park I-S, Ko J-K, et al. CT of congenital heart disease: normal anatomy and typical pathologic
conditions. Radiographics 2003; 23: S147-165
7. Gutierrez FR, Canter CE, Mirowitz SA: MR appearance of congenital heart defects. In: Gutierrez FR, Brown JJ,
Mirowitz SA (eds.): Cardiovascular magnetic resonance Imaging. St. Louis: Mosby Year Book, 1992;72-83.
8. Higgins CB: Congenital heart disease. In: Higgins CB, Hricak H, Helms CA (eds.): Magnetic Resonance Imaging
of the body. 3rd ed. Philadelphia: Lippincott-Raven, 1997; 461-518.
9. Lee E, Siegel MJ, Guttierez F, Hildebolt CF, Bhalla S, Fallah JH. Multidetector CT evaluation of thoracic aortic
anomalies in pediatric patients and young adults: comparison of thoracic axial, multiplanar, and 3D images. AJR
2004; 182:777-78410.
10. Kaemmerer H. Aortic coarctation and interrupted aortic arch. In: Gatzoulis MA, Wevbb GD, Daubeney PEF.
Adult Congenital Heart Disease. Churchill Livingstone. Edinburgh 2003; 253-264.
11. Becker C, Soppa C, Fink U et al. Spiral CT angiography and 3D reconstruction in patients with aortic coarctation.
Eur Radiol 1997; 7:1473-1477.
12. Roest AA, Helbing WA, van der Wall EE. Postoperative evaluation of congenital heart disease by magnetic
resonance imaging. J Magn Res Imag 1999; 10:656-666.
13. Donnelly LF, et al. MR imaging of cono-truncal abnormalities. AJR 1996; 166:925-928.
14. Connelly M. Common arterial trunk. In: Gatzoulis MA, Webb GD, Daubeney PEF. Adult Congenital Heart
Disease. Churchill Livingstone. Edinburgh 2003; 265-271.
15. Jacobs ML. Congenital heart surgery nomenclature and database project: truncus arteriosus. Ann Thorac Surg
2000; 69:S50-S55.
16. Kim TH, et al. Helical CT angiography and three-dimensional reconstruction of total anomalous pulmonary
venous connections in neonates and infants. AJR 2000; 175: 1381-1386.
17. Bardo DM, et al. Hypoplastic left heart syndrome. Radiographic 2001; 21:705-717.
18. Mavroudis C, Backer CL, Deal BJ. Venous shunts and the Fontan circulation in adult congenital heart disease. In:
Gatzoulis MA, Wevbb GD, Daubeney PEF. Adult Congenital Heart Disease. Churchill Livingstone. Edinburgh
2003; 79-83.
19. Feeedom RM, Li J, Yoo S-J. The complications following the Fontan operation. In: Gatzoulis MA, Wevbb GD,
Daubeney PEF. Adult Congenital Heart Disease. Churchill Livingstone. Edinburgh 2003; 85-91.
Topics
• Assessing the chest film
• Acyanotic CHD with increased PBF
• Cyanotic CHD with increased PBF
• Cyanotic CHD with decreased PBF
Caveat
• In infants, all forms of increased PBF may lead to pulmonary
edema
• Cannot reliably distinguishing arterial overcirculation from passive
congestion
• Consider the 3 causes of increased PBF:
➢ Intracardiac shunts
➢ Extracardiac shunts
➢ Cardiac failure
VSD: blood flows from LV to RV
VSD: Hemodynamics
• Blood flows from LV to RV
• Volume overload in RV
• RV enlarges and hypertrophies
• Blood in RV goes to lungs, LA, LV.
• When it arrives in LV, it “decompresses” into RV
➢ LV remains normal
• 4 basic types
➢ Membranous 80%
➢ Muscular (often multiple) 10%
➢ Supracristal 5%
➢ Inflow / AV canal type 5%
➢ Size matters, not location!
VSD: Presentation
• Usually in 2nd month of life
➢ Pulmonary vascular resistance has dropped
sufficiently to allow increased shunting Figure 6-15-4
• Presentation
➢ Frequent pneumonias
➢ Failure to thrive
➢ CHF
VSD
• All need to be closed
Figure 6-15-5
• Large:
➢ Significant L to R shunting
➢ Less turbulence
➢ Pulmonary HTN, Eisenmenger syndrome
• Small:
➢ Less L to R shunting
➢ More turbulence
➢ Higher risk of bacterial endocarditis
Figure 6-15-6b
ASD locations: uppermost is
sinus venosus, middle is
ostium secundum, lowest is
ostium primum
ASD
Figure 6-15-7
ASD: Complications
• Pulmonary HTN & Eisenmenger syndrome
➢ 30% with mod-large ASD develop HTN
• Atrial arrhythmias (volume overload)
• Paradoxical emboli
ASD
ASD: R to L Shunting [Figure 6-15-9]
• “Paradoxical” emboli
• R to L shunting may occur: Figure 6-15-8
➢ Pregnancy (decreased SVR)
➢ Diving,valsalva, cough
➢ COPD, pulmonary embolus
Paradoxical Embolus
• Ischemic stroke: no cause in
35-40%
Figure 6-15-9
➢ “Cryptogenic stroke”
➢ Paradoxical embolus from
ASD?
• Pts with cryptogenic ischemic
stroke and PFO, on
anticoagulant therapy: ASD at MR
➢ 1.2% risk/year of TIA
➢ 3.4% risk/year of TIA or
stroke
R to L shunting
across septal defect
PDA: shunt
• Shunt direction determined by:
➢ Pulmonary vs systemic pressure
• In otherwise normal infants, it will be L to R
Hemodynamics
• Shunt is from Ao to PA
• LA, LV, Ao: increased volume
• L heart enlarges
• RV: increased pressure from afterload; hypertrophy
PDA
• Anatomically closed by 3 weeks
• If open @6 months, certainly will remain
• Flow depends on:
➢ Width
➢ Length Figure 6-15-11
➢ Shape
Figure 6-15-15
Figure 6-15-19
Figure 6-15-20
Admixture Lesions
“5T’s” and H
• Transposition of the great vessels
• Total anom. pulmonary venous return
• Truncus arteriosus
• Tricuspid atresia
• Single chamber
➢ single ventricle R to L shunt lesions shunt PBF to L side of heart;
➢ double outlet right ventricle there is decreased PBF
➢ common atrium)
• Hypoplastic left heart syndrome Admixture lesions allow intracardiac mixing of R
and L circulations; blood preferentially flows to
lower pressure pulmonary vascular bed,
Complete Transposition of Great Vessels increased PBF results and patient is cyanotic
(d-TGV, D loop TGV) [Figure 6-15-24]
• Incidence 8%
• Most common cyanotic CHD presenting in neonate Figure 6-15-23
➢ TOF most common overall
• 2 : 1 male : female
• Classic TGV:
➢ Aorta arises from RV
➢ Pulm art from LV
• 2 closed circuits
➢ Incompatible with life w/o L-R communication
• All have ASD
• Half with VSD
Figure 6-15-25
Type 3 (infracardiac)
[Figure 6-15-33]
• 12%
• Common pulmonary vein descends thru esophageal hiatus
• Drains into portal vein/ductus venosus, hepatic vein, or IVC
• Pulmonary venous return is always obstructed because: Type 1 (supracardiac) TAPVR;
➢ Long course of vein PBF returns to SVC
➢ Passage through diaphragm
➢ Return through hepatic parenchyma when draining into Figure 6-15-32
PV/ductus venosus (most common)
• Pulmonary edema
• Heart size is NORMAL
➢ Lungs act as capacitor for obstructed pulmonary venous
return
• Distinctive appearance: normal size heart with pulmonary edema
• Type 4 = combination lesion of some the above (5%)
• Partial APVR (clinically insignificant) [Figure 6-15-34]
➢ Most commonly is return of RUL pulmonary vein directly into
SVC
➢ Scimitar syndrome is PAPVR of hypoplastic RML, RLL; drains
to IVC
Figure 6-15-37
TAPVR 1: “Snowman” heart & increased PBF
Figure 6-15-36
Figure 6-15-38
Figure 6-15-40
Figure 6-15-43
Single Ventricle/DORV/
Common Atrium
[Figure 6-15-48]
• All have single dominant
chamber (where normally
there are 2 separate L and R Tricuspid atresia with TGV:
chambers) into which all cardiomegaly + increased PBF
blood flows
• Admixture occurs in this Tricuspid atresia with transposition
single chamber of Ao & PA (increased PBF)
Figure 6-15-47
Figure 6-15-48
Figure 6-15-51
Figure 6-15-52
Surgical Repair
• Cardiac transplant
• Norwood (3 stage repair)
➢ Stage 1: (birth)
❖ Conduit RV to Ao root
❖ Divide PA from RV and ductus
❖ Perfuse PA via BT shunt
➢ Stage 2: (6 mos)
❖ Construct Glenn shunt (SVC to PA) to reduce RV volume HLHS: cardiomegaly + pulmonary
edema
load
➢ Stage 3: (18 mos)
❖ Extracardiac Fontan. Direct blood from IVC & SVC thru RA to PA Figure 6-15-54
Figure 6-15-55
Figure 6-15-57
Fontan: RA to PA graft
(adds atrial kick to perfusion
pressure)
R to L Shunts
• 2 common features:
➢ Opening between R and L sides of heart (allows R to L
shunting)
➢ R-sided outflow tract obstruction (pulmonary stenosis/ atresia,
tricuspid stenosis/atresia)
Associated Anomalies
• R aortic arch in 25% (usually mirror image branching)
➢ R arch also seen in 35–40% Truncus (most highly associated)
➢ But TOF much more common
• Pulmonary valvular stenosis (90%)
• Peripheral pulmonary stenoses (75%)
• ASD (10%) (w/ VSD=pentalogy of Fallot)
• Enlarged systemic collateral arteries
Figure 6-15-65
References
Textbooks
1. Gedgaudas E. Cardiovascular radiology. Philadelphia, Pa: WB Saunders, 1985.
2. Tonkin, ILD. Pediatric cardiovascular imaging. Philadelphia, Pa: WB Saunders, 1992.
3. Amplatz K, Moller JH. Radiology of congenital heart disease. St Louis, Mo: Mosby, 1993.
Journal Articles
1. Alexiou C, Mahmoud H, Al-Khaddour A, et al. Outcome after repair of tetralogy of Fallot in the first year of life.
Ann Thorac Surg. 2001;71:494-500
2. Bichell DP, Geva T, Bacha EA, Mayer JE, Jonas RA, del Nido PJ. Minimal access approach for the repair of atrial
septal defect: the initial 135 patients. Ann Thorac Surg. 2000;70:115-8.
3. Coussement AM, Gooding CA. Objective radiographic assessment of pulmonary vascularity in children.
Radiology 1973;109:649-654.
4. El-Najdawi EK, Driscoll DJ, Puga FJ, et al. Operation for partial atrioventricular septal defect: a forty-year review.
J Thorac Cardiovasc Surg. 2000;119:880-889.
5. Fisher RG, Moodie DS, Sterba R, et al. Patent ductus arteriosus in adults - long term follow-up: nonsurgical versus
surgical treatment. J Am Coll Card. 1986;8:280-284.
6. Harvey JR, Teague SM, Anderson JL, et al. Clinically silent atrial septal defects with evidence for cerebral
embolization. Ann Intern Med. 1986;105:695-687.
7. Jacobs ML, Pourmoghadam KK. The hemi-Fontan operation. Semin Thorac Cardiovasc Surg, 2003;6:90-97.
8. Kreutzer C, De Vive J, Oppido G, et al. Twenty-five-year experience with Rastelli repair for transposition of the
great arteries. J Thorac Cardiovasc Surg. 2000 Aug;120:211-223.
9. Murphy JG, Gersh BJ, McGoon MD, et al. Long term outcome after surgical repair of isolated atrial septal defect.
N Engl J Med 1990;323:1645-1650.
10. Ohye RG, Bove EL. Advances in congenital heart surgery. Curr Opin Pediatr. 2001;13(5):473-481.
11. Thibeault DW, Emmanouilides GX, Nelson RJ, et al. Patent ductus arteriosus complicating the respiratory distress
syndrome in preterm infants. J Pediatr 1975; 86:120-126.
12. Williams DL, Gelijns AC, Moskowitz AJ, et al. Hypoplastic left heart syndrome: valuing the survival. J Thorac
Cardiovasc Surg. 2000;119(4 Pt 1):720-731.
Figure 6-16-6
Figure 6-16-7
Healing of fractures1
• No callus fx < 14 days old
• Callus fx > 7 days old
• Caveat: these are general estimates and should not be thought of
as fixed time frames, as healing & callus formation are a
continuum
CT of healing left posterior rib
• The younger the child, the faster the healing fracture
1O’Connor JF, Cohen J., in: Kleinman PK Diagnostic Imaging of Child Abuse, 2nd
Figure 6-16-11
ed. Mosby, 1998 168–177.
High specificity
• Metaphyseal fracture
• Posterior rib fracture
• Spinous process fracture
• Sternal fracture
• Scapular fracture
Moderate specificity
• Multiple fractures, especially bilateral
• Fractures of different ages
• Epiphyseal separation
• Vertebral body fracture & subluxation
• Digital fractures
• Complex skull fractures
Cranial injury
• Leading cause morbidity & mortality
➢ Mortality peaks at 6 months
• Mechanisms:
➢ Shaking
➢ Direct blow
➢ Strangulation / suffocation
• Shaking alone is sufficient to cause fatal CNS injury (shearing forces)
Figure 6-16-16
Diagram of SDH
Figure 6-16-17
Interhemispheric hemorrhage
Cerebral edema
• Not specific for abuse
• May be seen in:
➢ Drowning
➢ Non-abusive head trauma
• When abuse-related, may be from:
➢ Direct brain injury
➢ Strangulation
➢ Venous pressure from chest compression
➢ Post-traumatic apnea
Sequellae
CT MRI
• Acute • Delayed presentation
• Polytrauma • Differing ages of injuries/blood collections
• Normal or equivocal CT with high suspicion (better than CT for
shear and SDH)
• Sequela
Stage Form T1 MR T2 MR
hyperacute (<12-24 hrs) oxy Hb iso-low high (slightly)
Cord injury
• In 9 of 11 abuse fatality autopsies in infants1,2
➢ Subarachnoid
➢ Subdural
➢ Epidural
➢ 4 of 6 with ventral cord contusion
• Probably overestimates real incidence
1Hadley MN, Sonntag VK, Rekate HL, Murphy A. The infant whiplash-shake
injury syndrome: a clinical and pathological study. Neurosurgery 1989;
24:536-540. Right transverse sinus thrombosis
2Feldman KW, Weinberger E, Milstein JM, Fligner CL. Cervical spine MRI in
abused infants. Child Abuse Negl 1997; 21:199-205.
Figure 6-16-21
Skull fracture [Figure 6-16-21]
• Overall, poorly correlated with CNS injury
(linear fx most common in NAT)
➢ 10% of all abuse cases have skull fx
• Non-specific (altho common) unless:
➢ Stellate / eggshell
➢ Multiple
➢ Diastatic (>3 mm)
➢ Occipital
➢ Inconsistent history (“rolled off changing table”)
Visceral Injury
• Seen in all ages of abused children
• Usually blunt trauma (punch or kick to abdomen, rapid deceleration after being
thrown)
• 50% mortality rate of clinically apparent visceral injury
➢ Delay in seeking treatment pivotal!
• Estimated to account for 12% of all abuse fatalities
➢ 2-4% of all abusive injuries
Bowel Injury
Duodenal hematoma
Pancreas
• Probably compressed against spine with blunt trauma
• Abuse is a common cause of pancreatitis (trauma is most Figure 6-16-23
common cause in children)
• May develop pseudocysts
Child abuse
• We as radiologists are uniquely able to diagnose abuse
• We may be the 1st to recognize abuse
• Radiographic findings in abuse are among the most specific & diagnostic in medicine
• Our findings may be PIVOTAL to investigation & prosecution
References
1. Billmire ME, Myers PA. Serious head injury in infants: accident or abuse? Pediatrics 1985; 75:340-342.
2. Block RW. Child abuse--controversies and imposters. Curr Probl Pediatr 1999; 29:249-272.
3. Bradley WG. MR appearance of hemorrhage in the brain. Radiology 1993 189: 15-26
4. Chen JC, Levy ML. Causes, epidemiology, and risk factors of chronic subdural hematoma. Neurosurg Clin N Am
2000; 11:399-406.
5. Chiaviello CT, Christoph RA, Bond GR. Stairway-related injuries in children. Pediatrics 1994; 94:679-681.
6. Child Maltreatment 2000: Reports from the States to the National Child Abuse and Neglect Data System. In: US
Department of Health and Human Services Children's Bureau (online). Available at:
http://www.calib.com/nccanch/prevmnth/scope/ncands/cfm
7. Feldman KW, Brewer DK. Child abuse, cardiopulmonary resuscitation, and rib fractures. Pediatrics 1984; 73:339-
342.
8. Feldman KW, Weinberger E, Milstein JM, Fligner CL. Cervical spine MRI in abused infants. Child Abuse Negl
1997; 21:199-205.
9. Hadley MN, Sonntag VK, Rekate HL, Murphy A. The infant whiplash-shake injury syndrome: a clinical and
pathological study. Neurosurgery 1989; 24:536-540.
10. Han BK, Towbin RB, De Courten-Myers G, McLaurin RL, Ball WS, Jr. Reversal sign on CT: effect of
anoxic/ischemic cerebral injury in children. 1990; 154:361-368.
11. Harwood-Nash DC. Abuse to the pediatric central nervous system. AJNR 1992; 13:569-575.
12. Helfer RE, Slovis TL, Black M. Injuries resulting when small children fall out of bed. Pediatrics 1977; 60:533-535.
Learning Objectives
• Review the differences in cranial anatomy of the preterm and term infant
• Review hemorrhagic (IVH) & nonhemorrhagic (PVL) injuries due to partial
asphyxia.
• Understand radiologic work up of hypoxic ischemic injury of the neonate
including neurosonographic techniques (transmastoid view, Doppler)
Figure 6-17-1
Sonographic Technique
• Anterior fontanelle
➢ Coronal and sagittal planes
• Axial views
➢ Posterior and mastoid fontanelle
• Doppler
➢ MCA/ACA resistive index
➢ Color Doppler of fluid collections
Germinal Matrix
• Origin of neuronal/glial development.
• Rich arterial supply perforators of ACA, MCA, PCA.
• Drain to deep venous system.
Axial CT demonstrates diffuse cortical
• Regression posterior to anterior b/w 24-28 wks infarction in a term infant with severe
• Involutes by 32 wks hypoxic ischemic injury
Periventricular Hemorrhagic
Infarction [Figure 6-17-9]
Figure 6-17-9
Coronal and sagittal US images demonstrate Grade II
intraventricular hemorrhage with blood extending into the
ventricle
Figure 6-17-7
Periventricular Hemorrhagic
Infarction (PHI/ Grade IV IVH) Figure 6-17-8
• 15% with IVH dev PHI
• Same side as IVH, after IVH has occurred
• Usually unilateral or asymmetric
IVH ? CT/MRI
• Difficult transporting unstable preterms
• CT may miss bleed after several days Pulsed Doppler demonstrates no flow
during diastole with resistive index of 1
• MRI - Hemosiderin staining can be seen up to 1 yr
➢ May demonstrate additional abnormalies
➢ Focal WM loss
➢ Diffuse hypoxic-ischemic changes
IVH: Outcome
• 3 mechanisms for poor outcome
➢ 1. Damage from ventricular dilatation-may be reversible if shunted
➢ 2. Shunt related complications: infection, sepsis, obstruction, seizures.
➢ 3. Hypoxic ischemic injury-white matter edema, gliosis, axonal swelling
• Spastic hemipareses, intellectual deficits.
• Prognosis parallels size of parenchymal echodensity
Periventricular Leukomalacia:Sonography
• Infarction occurs in deep cerebral WM
• Bilateral symmetric
• US not sensitive in detecting PVL
➢ Difficult to distinguish from anisotropic effect of periventricular
halo
➢ Echodensities resolve and can be missed
Periventricular Leukomalacia:Sonography
Coronal sonogram demonstrates
multiple cysts in the periventricular
Time Pathology US Findings white matter consistent with
periventricular leukomalacia
Acute focal necrosis patchy areas of inc
1-3 days petechial hemor echogenicity PVWM
Periventricular Leukomalacia
• Less severe PVL-diminished myelin result in dilated ventricles.
• Severe PVL will cavitate
• Cysts eventually resolve -gliotic scarring Figure 6-17-12
Periventricular Leukomalacia:CT
[Figures 6-17-12 and 6-17-13]
• Difficult transporting premature infants
• Due to high water content, difficult differentiating acute PVL from nl
preterm brain
• Chronic: CT useful extent of lesions, atrophy
➢ Irregular lateral ventricles
➢ Prominent sulci
➢ Subcortical gray matter abuts ventricles
➢ Small cysts missed
Figure 6-17-13
Periventricular Leukomalacia:Outcome
• Outcome correlates with cystic cavitation
• PVWM traversed by fibers of motor cortex results in spastic
diplegia
➢ Lower> Upper extremities
• Infants with larger lesions often delayed
Nonhemorrhagic Infarction
• Rare, term infants
• 90% major handicaps
• Perinatal asphyxia
➢ Emboli Axial T2w image demonstrates high
➢ Congenital Heart disease signal in the periventricular white
matter
➢ Meningitis
➢ Polycythemis
Profound Asphyxia
• Energy requirements related to state of myelination.
• Most metabolically active and mature regions with most advanced
➢ myelination, Figure 6-17-15
➢ perfusion
➢ glucose uptake
are regions that suffer the most damage
• Complete arrest - injury determined by
➢ metabolic maturity of brain
➢ myelination
➢ autoregulation
➢ watershed pattern
➢ excitatory neurotransmitter release
➢ severity and duration of event Coronal US demonstrates diffuse increased
echogenicity of the cerebral cortex with slit
ventricles
Profound Asphyxia: Sonography Anterior cerebral artery Resistive Index < .5
• Diffuse hypoxic ischemic encephalopathy often consistent with arterial vasodilatation due to loss
superimposed on IVH/PVL of sutoregulation
Profound asphyxia:
MRI findings in Preterm Infants
• PVWM changes dominate
➢ T1,T2 shortening in peritrigonal WM
➢ T1,T2 prolongation in cerebral WM
• Chronic - atrophy
➢ Relative sparing of cerebral cortex
➢ Hippocampal and brainstem atrophy
➢ Thin corpus collosum
Axial CT images demonstrate low
Profound asphyxia: MRI findings in term infants attenuation of the cortex, basal
ganglia as well as periventricular
• Short T, at times short T2 relaxation times white matter.in this term infant
➢ Basal ganglia following profound asphyxia
➢ Hippocampus
➢ Posterior and medial lentiform nuclei
➢ Lateral thalami Figure 6-17-17
➢ Cortical gyri
Figure 6-17-18
References
1. Barkovich AJ, Sargent SK: Profound asphyxia in the premature infant: imaging findings AJNR 1995;16;1837.
2. Benson JE et al. Intracranial Neonatal Neurosonography: An Update. Ultrasound Quarterly 2002: 18;89
3. Boo NY et al. Early cranial US changes as predictors of outcome during first yr of life. J Ped Child Healthy 2000;36:363
4. Bulas DI, Taylor GA, Fitz CR, Revenis ME, Glass P, Ingram JD. Posterior fossa intracranial hemorrhage in infants
treated with extracorporeal membrane oxygenation: Sonographic findings. AJR 1991; 156:571.
5. Bulas DI. Vezina G: Anoxic injury in the Preterm infant Radiologic evaluation Radiologic Clinics of North America,
Vol 37, Nov 1999:1147.
6. Bulas DI. TCD: Practical Applications in Pediatrics. Applied Radiology 1999, April 7-15.
7. Chadduck WM, Duong DH Kast JM et al: Pediatric cerebellar hemorrhage. Child Nerv Syst 1995;110:579.
8. Perlman JM, Rollins N: Surveillance protocol for the detection of intracranial abnormalities in premature neonates. Arch
Pediatr Adol Med 2000;154:822.
9. Rumack CM et al. Timing and course of neonatal intracranial hemorrhage using US. Radiology 1985:154:101
10. Rumack C, Drose J. Neonatal and Infant Brain Imaging ed Rumack et al. Diagnostic Ultrasound. Elsevier Mosby
2005
11. Taylor GA. Recent advances in neonatal cranial ultrasound and Doppler techniques. Clin Perinataol 1997;24:677
12. Seibert JJ et al. Use of power Doppler in pediatric neurosonography: a pictorial essay. Radiographics 1998;18:879
13. Volpe JJ: Neurobiology of periventricular leukomalacia in the premature infant Pediatr Res 2001;50:553-562
14. Vohr B, Allan WC, Scott DT et al: Early onset IVH in preterm neonates: Incidence of neurodevelopmental handicap.
Semin Perinatol 1999;23:212.
Categorization
• Benign Epithelial Tumors
• Benign Mesenchymal Tumors
• Malignant Epithelial Tumors
• Malignant Mesenchymal Tumors
• Metastases
Metastases
• Neuroblastoma
• Burkitt’s Lymphoma
• Sarcomas
• Wilms’ tumor
• Other
Mesenchymal Hamartoma
• Mesenchymal tissue, disorganized bile ducts, hepatocytes, fluid filled spaces
• Developmental disturbance:
➢ Portal/biliary obstruction, lymphangiomatous tissue
Figure 6-18-2
Figure 6-18-3
Photomicrograph with fibrous stroma
and cysts predominantly lined by flat
vascular endothelium from the
lympatic component of the
hamartoma
Figure 6-18-4
Mesenchymal Hamartoma
• Age: Young (less than 3y/o)
• Biologic imaging: Cystic
• Chemistry: Normal alpha-fetoprotein
Infantile Hemangioendothelioma
• Most common hepatic tumor- first year of life Large vascular spaces in
• Usually Dx in first few months of life hemangioendothelioma with normal
• Female predominance 1.5:1 adjacent liver
• Growing mass, clinically symptomatic
• Vascular, high flow, mass-stroma
• History of involution in first year, if survivor
Figure 6-18-8
Figure 6-18-9
Figure 6-18-10
Figure 6-18-12
Figure 6-18-13
Diffuse hepatic involvement of
hemangioendothelioma
Figure 6-18-14
Figure 6-18-15
Hemangioendothelioma
• Age: Young (Infants)
• Biologic imaging: Photomicrograph of hepatoblastoma
➢ Vascular-High flow state demonstrating cords and nests of
➢ Solid stroma malignant cells
• Chemistry: Normal alpha-fetoprotein
➢ Positive endothelial growth factor
Figure 6-18-17
Hepatoblastoma
• Most common primary liver tumor in childhood
• Third most common abdominal malignancy
➢ After neuroblastoma, Wilms’ tumor
• May be familial
• Associations: Trisomy 18, Beckwith-Wiedemann,
hemihypertropy, familial polyposis, exposure- metals,
petroleum products, paints, oral contraceptives, Fetal
Alcohol Syndrome
Hepatoblastoma: Clinical
• Abdominal mass, hepatomegaly
• Anemia
• Child 90% < 5 yrs old, 65–70% under 2 yrs
• Males> females 2:1
• Positive alpha-fetoprotein
• No prior history of liver disease
Hepatoblastoma: Imaging
[Figures 6-18-17 to 6-18-19]
• Hepatomegaly, abdominal mass, 10–15% Ca2+
• US: Heterogeneous, predominantly solid
• CT: Heterogeneous, lobulated Unenhanced CT with focus of
• MR: Low T1, High T2 calcification in a teratoid variety of
• Angio: Tumor neovascularity hepatoblastoma. Heterogeneous
enhancement of same tumor involving
left and right hepatic lobes
Hepatoblastoma
Heptoblastoma with solid nature in CT and gross
• Age: Young (infants, young children) specimen. Cystic change is irregular due to
• Biologic imaging features: Solid central necrosis of the solid tumor
• Chemistry: Positive alpha-fetoprotein
Figure 6-18-20
Hepatocellular Carcinoma
• #2 primary liver malignancy in childhood
• Often underlying liver disease/cirrhosis
➢ Tyrosinemia, alpha-1-antitrypsin deficiency, glycogen storage
dz, biliary atresia, chronic hepatitis (HBsAg +), Fanconi
anemia, methotrexate induced hepatic fibrosis
• May be primary
Nodular
appearance of
solid epithelial
tumor
(hepatocellular
carcinoma) in
14 year old
patient, with
positive AFP
Nests of inhomogeneously enhancing
HCC
Hepatocellular Carcinoma
• Age of patient: Teens
• Biologic imaging: Solid, multifocal
• Chemistry-blood
➢ Positive alpha-fetoprotein
Complex US appearance of
embryonal sarcoma in 11 year female
Demonstrable pseudocapsule
anteriorly surrounding mesenchymal
sarcoma
1. Von Schweinitz, D. Management of liver tumors in childhood. Semin Ped Surg 2006; 15(1):17-24
2. Stocker JT. Hepatic tumors in children. Clin Liver Dis. 2001 Feb;5(1):259-81, viii-ix.
3. von Schweinitz D. Neonatal liver tumours. Semin Neonatol. 2003 Oct;8(5):403-10.
4. Tiao GM, Bobey N, Allen S, Nieves N, Alonso M, Bucuvalas J, Wells R, Ryckman F. The current management of
hepatoblastoma: a combination of chemotherapy, conventional resection, and liver transplantation. J Pediatr. 2005
Feb;146(2):204-11.
5. Burrows PE, Dubois J, Kassarjian A. Pediatric hepatic vascular anomalies. Pediatr Radiol. 2001 Aug;31(8):533-45.
6. Dubois J, Hershon L, Carmant L, Belanger S, Leclerc JM, David M. Toxicity profile of interferon alfa-2b in children:
A prospective evaluation. J Pediatr. 1999 Dec;135(6):782-5.
7. Dachman AH, Pakter RL, Ros PR, Fishman EK, Goodman ZD, Lichtenstein JE. Hepatoblastoma: radiologic-pathologic
correlation in 50 cases. Radiology. 1987 Jul;164(1):15-9.
8. Gerber DA, Arcement C, Carr B, Towbin R, Mazariegos G, Reyes J. Use of intrahepatic chemotherapy to treat advanced
pediatric hepatic malignancies. J Pediatr Gastroenterol Nutr. 2000 Feb;30(2):137-44.
9. Sun XY, Wu ZD, Liao XF, Yuan JY. Tumor angiogenesis and its clinical significance in pediatric malignant liver tumor.
World J Gastroenterol. 2005 Feb 7;11(5):741-3.
10. Rhim H, Dodd GD 3rd, Chintapalli KN, Wood BJ, Dupuy DE, Hvizda JL, Sewell PE, Goldberg SN. Radiofrequency
thermal ablation of abdominal tumors: lessons learned from complications. Radiographics. 2004 Jan-Feb;24(1):41-
52.
11. Iannitti DA, Dupuy DE, Mayo-Smith WW, Murphy B. Hepatic radiofrequency ablation. Arch Surg. 2002
Apr;137(4):422-6.
Figure 6-19-3
Figure 6-19-4
Figure 6-19-8
References
1. Harcke HT, Grissom LE. Pediatric hip sonography. Diagnosis and differential diagnosis. Radiol Clin North Am.
1999 Jul;37(4):787-96.
2. Grissom LE, Harke HT. Developmental Dysplasia of the Pediatric Hip with Emphasis on Sonographic Evaluation.
Semin Musculoskelet Radiol. 1999;3(4):359-370
3. ACR Practice Guideline for the Performance of the Ultrasound
Examination for Detection of Developmental Dysplasia of the Hip. American College of Radiology Practice
Standards/Guidelines 2004. American College of Radiology, Reston, VA.Headquarters Office: 1891 Preston White
Dr, Reston, VA 20191, (703) 648-8900© 2004 American College of2004 American College of Radiology
4. Eich GF, Superti-Furga A, Umbricht FS, Willi UV. The painful hip: evaluation of criteria for clinical decision-
making. Eur J Pediatr. 1999 Nov;158(11):923-8.
5. Buchmann RF, Jaramillo D. Imaging of articular disorders in children. Radiol Clin North Am. 2004 Jan;42(1):151-
68, vii.
6. Givon U, Liberman B, Schindler A, Blankstein A, Ganel A. Treatment of septic arthritis of the hip joint by repeated
ultrasound-guided aspirations. J Pediatr Orthop. 2004 May-Jun;24(3):266-70.
Follow-up
Normal Thymus
• Sail sign, wave sign, notch or sulcus
• No mass effect on trachea or vessels
• Homogeneous in density
• Commonly seen on CXR up to age 5 years then regresses in latter half of first
decade
• Thymic rebound
• Masses can arise in thymus – leukemia/lymphoma, teratoma, thymolipoma,
lymphatic malformation
Round Pneumonia
• Unique to children – usually < 8 yo
• Usually posterior lower lobes
• Almost always bacterial –
pneumococcus
• Exclude bone erosion – ddx: neoplasm
Pulmonary Blastoma
• Arises from primitive mesenchymal blastema
• Histologically reminiscent of Wilms tumor
• Unlike other embryonal tumors, it is more commonly found in adults
• May present as solitary nodule or huge mass
• Heterogeneous, cystic areas
PA and lateral chest radiographs show dense opacification of the right Ultrasound of the right chest
lower lobe with silhouetting of the right hemidiaphram. Right lateral shows pleural fluid with
pleural thickening is also seen septations and consolidated,
airless lung that transmits sound.
Complicated Pneumonia The hyperechoic foci with ring-
• Suspect in cases of near white out down artifact represent round air
• H. flu less than 2 y.o. collections
• Pneumococcus
• S. aureus
• CT vs. US
➢ Ultrasound may be
better determining
which fluid collections
need drainage
Pulmonary Abscess
• CT – fluid or air-filled cyst with enhancing, thick, irregular wall
• Both necrosis and small abscesses in children have good outcomes with
antibiotics only
Pneumatoceles
• Thin walled cavity seen in the recovery phase usually
of infection
• Staphylococcus, pneumococcus, tuberculosis
• Blunt chest trauma, hydrocarbon pneumonitis,
Langerhans cell histiocytosis
• Bronchial obstruction leading to air trapping and
alveolar rupture Pulmonary necrosis. Contrast this appearance to
• Pneumothorax or mediastinum case #3 with empyema and abscesses. Note
decreased enhancement of surrounding
parenchyma compared to more anterior
parenchyma with preservation of enhancement of
the visceral pleura (arrow)
Swyer-James Syndrome
• Bronchiolitis obliterans
➢ Idiopathic, viral, toxic inhalation,drug reaction, collagen vascular dz,
transplant, chronic aspiration.
➢ Adenovirus as child – unilateral hyperlucent lung
• Small hyperlucent lung, hypoplastic ipsilateral artery
• Reticular nodular pattern with hyperinflation, central bronchiectasis
Differential Diagnosis
• Bronchopulmonary foregut
malformation
• CPAM
• Neurogenic tumor
• Sequestration
Sequestration
• Area of pulmonary tissue that
does not have a normal
connection to the bronchial tree
• Systemic arterial supply
• Can present as an infant or
young child or as a young adult
• Often a history of recurrent
infections in the same lobe
• May contain air
Sequestration
• LLL most common
• Multiloculated cystic or solid
mass
• Intralobar vs. extralobar
➢ Pleural investment CT reveals a predominantly cystic mass with focal nodular thickening
➢ Extalobar – own pleural along the posterior wall in the right posterior mediastinum. The lower
investment right image reveals an additional simple cyst in the left superior
mediastinum
➢ Extralobar – systemic venous
drainage
➢ Extralobar – infants, associated anomalies
➢ Extralobar-congenital/intralobar-acquired
• CT vs. MRI vs. US – define vascular supply and drainage
Radiologic Approach
• Assess Proportion
➢ Rhizo-, meso-, or acromelia
➢ +/- platyspondyly
• Assess Components of Bone
➢ Epiphyses small or irregular ◗ epiphyseal dysplasia
➢ Metaphyses widened, flared, or irregular ◗ metaphyseal dysplasia
➢ Diaphyses widened or thickened ◗ diaphyseal dysplasia
Achondroplasia Group
• All have abnormalities of the same chromosomal locus and gene product,
fibroblast growth factor receptor 3 (FGFR3)
➢ Thanatophoric dysplasia
➢ Achondroplasia
➢ Hypochondroplasia
Thanatophoric Dysplasia
• AD
• Probably the most common lethal bone dysplasia
• Skull - kleeblatschadel in type II
• Thorax - very short ribs and handlebar clavicles
• Spine – small flat vertebral bodies with round
anterior ends, U or H-shaped on AP
Thanatophoric Dysplasia
• Pelvis
➢ Small, flared iliac bones
➢ Very narrow sacrosciatic notches, flat dysplastic Thanatophoric dysplasia. Note small flat vertebral
bodies, very short ribs, and “telephone receiver”
acetabula femora
• Extremities – telephone receiver
• Femora
Achondroplasia
• Most common nonlethal skeletal dysplasia
• AD, spontaneous mutation rate 8-%
• Skull
➢ Large with midface hypoplasia
➢ Small skull base and foramen magnum
Achondroplasia
• Spine
➢ Very short pedicles – risk of spinal canal stenosis
➢ Decrease in interpediculate distance – lumbar spine
• Pelvis
➢ Elephant-ear iliac wings
➢ Flat acetabular roofs
➢ Narrow sacrosciatic notches
Achondroplasia
• Extremities
➢ Rhizo- > meso- and acromelia
➢ Hands – brachydactyly with metaphyseal cupping of MC’s
➢ Knees – chevron and inverted chevron deformities
➢ Hips proximal femoral fade out and hemispheric capital femoral epiphyses
Short Rib-Polydactyly
• Thorax – shortest ribs, horizontal ribs
• Pelvis – small ilia, notched acetabula
• Extremities
➢ Micromelia
➢ Rolling pin-shaped or round-ended or spiked
femora
➢ Ovoid tibiae
➢ Polydactyly in some types
Chondroectodermal dysplasia. AP
views of the hands show bilateral
postaxial polydactyly and cone
shaped epiphyses (arrows)
Chondroectodermal dysplasia. AP
view of pelvis and LE’s shows short
long bones and short, flared iliac
wings, with trident-shaped acetabular
roofs
Metaphyseal Chondrodysplasias
• Schmid-type – mildest, metaphyseal flaring, especially around knees
• Shwachman-Diamond – AR
➢ Pancreatic insufficiency – malabsorption and lipomatosis of pancreas
➢ Cyclic neutropenia – recurrent infections
Metaphyseal Chondrodysplasias
• McKusick-type
➢ Cartilage-hair hypoplasia
➢ High frequency in the Amish and Finnish populations
➢ Hirschprung disease
➢ Immune deficiency and increased risk of malignancy, especially leukemia
and lymphoma
McKusick-Type
• Spine – square vertebral bodies
• Extremities – flaring, cupping and fragmentation of
metaphyses, especially at the knees
• Hands – shortening with metacarpal and phalangeal
cupping and coning
Hurler Syndrome
• Present in infancy or early childhood
• Skull – J-shaped sella
• Thorax
➢ Short thick clavicles
➢ Oar-shaped ribs
• Spine
➢ Gibbus deformity
➢ Inferior beaked T-L vertebral bodies
Hurler Syndrome
• Pelvis – small flared iliac wings with inferior tapering and steep acetabular
roofs
• Extremities
➢ Wide diaphyses of long bones and metacarpals
➢ Pointed proximal metacarpal poles
Osteogenesis Imperfecta
• Type II
➢ Spine – very poor ossification with collapse of vertebral bodies
➢ Extremities – accordion femora
• Other types
➢ Skull – more than 8-10 wormian bones, variable ossification
➢ Extremities – variable osteoporosis and fractures
Osteopetrosis. Acute
Osteopetrosis with sandwich femoral neck fracture on
vertebrae earlier film
Pyknodysostosis
• AR, presents in infancy
• Micrognathia, short fingertips, fractures
• Generalized osteosclerosis
• Skull
➢ Wormian bones
➢ Marked delay in closure of sutures and fontanelles
➢ Obtuse mandibular angle
• Thorax – resorption of acromial ends of clavicles
• Extremities – resorption of phalangeal tufts
“Pancreatic Sufficiency”
• 10-15% of CF patients
• Do not require enzyme supplements
• Better nutritional status
• Older at diagnosis – later onset of lung disease
• Lower Pseudomonas colonization rates
• Better prognosis
• May convert to pancreatic insufficiency with age (genetically determined)
I1
Benign Sacrococcygeal Teratoma 1422 Child Abuse 1491
Benign sinus lesions 1247 Differential Diagnosis 1499
Berdon Syndrome 1349 Childhood Neck Neoplasms 1370
Bezoar 1356 Choanal Atresia 1366
Bezold abscess 1078 Cholesteatoma 1074, 1076
Biliary Cirrhosis (Cystic Fibrosis) 1541 Cholesterol Granuloma (Cyst) 1083
Binswanger's 1039 Chondrodysplasia Punctata 1530
Bladder Diverticula 1332 Chondroectodermal Dysplasia (Ellis-van Creveld Syndrome)
Blood Brain Barrier 1131 1529
Blowout Orbital Trauma 1093 Chondrosarcoma 1084
Blunt trauma 1498 Chordoma 1158
Blyth and Ockenden Clinical Classification (ARPKD) 1384 Choriocarcinoma 1178
Bone Marrow Components 1425 Chorioretinitis 1092
Bone Marrow Imaging (Pediatric) 1425 Choroid Plexus
Bony Orbit 1088 Carcinoma 1063, 1064
Borden Classification (Dural AVF) 1225 Metastasis 1065
Borrelia burgdorferi 1237 Neoplasms 1151
Bourneville Disease 1197 Papilloma 1063
Brachial Plexus Traction Injury 1296
Tumors 1063
Brain (Congenital Abnormalities) 1307 Choroidal Detachment 1090
Brain Tumor 1137 Chylothorax 1448, 1451
Branchial Cleft Cyst 1269, 1278 Clear Cell Sarcoma (Kidney) 1396
Bright cerebellum sign 1496 Cleft Brain 1314
Bronchial Atresia 1372 Clivus 1115
Bronchogenic Cyst 1437 Cloquet’s canal 1091
Bronchopulmonary Dysplasia 1447 Closed-Lip (Fused) 1314
Butterfly pattern 1046 CNS Bacterial Infections 1130
Callosal Dysgenesis 1316 CNS infections (acquired) 1232
Calyceal Diverticulum 1381 CNS Lyme Disease 1237
Capillary Telangiectasia (Brain) 1229 CNS Lymphoma 1045
Carbon monoxide poisoning 1041 CNS Neoplasms – Chromosome Loss of Heterozygosity 1192
Carcinoma (Choroid Plexus) 1151 CNS Neoplasms: Chromosomes 1184
Cardiac Imaging (Pediatric) 1453 CNS Tuberculosis 1235
Cardiomediastinal Silhouette Size 1473 Coats’ Disease 1092
Carotid Artery 1073 Cochlea 1068
Carotid Body Paragangliomas 1272 Colloid Cyst 1058, 1062, 1116, 1163
Carotid Space 1269 Colonic Aganglionosis (Total) 1351
Catecholamine Production 1402 Colonic Atresia 1349
Caudal Regression Syndrome 1265 Common Atrium 1485
Cavernous Angioma (Brain) 1228 Complete Atrioventricular Septal Defect 1464
Cavernous Hemangioma 1098 Complete Labrynthine Aplasia 1072
Cavernous Malformation (Brain) 1229 Complete Transposition of Great Vessels 1479
Cavernous Sinus Invasion (Pituitary Macroadenoma) 1254 Complicated Pneumonia 1523
Cellulitis (Orbit) 1101 Compression Fractures 1430
Central Neurocytoma 1058, 1060, 1061 Conal Lesions 1094
Central Posterior Fossa Lesion 1109 Congenital
Cephaloceles 1307 Abnormalities of the Brain 1307
Cerebellar Infarction 1507 Adrenal Hyperplasia 1411
Cerebellar Liponeurocytoma 1050
Anomalies (UTI) 1329
Cerebellopontine Angle Masses 1079
Cerebral edema 1496 Cholesteatoma (Epidermoid) 1074
Cerebral Hemiatrophy (Dyke-Davidoff-Masson Syndrome) Dehiscence of Tegmen Tympani 1074
1312 Heart Disease 1379, 1463, 1472
Cerebral Infarction 1123 hyperplasia (Adrenal) 1410
Cerebral Intraventricular Neoplasms 1058 Lobar Emphysema 1435
Cerebral Neuroblastoma 1157 Lung Malformations 1435
Cerebritis 1231 Megacalyces 1339
Ceruminoma 1079 Megacystis-Megaureter 1339
Cervical aortic arch 1378
Midline Nasal Mass 1367
Cervical Fascia 1266
Chamber Assessment 1472 Spinal Anomalies 1260
Congenitally Corrected TGV 1480
CHARGE Syndrome 1366 Contrast Enema (Malrotation) 1344
Chemotherapy 1042, 1155 Contrast Enhancement 1126
Chiari I Malformation 1308 Contrast Enhancement- Abscess 1133
Chiari II Malformation - (Arnold Chiari Malformation) 1308 Contrast Enhancement: Hematoma 1134
Chiari III Malformation 1309 Contusion (CNS) 1324
Chiari IV Malformation 1309 Convexity Extraaxial Differential 1124
Chiasmatic-hypothalamic glioma 1256 Convexity Intraaxial 1123
I2
Cord Herniation (Idiopathic Transdural) 1296 Distal Intestinal Obstruction Syndrome (DIOS) 1540
Cord injury 1497 Dorsal Induction (Disorders of) 1307
Coronary Artery Aneurysms-Kawasaki 1460 Double Aortic Arch 1378
Cortical Tubers 1200 Double Arch 1454
Cranial injury 1494 Double Outlet Right Ventricle 1485
Cranial Double Ring sign 1085
Nerve Enhancement 1129 Drug abuse 1041
Nerves 1107 Ductus Arteriosus 1456
Nerves III, IV, VI 1090 Duodenal
Vascular Development 1194 Atresia/Stenosis/Web 1345
Craniopharyngioma 1114, 1253, 1255, 1319 Hematoma 1356
Creutzfeldt-Jakob Disease 1235 Duplication Cyst (GI tract location) 1360
Crohn Disease 1360 Dural Tail 1131, 1169
Crohn's 1037 Dyke-Davidoff-Masson Syndrome 1196, 1312
Cryptococcus meningitis 1238 Dysembryoplastic Neuroepithelial Tumor 1051
Cryptococcus neoformans 1238 Dysgenesis (Callosal) 1316
CSF Dysgerminoma 1419
Dissemination 1156 Dysostosis Multiplex 1532
Dysphagia 1374
Homeostasis 1152
Dysplasias with Prominent Membranous Bone Involvement
Spread - Zuckerguss (Sugar Icing) 1157
CT Angiography: Basic Protocol 1453 1531
Cyanotic CHD 1467, 1472, 1478 Dysplastic Cerebellar Gangliocytoma (Lhermitte-Duclos
Cyanotic CHD with Decreased PBF 1487 Disease) 1049
Cyst (Neurenteric) 1264 EAC cholesteatoma 1078
Cystadenoma (Ovary) 1418 Ear 1068
Cystic Ebstein Malformation 1488
Echogenic Kidneys in Neonate 1386
Adenomatoid Malformation 1436
Ectopic Ureter 1332
Fibrosis 1535
Eisenmenger Physiology 1478
CF Gene 1535 Elevated Prolactin 1113
of the Pancreas 1539 Ellis-van Creveld Syndrome 1529
Masses (Pediatric Renal Tumors) 1398 Embryonal
neoplasms (Ovary) 1415 Sarcoma 1515
Neoplasms: Ovarian Teratoma 1417 small cell tumor 1053
nephroma 1398 Emphysema (Pulmonary Interstitial) 1446
Partially Differentiated Nephroblastoma 1398 Encephalitis 1040, 1231
Encephalocele 1074
Renal Disease of Childhood 1381
Endocardial Cushion Defect 1477
Renal Tumor (Multilocular) 1398
Cysticercosis (Intracranial) 1236 Endolymphatic Sac Tumor 1205
Cysts of the CNS 1160 Enteric Duplication Cyst 1360
Dandy-Walker Malformation 1312 Enteric Fistula (Dorsal) 1263
Darling’s Classification 1481 Enterocolitis (Necrotizing) 1353
Dating of intracranial blood 1496 Enterocolitis (Neutropenic) 1361
DAVF (Dural AVF) 1225 Ependymitis granularis 1037
Dawson's fingers 1038 Ependymoma 1058, 1109, 1112, 1149
DBO’s MR Signal Abnormalities 1191 Epidermoid 1081, 1161
Deep and Periventricular 1121 Epidermoid Inclusion Cyst 1109
Degenerative Disc Disease 1290 Epidermoid vs. Arachnoid Cyst 1109
Degenerative Disease (Spine) 1290 Epidural abscess 1231
Dehiscence of Tegmen Tympani 1074 Epidural Phlegmon / Abscess 1295
Dehiscent jugular bulb 1073 Epiglottitis 1364
DeMorsier’s Syndrome (Septo-Optic Dysplasia) 1310 Epstein-Barr virus (EBV) 1037
Demyelinating Diseases 1037 Esophageal Atresia 1341
Demyelination 1039, 1040, 1041 Esthesioneuroblastoma 1248, 1368
Ethmoid sinus 1240
Imaging 1043
Dermal Sinus (Dorsal) 1264 Exocrine Pancreatic Insufficiency 1538
DERMOID 1162 Exostoses 1288
Dermoid / Epidermoid (Orbit) 1101 Exostosis (External Ear) 1078
Dermoid Cysts 1287 External auditory canal (EAC) atresia 1071
Desmoplastic Infantile Ganglioglioma / Astrocytoma 1048 External Ear Masses 1078
Differential diagnosis of abuse injuries 1499 External Ear Neoplasms 1079
Dilated Azygous Vein 1460 External Otitis 1078
Dirty retrobulbar fat (Grave's Disease) 1094 Extraaxial Lesions 1106
Disc Extraaxial Tumors 1158
Disease 1290 Extraconal Lesions 1100
Extrusion with Migration 1291 Extralobar Sequestration 1440
Extraocular muscles (EOM) 1089
herniations and types 1291
Disorders of Neuronal Proliferation 1313, 1314 Extrapontine myelinolysis 1041
I3
Facet Joint Synovial Cysts 1292 Hemangioendothelioma 1511
Facial Nerve Palsy 1081 Hemangioma 1370
Failed Back Surgery Syndrome (see also FBBS) 1292 Hemangiomas (suprahyoid Neck) 1266
Fallot 1487 Hemangiopericytoma 1173
FBSS (Failed Back Surgery Syndrome) 1293 Hemangiopericytoma vs. Meningioma 1173
Cervical Spinal Canal Stenosis 1293 Hematoma (Duodenal) 1356
Ossification (Posterior Longitudinal Ligament) 1294 Hemimegalencephaly 1313
Posterior Longitudinal Ligament (Ossification) 1294 Hemorrhage 1502
Type I Arachnoiditis 1293 Adrenal 1410
Type II Arachnoiditis 1293 Child Abuse 1495
Fibromatosis (Aggressive - Masticator Space) 1276 Intracranial 1221
Fibromatosis Colli 1267, 1371 Hemorrhagic Cysts (Ovary) 1416
Fibrosing Colonopathy (Cystic Fibrosis) 1540 Hemorrhagic Infarction 1131
Fibrous Dysplasia (Paranasal Sinuses) 1246 Hemorrhagic Ovarian Cysts 1416
Fibrous Histiocytoma (Orbit) 1099 Henoch-Schönlein Purpura 1356
Filum Terminale (Congenital Anomalies) 1263 Hepatobiliary Disease (Cystic Fibrosis) 1541
Fissures of Santorini 1078 Hepatoblastoma 1513
Focal Biliary Cirrhosis 1541 Hepatocellular Carcinoma 1514
Follicular cysts 1415 Hernia (Inguinal) 1357
Foreign Body 1365, 1366 heroin 1041
Forensic Radiology of Child Abuse 1491 Herpes encephalitis 1234
Fourth Ventricle 1109 Heterotopias (Gray Matter) 1315
Fractures (Healing) 1493 High Jugular Bulb (“Megabulb”) 1073
Fried egg appearance 1061 Highly Active Antiretroviral TX (HAART) 1239
Frontal horn “capping” 1037 Hip Effusion 1519, 1520
Frontal Lipoencephalocystocele 1307 Hip Sonography 1518
Frontal sinus 1241 Hirschprung Disease 1350
Functional Ovarian Cyst 1416 HIV encephalitis 1040, 1041
Fungal sinusitis 1102, 1245 HIV Leukoencephalopathy 1238
Ganglioglioma / Gangliocytoma 1047 Holoprosencephaly (Alobar) 1310
Ganglioneuroblastoma 1402, 1408 Holoprosencephaly (Semilobar) 1310
Ganglioneuroma 1402 Horseshoe kidney 1330
Gastric Atresia 1342 HSV Encephalitis 1131
Gastrostomy Tubes 1356 Hurler Syndrome 1532
Gastrulation 1263 Hyaline Membranes 1444
Gaucher Disease 1431 Hydranencephaly 1310
Germ Cell Tumors 1176, 1418 Hydrocarbon aspiration 1366
Germ Cell Tumors-AFIP Series 1177 Hydrocephalus 1181
Germinal Matrix 1502 Hydrocolpos 1420
Germinoma 1121, 1177 Hydronephrosis 1338
Germinoma (Infundibular) 1257 Hyperostosis in Meningiomas 1171
Ghost tumor 1046 Hypertrophic Pyloric Stenosis 1354
GI Disorders (Acute - Infants and Chidren) 1353 Hypogenetic Lung Syndrome 1439
GI Tract Obstruction 1341 Hypoperfusion complex (Child Abuse) 1499
Glioblastoma Multiforme 1119, 1147, 1322 Hypopharyngeal cyst 1369
Glioma 1109 Hypoplastic left heart syndrome 1466, 1485
Glioma (Chiasmatic-hypothalamic) 1256 Hypothalamic Hamartoma 1257
Globe 1088 Hypothalamus 1115
Globus pallidus 1191 Hypoxic-ischemic encephalopathy 1039
Glomerulocystic Disease 1386 Iatrogenic Demyelinating Disorders: Chemotherapy 1042
Glomus jugulare 1082 Iatrogenic white matter degeneration 1037
Glomus tympanicum 1082 Idiopathic Transdural Cord Herniation 1296
Gradenigo’s syndrome 1078 Ileal Atresia 1347
Grading Problems in Gliomas 1140 Ileus (Meconium) 1348
Graf System (Pediatric Hip) 1519 Imaging Studies (UTI) 1331
Granulocyte Colony Stimulating Factor 1429 Immaturity of the Colon (Functional) 1349
Granulosa-theca Cell Tumor 1419 Immune reconstitution syndrome 1239
Graves’ 1037 Immunocompromised Child 1535
Graves’ Disease 1094 Immunocompromised Patient 1045
Great Vessels (Transposition) 1468 Imperforate Anus 1351
Grey Matter Heterotopias 1315 Incudostapedial disruption 1085
HAART 1239 Infantile Hemangioendothelioma 1511
Hamartoma 1510 Infarction 1506, 1507
Hamartoma (hypothalamic) 1257 Infections (Intracranial) 1231
Healing of fractures 1493 Infections (Spine) 1290, 1295
Healing of metaphyseal fractures 1492 Inferior orbital fissure 1088
Hemangioblastoma 1109, 1111, 1203, 1320 Inflammatory disease of the salivary glands 1369
Hemangioblastomatosis 1202 Infratentorial 1106
I4
Inguinal Hernia 1357 Lipoma (Intraspinal) 1262
Inner Ear Anomalies 1071 Liposarcoma (Suprahyoid Neck) 1267
Innominate Artery Compression 1455 Lissencephaly 1314
Innominate Artery Compression Syndrome 1379 Listeria Monocytogenes 1130
Interhemispheric extra-axial hemorrhage 1495 Liver Metastases 1516
Internal Auditory Canal 1107 Liver Tumors (Pediatric) 1509
Internal Carotid Artery 1073 Lobar emphysema 1435
Interrupted Pulmonary Artery 1455 Long bone shaft fracture 1491
Intestinal Obstruction (Neonatal) 1341 Long Parotid Tails 1275
Intraaxial Lesions 1106 Low Back Pain 1290
Intraconal Lesions 1097 Low Intestinal Obstruction 1347
Intracranial Lumbar 1292
Aneurysms 1210 Facet Arthropathy 1292
blood (Dating) 1496 Spinal Canal and Foraminal Stenosis 1292
Germ Cell Tumors 1176 Lung Agenesis 1439
Lung Disease(Cystic Fibrosis) 1537
Germinoma 1177
Lung Diseases in Neonates 1444
Infections 1231
Lyme disease 1231
Lipoma 1182 Lymphangioma (Orbit) 1100
Vascular Malformations 1220 Lymphatic Malformations (SupraHyoid Neck) 1267
Intralobar Sequestration 1440
Lymphocytic hypophysitis 1252
Intramural Hemorrhage (GI - Differential) 1356
Lymphoepithelial Lesions (Benign - Suprahyoid Neck) 1278
Intrarenal Collecting System (Abnormal Axis) 1333
Lymphoma 1324, 1371
Intrarenal Reflux 1334
CNS 1045
Intrasellar Pathology 1251
Intraventricular Lesions 1106 Orbit) 1098
Intraventricular Meningioma 1065 Pediatric Renal Tumors) 1400
Intussusception 1357 Sella) 1258
Cystic Fibrosis 1540 in AIDS 1324
Reduction 1358 vs. Toxoplasmosis 1324
Inverted Papilloma (Paranasal Sinuses) 1247 Macroglossia 1369
Irritable Hip 1519 Madelung’s Disease 1267
Ischemic Enhancement 1131 Malfixation (Duodenum) 1343
Jantene Procedure 1469 Malignant
Jejunal Atresia 1347 Astrocytoma 1145
Jeune Syndrome 1528 Compression Fracture 1430
JNA (Juvenile Nasopharyngeal Angiofibroma) 1246 Germ Cell Tumors 1418
Joubert’s Syndrome 1313 Meningioma 1172
Jugular bulb 1073
Sinus Lesions 1247
Jugular Malrotation – UGI 1344
Diverticulum 1073 Malrotation (Duodenum) 1343
Foramen Masses 1083 Mandibular Hypoplasia 1369
Paragangliomas 1270 Marburg 1039
Jugulotympanic Paraganglioma 1082 Marchiafava-Bignami disease 1042
Juvenile Angiofibroma 1367 Marfan syndrome 1460
Juvenile Nasopharyngeal Angiofibroma (JNA) 1246 Marrow
Kawasaki disease 1460 Components 1425
Keratosis obturans 1078 Conversion 1427
Kernohan-Sayre (AFIP) Grading System 1137
Depletion Fatty Replacement 1432
Kidney (Medullary Sponge) 1382
Distribution 1427
Kidney (Multicystic Dysplastic) 1399
Kidney (Rhabdoid Tumor of) 1395 Reconversion 1428
Labrynthine Aplasia 1072 Replacement or Infiltration 1429
Masses - Ring Enhancing (CNS) 1322
Lacrimal Gland Lesions 1102
Masticator Space 1274
Lacrimal Sac Lesions 1103
Mastoiditis 1078
Langerhans Cell Histiocytosis (Sella) 1258
Mature Teratoma (Ovary) 1417
Large Endolymphatic Duct and Sac (LEDS) 1072
Maxillary sinus 1241
Laryngeal- Tracheopapillomatosis 1372
McKusick 1531
Laryngomalacia 1371
Measles 1037
Laryngotracheal cleft 1371
Meckel Diverticulum 1359
Left (Double) Superior Vena Cava 1458
Meckel-Gruber Syndrome 1388
Left paramediastinal structures (Differential Diagnosis) 1458
Meconium Aspiration Syndrome 1449
Left Superior Vena Cava 1458
Meconium Ileus 1348
Leukocoria 1090
Leukoencephalopathy (HIV) 1238 Cystic Fibrosis 1540
Meconium Peritonitis 1348
Lhermitte-Duclos Disease 1049 Meconium Plug Syndrome 1540
Lingual Thyroid 1370 Mediastinal Bronchogenic Cysts 1438
Lingual Thyroid Gland 1285 Medullary Cystic Disease Complex 1387
Lipoencephalocystocele (Frontal) 1307
I5
Medullary Sponge Kidney 1382 polyps 1368
Medullary Tumors (Adrenal) 1402 Nasopharyngeal Carcinoma (NPSCCa) 1283
Medulloblastoma 1109, 1154, 1318 Neck Neoplasms (Child) 1370
Medulloblastoma - Desmoplastic 1157 Necrotizing Enterocolitis 1353
Megabulb 1073 Necrotizing External Otitis 1078
Megacalyces 1339 Neonatal
Megalencephaly (Unilateral) 1313 Brain 1501
Megaureter 1339 GI Tract Obstruction 1341
Melanoma (Uveal) 1092 Hypoxic-Ischemic Injury 1502
Membranous Tracheitis 1365 Low Intestinal Obstruction (Differential Diagnosis) 1351
Meninges (Neoplasms) 1164 Pneumonia 1450
Meningioma 1065, 1081, 1108, 1125, 1164
Respiratory Distress 1444
MENINGIOMA
Lung Diseases 1444
*Imaging Features: CT vs. MR 1169 Neoplasms (Benign - Masticator Space) 1276
Angiography Transit Time 1170 Neoplasms (Malignant - Masticator Space) 1277
Atypical Imaging 1172 Neoplasms of the Meninges 1164
Dural Tail 1131 Nephroblastoma (Cystic Partially Differentiated) 1398
Hyperostosis 1171 Nephroblastomatosis 1394
Vasogenic Edema 1167 Cortical Nodule 1395
Suprahyoid Neck 1270 Diffuse 1394
Nephrogenic Rests: Location 1394
Suprasellar 1254 Nephroma (mesoblastic) 1396
Tentorial 1320 Nerve Sheath Tumors 1187
MR Imaging 1167 Neuroblastic Tumors 1402
Meningitis 1231 Neuroblastoma 1371, 1402
Meningocele 1262
Stage Distribution 1408
Mesenchymal Hamartoma 1509 Neuroectodermal Tumor 1053
Mesoblastic Nephroma 1396 Neuroepithelial Tumors 1047
Metabolic imaging 1043 Neurofibroma vs. Schwannoma 1188
Metaphyseal Chondrodysplasia 1530 Neurofibromas (Pelvis) 1423
Metaphyseal fracture 1491-1492 Neurofibromatosis 1185
Metastasis (Pituitary and Infundibulum) 1259 Type 2 1191
Metastatic Lesions (Orbit) 1100
Type 1 or von Recklinghausen Disease 1185
Methotrexate 1042 Neuromyelitis optica (Devic syndrome) 1039
Michel’s deformity 1072 Neuronal Proliferation (Disorders of) 1313, 1314
Microangiopathy 1039 Neutropenic Enterocolitis 1361
Microgastria 1342 Non-Astrocytic Gliomas 1149
Microgyria 1314 Non-Glial Lesions 1158
Middle Ear 1068 Nonhemorrhagic Infarction 1506
Midgut Loop (Normal Rotation) 1343 Non-Hodgkin Lymphoma (NHL) -Pharyngeal Mucosal Space
Midgut Volvulus 1343 1283
Migraine 1039 Non-Lissencephalic Cortical Dysplasias
Mirror Image Right Arch 1376 Microgyria/Polymicrogyria 1314
Modic Changes 1291 Normal
Modified Papile Classification 1502 Cranial Nerve Enhancement 1129
Brain (Neonatal) 1501 Enhancement 1128
Mondini’s dysplasia 1072
Monosymptomatic demyelinating 1037 Marrow (MR Features) 1426
Morquio Syndrome 1533 Pineal Calcification 1175
MR Angiography: Basic Technique 1453 Thymus 1521
Mucocele 1246 Vertebral Marrow: MRI 1428
Mucoepidermoid Carcinoma 1281 Norrie’s 1091
Mucopolysaccharides 1094 Obstruction (GI Tract - Neonatal) 1341
Multicystic Dysplastic Kidney 1382, 1399 Olfactory Neuroblastoma 1248
Multilocular Cystic Renal Tumor 1398 Olidodendroglioma 1152
Multiple sclerosis 1037, 1039, 1325 Oncocytoma (Suprahyoid Neck) 1280
MR 1038 Ophthalmic veins 1088
Mustard Procedure 1469 Opportunistic neoplasm 1045
myasthenia gravis, 1037 Optic Nerve
myelinolysis 1041 Glioma 1097
myelitis 1040 Sheath Meningioma 1097
Myelocystocele (Terminal) 1262 Optic neuritis 1040
Myelofibrosis 1431 Oral Cavity Normal Anatomy 1286
Myeloid Depletion: MRI 1432 Orbit 1088
Myelomeningocele 1260 Orbital
Nasal Cellulitis 1101
Cycle 1128 fissures 1088
Dermoid 1367 Lymphoma 1098
I6
septal system 1088 Persistent Interstitial Pulmonary Emphysema 1446
Trauma 1093 Persistent Stapedial Artery 1073
Varix 1099 Petrous Apex (Differential Diagnosis) 1083
Organic toxins 1041 Phakomatoses 1184
Oropharynx 1284 Pharyngeal Mucosal Space 1282
Osmotic myelinolysis 1041, 1042 Pharyngeal Perforation 1342
Ossicular Derangement 1085 Pheochromocytoma 1408
Ossifying Renal Tumor of Infancy 1397 Phlegmon / Abscess (Epidural) 1295
Osteogenesis Imperfecta 1533 Pial A-V Fistula 1225
Osteoma (Paranasal Sinuses) 1246 Pilocytic Astrocytoma 1110, 1134, 1139
Osteomyelitis 1431 Pilocytic Astrocytoma (Juvenile Pilocytic) 1141
Osteomyelitis (Spine) 1295 Pineal Calcification 1175
Pyogenic 1295 Pineal Cyst 1121, 1181
Tuberculous 1295 Pineal
Osteopetrosis (Albers-Schonberg Disease) 1533 Neoplasms Laboratory Tests 1179
Osteoporotic Fracture 1430 Parenchyma 1180
Ostiomeatal complex (Paranasal Sinuses) 1241 Region Masses 1175, 1320
Ostium Primum ASD 1464
Region Neoplasms 1178
Otitis 1078 Pineal/Quadrigeminal Cistern Region 1121
Otosclerosis 1085 Pinealomas 1121, 1175
Otospongiosis 1085 Pineoblastoma 1121, 1180
Outer Ear Anomalies 1071 Pineocytoma 1121, 1180
Ovarian Pituitary 1250
Cancer 1420 Pituitary
Cyst 1416 Adenoma 1113, 1253
Cystadenoma 1418 Apoplexy 1254
Maturation 1414 Macroadenoma 1253
Tumors 1415 Neoplasms 1251
Ovary (Prepubertal vs Postpubertal) 1414 Plasma Cell Granuloma 1522
Palatine Tonsil Enlargement 1368 Pleomorphic Adenoma 1279, 1288
Pancreas (Child Abuse) 1498 Pleomorphic Xanthoastrocytoma 1051, 1141
Pancreatic injury 1498 Plexiform Neurofibromatosis 1423
Papillary Cystadenoma Lymphomatosum 1280 Pneumatoceles 1524
Papillary Endolymphatic Sac Tumor 1083 Pneumonia 1523
Papilloma 1151 Pneumonia (term & premature neonates) 1448
Papovavirus 1238 Polycystic Kidney Disease (autosomal Recessive) 1383
Paradoxical Embolus 1475 Polymicrogyria 1314
Paragangliomas 1082, 1270 Port Wine Stain 1193
Paranasal Sinuses 1240 Post fossa cysts 1109
Paraovarian cysts 1415, 1417 Posterior chamber 1088
Parapharyngeal Abscess 1365 Posterior Fossa
Parapharyngeal Space 1267, 1268 Malformations 1312
Parasellar Region 1250 Tumors (Pediatric) 1318
Parinaud Syndrome 1175 Posterior Hyaloid Detachment 1090
Parotid Space 1278 Posterior Reversible Encephalopathy Syndrome (PRES)
Parotid Tail 1275 1039, 1040
Partial Anomalous Venous Return (Pulmonary) 1456 Posterior rib fractures (visualization) 1493
Patent Ductus Arteriosus 1456, 1476 Posterior Urethral Valves 1337
Patterns of Enhancement 1126 Precocious Puberty 1175
Patterns of Location 1106 Premature Births 1444
Pediatric Premature Brain 1501
Adrenal Masses 1402 Prepubertal ovary 1414
Airway 1363 Primary Megaureter 1339
Hip Sonography 1518 Pringle’s Disease 1199
Liver Tumors 1509 Profound Asphyxia 1506
Progressive multifocal leukoencephalopathy 1040
Pelvic Masses 1414
Progressive Multifocal Leukoencephalopathy (PML) 1041
Posterior Fossa Tumors 1318
Prolactin 1113
Renal Tumors 1390 Prolactinoma 1251, 1253
Tuberculosis 1526 Proteinosis (Alveolar) 1451
Pelvic Masses (Pediatric) 1414
Proximal Neonatal Intestinal Obstruction 1347
Pelvicaliectasis (Antenatal) 1336
Pseudotumor (Orbit) 1095
Peritonitis (Meconium) 1348
Pubertal ovary 1414
Periventricular Hemorrhagic Infarction 1503
Pulmonary
Sonography 1503
Periventricular Leukomalacia 1504 Abscess 1524
periventricular white matter 1039 Arterial Anomalies 1455
Persistent hyaloid (Cloquet’s) canal 1091 Artery Stenosis 1470
Persistent Hyperplastic Primary Vitreous (PHPV) 1091
I7
Atresia with Intact Ventricular Septum 1489 Rotation of Midgut Loop 1343
AVM 1442 Round Pneumonia 1522
Blastoma 1522 Rules for Ring Enhancing Mass 1132
Blood Flow 1472 Sacrococcygeal Teratoma 1421
SAH (Subarachnoid Hemorrhage) 1210
Bronchogenic Cyst 1438
Aneurysms (Intracranial) - Infectious 1218
Hypoplasia 1439
Aneurysms (Intracranial) - Treatment Options 1218
Infections 1521
Clinical Grading Scale 1213
Infections (Immunocompromised Child) 1535
CT 1214
Interstitial Emphysema 1446
CTA 1215
Sequestration 1440
DSA 1215
Sling 1379, 1455
induced Vasospasm 1214
Underdevelopment 1439
Infectious Intracranial Aneurysms 1218
Venous Anomalies 1456
Pulsatile Tinnitus Lesions 1074 Lumbar puncture 1214
Pyeloneprhitis 1335 MRA 1215
Pyknodysostosis 1534 MRI 1215
Pyloric Stenosis 1354 Outcomes 1213
Pyogenic Abscess (Intracranial) 1234 Patterns 1213
Pyogenic Osteomyelitis 1295
Radiologic Grading Scale 1213
Pyriform Aperture stenosis 1367
Risk Factors 1210
Radiation 1155
Screening 1217
Injury (Brain) 1043 Salivary glands (Inflammatory disease) 1369
Necrosis vs. Tumor (CNS) 1323 Salt and pepper appearance 1082
Ranulas 1287
Sarcoidosis (CNS) 1321
Rathke Cleft Cyst 1252
Sarcoidosis (Sella) 1258
Reactive Airways Disease 1365
SATCHMO 1319
Rebleeding 1497
SCCa (Squamous Cell Carcinoma) 1248
Rectal Prolapse (Cystic Fibrosis) 1540
Schizencephaly 1314
Rectus: medial, lateral, superior, inferior 1089
Schwannoma 1107, 1188, 1192
Red Marrow Signal 1427
Acoustic - Vestibular 1079
Reflux Nephropathy 1335
Renal Agenesis 1329 Orbit 1098
Scimitar Syndrome 1457
Renal Cell Cancer 1399
Sclera 1089
Renal Cyst 1381
Scutum 1076
Renal Ectopia 1330
Second Branchial Cleft Cyst 1269
Renal Ectopia and Fusion 1330
Secundum ASD 1464
Renal Tumors (Infancy and Young Children) 1390
Segmental Spinal Dysgenesis 1265
Respiratory Distress (Neonatal) 1444
Sella 1250
Respiratory Distress Syndrome (RDS) 1444
Sella/Parasellar Region - Differential 1113
Retained fetal lung fluid 1448, 1449
Sellar Masses: “SATCHMO” 1319
Retina 1089
Semicircular Canals (SCC) 1068
Retinal Detachment (RD) 1090
Semilobar Holoprosencephaly 1310
Retinoblastoma 1091
Senescent White Matter Changes 1039
Gene 1091 Senile Macular Degeneration 1090
Retinopathy of prematurity 1092
Septic Arthritis (Hip) 1520
Retrobulbar (“Postseptal”) Space 1089
Septo-Optic Dysplasia (DeMorsier’s Syndrome) 1310
Retropharyngeal Cellulitis 1364
Sequestration 1525
Reversal sign 1496
Sertoli-Leydig cell tumor 1419
Rhabdoid Tumor 1054
Sex Cord-Stromal Tumors 1419
Rhabdoid Tumor of Kidney 1395
Shaking mechanism 1492
Rhabdomyosarcoma 1368, 1420
Short Rib-Polydactyly 1528
Orbit 1101
Shunt Lesions 1463, 1487
Male Bladder & Prostate 1421 Sickle Cell Anemia 1429
Rhabdomyosarcomatoid variant of Wilms tumor 1053
Rhombencephalosynapsis 1313 Simple Renal Cyst 1381
Rib fracture 1492 Single Ventricle 1484
Rib Notching 1189 Physiology 1489
Sinus Mass Differential 1368
Right aortic arch 1454
Sinus Venosus ASD 1464
Right Arch 1376
Sinuses (Paranasal) 1240
Right paramediastinal structures (Differential Diagnosis)
Sinusitis 1243
1459
Sinusitis (Fungal) 1102
Right to Left Shunts 1487
Sjogren’s Syndrome 1279
Ring Enhancing Mass 1132
Skeletal Dysplasia 1527
Ring Lesion Features For Infection 1132
Skeletal injury (evaluation) 1494
Ring Lesions Differential 1132
Skull fracture 1497
Ring-enhancing Masses (CNS) 1322
SLE 1037
Risk Factors (subarachnoid Hemorrhage) 1211
Soap-bubble appearance 1051
I8
Spetzler-Martin Grading System (Intracranial Vascular Temporomandibular joint (TMJ) anomalies 1071
Malformations) 1222 Tenon’s capsule 1089
Sphenoid sinus 1242 Tentorial Meningioma 1320
Spina Bifida 1262 Teratoid Tumor 1053
Spinal Anomalies (Congenital) 1260 Teratoma 1178, 1371
Caudal Regression Syndrome 1265 Ovary 1417
Chiari II Malformation 1261 Sacrococcygeal 1421
Complex Dysraphic States 1263 vs. Dermoid (Pineal Region) 1178
Dorsal Dermal Sinus 1264 Tetralogy of Fallot 1455, 1467, 1487
Thanatophoric Dysplasia 1527
Dorsal Enteric Fistula 1263
Thiamin deficiency 1042
Fibrolipomatous Infiltration of Filum 1263
THIRD VENTRICLE 1116
Gastrulation 1263 Thoracic MRA & CTA 1453
HemiMMC/Hemimyelocele 1261 Thymus (Pediatric - Normal) 1521
Intraspinal Lipoma 1262 Thyroglossal Duct Cysts 1284
Lipoma with Dorsal Defect 1261 Thyroid Gland (Lingual) 1285
Lipomyelomeningocele 1261 Thyroid Orbitopathy (Graves’ Disease) 1094
Meningocele 1262 Time Density Curves 1126
Myelocele (Myeloschisis) 1261 Tinnitus 1074
Tongue Base Mass 1369
Myelomeningocele 1260
Top 10 Pelvic Lesions 1423
Neurenteric Cyst 1264
Total Anomalous Pulmonary Venous Return 1480
Persistent Terminal Ventricle 1263 Total Anomalous PV Return 1469
Posterior Spina Bifida 1262 Total Colonic Aganglionosis 1351
Segmental Spinal Dysgenesis 1265 Toxic Demyelination 1041
Spinal Dysraphism 1260 Toxocara canis 1092
Split Cord Malformation 1264 Toxocariasis 1092
Terminal Myelocystocele 1262 Toxoplasmosis 1119
Tight Filum Terminale 1263 Intracranial 1238
Spinal Dysraphism 1260 Tracheal bronchus 1372
Spine 1290 Tracheal Stenosis 1372
Spine injury 1493 Tracheomalacia 1371
Split Cord Malformation 1264 Transient Tachypnea of Newborn 1449
Squamous cell carcinoma 1248 Transposition of Great Vessels 1468
Stapedial Artery 1073 Transverse Myelitis 1039
Stridor 1363, 1374 Tricuspid Atresia 1468, 1484, 1489
Sturge-Weber Syndrome 1193 Trilateral Retinoblastoma 1180
Subacute sclerosing panencephalitis 1040 Truncus Arteriosus 1469, 1483
Subarachnoid Hemorrhage 1210 Tuberculosis (Intracranial) 1231
Subdural empyema 1231 Tuberculosis Pediatric 1526
Subependymal Giant Cell Astrocytoma 1058, 1061 Tuberous Sclerosis or Bourneville Disease 1197
Subependymal Nodules 1200 Tumefactive Demyelination 1134
subependymal veins 1039 Tumor Blush 1171
Subependymoma 1058, 1059 UGI (Upper GI Tract - Malrotation) 1344
Subepidermal Fibrosis 1199 ulcerative colitis 1037
Subglottic edema 1363 Uncommon Neuroepithelial Tumors 1045
Subglottic Hemangioma 1370 Undifferentiated Embryonal Sarcoma 1515
Sugar Icing 1156 Unilateral Megalencephaly (Hemimegalencephaly) 1313
Superior and inferior ophthalmic veins 1088 Upper esophageal foreign body 1366
Superior Left Intercostal Vein 1458 Ureterocele 1333
Superior orbital fissure 1088 Ureteropelvic duplication 1333
Suprahyoid Neck 1266 Ureteropelvic Junction Obstruction 1338
Suprasellar Masses 1253 Urethral Valves (Posterior) 1337
Supratentorial 1106 Urinary Tract Infection (Child) 1329
Supratentorial Primitive Neuroectodermal Tumor 1052 US Guidance 1520
Surfactant 1445 Uterine Morphology: Maturation 1415
Surfactant B protein deficiency 1448 Uvea: choroid 1089
Swyer-James Syndrome 1436, 1524 Uveal Melanoma 1092
Systemic Gas Embolism 1447 Uveal Metastasis 1093
Systemic Venous Anomalies 1458 VACTERL 1342
Taenia solium 1236 Vagal paraganglioma 1082
Tegmen Tympani 1074 Vagale Paragangliomas 1271
Temporal Bone Fracture 1084 Vaginal Rhabdomyosarcoma 1421
Temporal Bone: Vallecular Cyst 1369
Anatomy 1068 Valvular Pulmonic Stenosis 1470
Varix (Orbit) 1099
Congenital Lesions 1068
Vascular Anomalies (Pediatric Cardiac Imaging) 1453
Infectious Lesions 1076
Vascular Malformations (Intracranial) 1220
Neoplastic Lesions 1076
I9
Vascular Mediated Disorders (Bone Marrow) 1433
Edema 1433
Ischemia 1433
Ischemia & Edema: Causes (Bone Marrow) 1433
Vascular Rings and Slings 1374
Vascular White Matter Disease 1039
Vasculitis 1039
Vein Of Galen Malformation 1181
Venous Anomaly (Intracranial - Developmental) 1226
Venous Collagenosis 1039
Ventral Induction (Disorders of) 1310
Ventricular Septal Defect 1474
Ventricular Septal Defects 1465
Vesicoureteric Reflux 1332
Vestibular Schwannoma 1079, 1108
Vestibule 1068
Viral and Postviral Demyelination 1040
Viral Croup 1363
Virchow-Robin spaces 1037
Visceral injury 1498
Vitreous body 1088
Volvulus (Midgut) 1343
von Hippel-Linmdau Syndrome: NIH Classification 1202
von Recklinghausen Disease 1185
Warburg’s 1091
Warthin’s Tumor 1280
Wernicke encephalopathy 1042
White Matter Changes (Senescent) 1039
WHO 2000 Brain Tumor Classification 1137
Whole-body MRI 1426
Wilms Tumor 1390
Wishart Disease 1191
Wolman Disease 1411
Xanthoastrocytoma 1052
Xanthoastrocytoma (Pleomorphic) 1141
Yellow Marrow Signal 1427
Zellweger Syndrome 1388
I 10