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Comprehensive Radiographic

PATHOLOGY SIXTH EDITION

Ronald L. Eisenberg, MD, JD, FACR Associate Professor of Radiology Harvard Medical School Staff Radiologist Beth Israel Deaconess Medical Center Boston, Massachusetts

Nancy M. Johnson, MEd, RT(R)(CV)(CT)(QM), FASRT Faculty, Diagnostic Medical Imaging GateWay Community College Phoenix, Arizona

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3251 Riverport Lane St. Louis, Missouri 63043 COMPREHENSIVE RADIOGRAPHIC PATHOLOGY, SIXTH EDITION Copyright © 2016 by Mosby, Inc., an affiliate of Elsevier Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher, except that, until further notice, instructors requiring their students to purchase Comprehensive Radiographic Pathology by Eisenberg, may reproduce the contents or parts thereof for instructional purposes, provided each copy contains a proper copyright notice as follows: Copyright © 2016 by Elsevier Inc. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein). Permission is hereby granted to reproduce the test questions in this publication in complete pages, with the copyright notice, for instructional use and not for resale. Although for mechanical reasons some/all pages of this publication are perforated, only those pages imprinted with an Elsevier Inc. copyright notice are intended for removal.

Notices Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become n ­ ecessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. Previous editions copyrighted 2012, 2007, 2003, 1995, 1990. Library of Congress Cataloging-in-Publication Data Eisenberg, Ronald L., author. Comprehensive radiographic pathology / Ronald L. Eisenberg, Nancy M. Johnson. -- Sixth edition. p. ; cm. Includes index. ISBN 978-0-323-35324-3 (pbk. : alk. paper) I. Johnson, Nancy M., author. II. Title. [DNLM: 1. Radiography--methods. 2. Pathology. WN 200] RC78 616.07’572--dc23 2015016178

Content Strategist: Sonya Seigafuse Content Development Manager: Laurie Gower Content Development Specialist: Laura Goodrich Publishing Services Manager: Jeff Patterson Project Managers: Jeanne Genz and Lisa A. P. Bushey Design Direction: Julia Dummitt Printed in China Last digit is the print number: 9 8 7 6 5 4 3 2 1

This text is dedicated to all the students and medical imaging professionals who wish to better understand the value of pathology to improve their diagnostic images. Thank all of you who helped in making this endeavor successful. Special credit to the contributors of this edition who assisted in updating the content and images. – Raymond Johnson, BS, NMTCB, PET and Bartram Pierce, BS, RT(R)(MR), FASRT Nancy M. Johnson

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REVIEWERS Elaine Beaudoin, MS, RT(R) Clinical Coordinator Niagara County Community College Sanborn, New York

Joy Menser, EdD, RT(R)(T) Program Director of Radiography Owensboro Community and Technical College Owensboro, Kentucky

Chris Beaudry, MEd, ARRT(R)(M)(CT) Program Coordinator Yakima Valley Community College Yakima, Washington

Cynthia A. Meyers, MSRT(R) Program Director, Professor Niagara County Community College Sanborn, New York

Dena L. Blevins, BSRT(R) Clinical Coordinator Collins Career Technical College Chesapeake, Ohio

Sandra E. Moore, MA, RT(R)(M) Radiography Program Director The Johns Hopkins Hospital Baltimore, Maryland

Robin T. Cornett, MAEd, RT(R)(CV) Program Director, Radiography Catawba Valley Community College Hickory, North Carolina

April H. Pait, BS, RT(R)(M) Clinical Coordinator Guilford Technical Community College Jamestown, North Carolina

Kristi Klein, MSEd, RT(R)(M)(CT) Program Director Madison Area Technical College Madison, Wisconsin

Paula Pate-Schloder, MS, RT(R)(CV)(CT)(VI) Associate Professor Misericordia University Dallas, Pennsylvania

Nancy I. Lamouroux, BS, RT(R) Clinical Coordinator/Instructor Kilgore College Kilgore, Texas

Lorrie Scott Teeter, MS, RT(R)(CT) Assistant Professor Adventist University of Health Sciences Orlando, Florida

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P R E FAC E Understanding the basic principles of pathology is an essential part of the radiologic technologist’s education. Knowing how disease processes work and recognizing the radiographic appearance of specific diseases aids the technologist in selecting proper modalities and determining the need for repeat radiographs in different situations. This kind of knowledge enables the radiologic technologist to become a more competent professional and a contributing member of the diagnostic team.

ORGANIZATION Fully illustrated and well organized, Comprehensive Radiographic Pathology meets the needs of today’s student and practicing image personnel. The book opens with a chapter on disease processes that introduces the pathologic terms used throughout the text. Chapter 2 describes the advantages and limitations of eight widely used modalities: mammography, ultrasound, computed tomography (CT), magnetic resonance imaging (MRI), nuclear medicine, single-photon emission computed tomography (SPECT), positron emission tomography (PET), and fusion imaging. Summary tables describe imaging terminology used in each of the seven modalities. Each of the remaining chapters is a systematic approach to the diseases involving a specific organ system. These chapters begin with an overview of physiology. For each of the most common pathologic conditions associated with the system, there is a brief description of the disease and its clinical manifestations, followed by imaging findings and treatment. Summary tables follow each major discussion, reiterating the location, imaging appearance, and treatment of the diseases just presented.

DISTINCTIVE FEATURES • Comprehensive coverage provides the most thorough explanations of any radiographic pathology text of those pathologies that can be diagnosed with medical imaging. • Navigating the chapters is easy with the standardized heading scheme and chapter outlines for the systems chapters. • Radiographer Notes in every chapter instruct students on how to deal effectively with varying patient needs and provide perspective on why learning pathology is important for radiography practice. • A systems approach makes it easy to locate information and to study one area at a time, assimilating details in a logical sequence. It provides the best framework for building understanding of pathology. • Summary tables list the imaging appearance and treatment of each disease and have been updated to include pathologic conditions included in the text. • Coverage of the alternative imaging modalities that supplement radiographic imaging for diagnosis of some pathology conditions orients readers to other modalities

that may be needed to ensure proper diagnosis of certain pathologies. • Treatment sections provide useful background treatment and prognosis. • The student workbook provides extra opportunities for review and self-assessment.

NEW TO THIS EDITION • Expanded terms related to disease process and imaging features • Updates and additions of the following: fusion imaging, SPECT, PET/CT, MR pulse sequences, and their correlation with general radiography • Color images, where appropriate, of MR, nuclear medicine, and PET/CT • Updated Radiographer Notes to incorporate analog and digital information

PEDAGOGICAL FEATURES • Each chapter opens with an outline and a key terms list to aid the student in navigating the content. • Radiographer Notes offer helpful suggestions for producing optimal radiographs of the organ system featured in each chapter. Information especially relevant to radiologic technologists is included, such as positioning and exposure factor adjustments for patients with specific conditions and special patient handling requirements. If multiple imaging modalities can be used, the most appropriate initial procedure is indicated, as well as the sequence in which various imaging studies should be performed. • The body system chapters are organized as follows: physiology, identification of anatomic structures on anatomy figures and radiographs, pathologic conditions, radiographic appearance, and treatment. • Each section of related pathologies is summarized in a table at the end of the section. The table names the disorder and then lists the location, radiographic appearance, and treatment for easy review and enhanced retention. • Finally, each chapter ends with a series of review questions to help readers assess their comprehension of the material. An answer key is found at the back of the book, along with several appendices, an extensive glossary, and a list of major prefixes, roots, and suffixes to help readers determine the meaning of unfamiliar words.

ANCILLARIES For the Instructor • Instructor Resources on Evolve include a test bank with approximately 500 questions, PowerPoint slides, and an image collection with approximately 900 images.

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PREFACE

For the Student • The Evolve site offers 10 student review questions per chapter and access to the image collection for further review. • The workbook contains a variety of exercises for each of the 12 chapters in the book. Examples include matching terms with their definitions; labeling diagrams; fill-inthe-blank, short-answer, and multiple-choice questions;

pathology case studies; and a post-test. Completing the workbook activities will ensure understanding of disease processes, their radiographic appearance, and their likely treatment. The answers for the exercises are located in the back of the workbook. • By understanding the disease processes, their image appearance, and their treatment, the technologist will be prepared to contribute to the diagnostic team.

CONTENTS Preface, vii 1 Introduction to Pathology, 1 Disease, 2 Inflammation, 3 Edema, 4 Ischemia and Infarction, 5 Hemorrhage, 5 Alterations of Cell Growth, 6 Neoplasia, 7 Hereditary Diseases, 9 Disorders of Immunity, 11 Infectious Disease Exposure, 11 Acquired Immunodeficiency Syndrome, 12 2 Specialized Imaging Techniques, 15 Diagnostic Imaging Modalities, 15 Imaging Features, 16 Mammography, 16 Ultrasound, 17 Computed Tomography, 20 Magnetic Resonance Imaging, 24 Nuclear Medicine, 28 Single-Photon Emission Computed Tomography, 28 Positron Emission Tomography, 29 Fusion Imaging, 31 3 Respiratory System, 36 Physiology of the Respiratory System, 38 Internal Devices, 40 Endotracheal Tube, 40 Central Venous Catheters, 40 Swan–Ganz Catheters, 41 Transvenous Cardiac Pacemakers, 42 Congenital/Hereditary Diseases, 43 Cystic Fibrosis, 43 Hyaline Membrane Disease, 44 Inflammatory Disorders of the Upper Respiratory System, 44 Croup, 44 Epiglottitis, 44 Inflammatory Disorders of the Lower Respiratory System, 45 Pneumonia, 45 Anthrax, 47 Lung Abscess, 48 Tuberculosis, 49 Pulmonary Mycosis, 52 Respiratory Syncytial Virus, 53 Severe Acute Respiratory Syndrome, 53

Diffuse Lung Disease, 54 Chronic Obstructive Pulmonary Disease, 54 Sarcoidosis, 57 Pneumoconiosis, 59 Neoplasms, 61 Solitary Pulmonary Nodule, 61 Bronchial Adenoma, 63 Bronchogenic Carcinoma, 63 Treatment of Pulmonary Neoplastic Diseases, 65 Pulmonary Metastases, 65 Vascular Diseases, 68 Pulmonary Embolism, 68 Septic Embolism, 71 Pulmonary Arteriovenous Fistula, 72 Miscellaneous Lung Disorders, 72 Atelectasis, 72 Adult Respiratory Distress Syndrome, 73 Intrabronchial Foreign Bodies, 74 Mediastinal Emphysema (Pneumomediastinum), 75 Subcutaneous Emphysema, 75 Treatment of Mediastinal and Subcutaneous Emphysema, 75 Disorders of the Pleura, 76 Pneumothorax, 76 Pleural Effusion, 77 Empyema, 79 Mediastinal Masses, 80 Disorders of the Diaphragm, 82 Diaphragmatic Paralysis, 82 Eventration of the Diaphragm, 83 Other Causes of Elevation of the Diaphragm, 83 4 Skeletal System, 85 Physiology of the Skeletal System, 87 Congenital/Hereditary Diseases of Bone, 89 Vertebral Anomalies, 89 Spina Bifida, 89 Osteopetrosis, 90 Osteogenesis Imperfecta, 91 Achondroplasia, 92 Congenital Hip Dysplasia (Dislocation), 92 Inflammatory and Infectious Disorders, 95 Rheumatoid Arthritis, 95 Rheumatoid Variants: Ankylosing Spondylitis, Reiter’s Syndrome, and Psoriatic Arthritis, 96 Osteoarthritis (Degenerative Joint Disease), 98 Infectious Arthritis, 98 Treatment of Arthritis, 100 Bursitis, 101 Rotator Cuff Tears, 102 Tears of the Menisci of the Knee, 103

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CONTENTS Bacterial Osteomyelitis, 103 Tuberculous Osteomyelitis, 106 Metabolic Bone Disease, 108 Osteoporosis, 108 Osteomalacia, 109 Rickets, 110 Gout, 111 Paget’s Disease, 112 Lead Poisoning, 114 Fibrous Dysplasia, 116 Ischemic Necrosis of Bone, 116 Benign Bone Tumors, 119 Treatment of Benign Bone Tumors, 123 Malignant Bone Tumors, 124 Treatment of Malignant Bone Tumors, 127 Bone Metastases, 127 Fractures, 131 Types of Fractures, 131 Fracture Healing, 134 Pathologic Fractures, 135 Stress Fractures, 136 Battered-Child Syndrome, 137 Common Fractures and Dislocations, 137 Fractures and Dislocations of the Spine, 141 Herniation of Intervertebral Disks, 144 Scoliosis, 147 Spondylolysis and Spondylolisthesis, 148

5 Gastrointestinal System, 152 Physiology of the Digestive System, 153 Esophagus, 156 Tracheoesophageal Fistula, 156 Esophagitis, 158 Ingestion of Corrosive Agents, 160 Esophageal Cancer, 161 Esophageal Diverticula, 163 Esophageal Varices, 163 Hiatal Hernia, 165 Achalasia, 166 Foreign Bodies, 166 Perforation of the Esophagus, 168 Stomach, 170 Gastritis, 170 Pyloric Stenosis, 170 Peptic Ulcer Disease, 171 Cancer of the Stomach, 174 Small Bowel, 176 Crohn’s Disease (Regional Enteritis), 176 Small Bowel Obstruction, 177 Adynamic Ileus, 180 Intussusception, 181 Malabsorption Disorders, 182 Colon, 183 Appendicitis, 183 Diverticulosis, 185 Diverticulitis, 186

Ulcerative Colitis, 187 Crohn’s Colitis, 189 Ischemic Colitis, 191 Irritable Bowel Syndrome, 191 Cancer of the Colon, 191 Large Bowel Obstruction, 193 Volvulus of the Colon, 193 Hemorrhoids, 195 Gallbladder, 197 Gallstones (Cholelithiasis), 197 Acute Cholecystitis, 198 Emphysematous Cholecystitis, 199 Porcelain Gallbladder, 199 Liver, 201 Hepatitis, 201 Cirrhosis of the Liver, 202 Hepatocellular Carcinoma, 203 Hepatic Metastases, 205 Pancreas, 206 Acute Pancreatitis, 206 Chronic Pancreatitis, 206 Pancreatic Pseudocyst, 208 Cancer of the Pancreas, 209 Pneumoperitoneum, 210 Spleen, 212 Enlargement, 212 Rupture, 213 6 Urinary System, 216 Physiology of the Urinary System, 216 Congenital/Hereditary Diseases, 218 Anomalies of Number and Size, 218 Anomalies of Rotation, Position, and Fusion, 219 Anomalies of Renal Pelvis and Ureter, 220 Treatment of Congenital/Hereditary Anomalies, 221 Ureterocele, 221 Posterior Urethral Valves, 222 Inflammatory Disorders, 224 Glomerulonephritis, 224 Pyelonephritis, 224 Tuberculosis, 225 Papillary Necrosis, 226 Cystitis, 227 Urinary Calculi, 228 Urinary Tract Obstruction, 231 Cysts and Tumors, 234 Renal Cyst, 234 Polycystic Kidney Disease, 236 Renal Carcinoma, 237 Wilms’ Tumor (Nephroblastoma), 240 Carcinoma of the Bladder, 240 Renal Vein Thrombosis, 242 Acute Renal Failure, 243 Chronic Renal Failure, 245

CONTENTS 7 Cardiovascular System, 248 Physiology of the Cardiovascular System, 248 Congenital Heart Disease, 252 Left-to-Right Shunts, 252 Tetralogy of Fallot, 254 Coarctation of the Aorta, 254 Acquired Vascular Disease, 256 Coronary Artery Disease, 256 Congestive Heart Failure, 260 Pulmonary Edema, 261 Hypertension, 263 Hypertensive Heart Disease, 265 Aneurysm, 266 Traumatic Rupture of the Aorta, 267 Dissection of the Aorta, 268 Atherosclerosis, 270 Thrombosis and Embolism, 271 Valvular Disease, 275 Rheumatic Heart Disease, 275 Mitral Stenosis, 275 Mitral Insufficiency, 276 Aortic Stenosis, 277 Aortic Insufficiency, 278 Infective Endocarditis, 278 Pericardial Effusion, 280 Venous Disease, 281 Deep Venous Thrombosis, 281 Varicose Veins, 281 8 Nervous System, 286 Physiology of the Nervous System, 287 Infections of the Central Nervous System, 290 Meningitis, 290 Encephalitis, 291 Brain Abscess, 292 Subdural Empyema, 293 Epidural Empyema, 293 Treatment of Subdural and Epidural Empyemas, 294 Osteomyelitis of the Skull, 294 Tumors of the Central Nervous System, 295 Glioma, 295 Meningioma, 299 Acoustic Neuroma, 299 Pituitary Adenoma, 300 Craniopharyngioma, 303 Pineal Tumors, 305 Chordoma, 306 Metastatic Carcinoma, 307 Traumatic Processes of the Brain and Skull, 309 Skull Fracture, 309 Epidural Hematoma, 311 Subdural Hematoma, 311 Cerebral Contusion, 312 Intracerebral Hematoma, 313 Subarachnoid Hemorrhage, 313

Carotid Artery Injury, 313 Facial Fractures, 313 Vascular Disease of the Central Nervous System, 317 Cerebrovascular Disease, 317 Stroke Syndrome, 317 Transient Ischemic Attacks, 319 Intraparenchymal Hemorrhage, 320 Subarachnoid Hemorrhage, 321 Multiple Sclerosis, 324 Epilepsy and Convulsive Disorders, 326 Degenerative Diseases, 327 Normal Aging, 327 Alzheimer’s Disease, 327 Huntington’s Disease, 328 Parkinson’s Disease, 329 Cerebellar Atrophy, 329 Amyotrophic Lateral Sclerosis (Lou Gehrig’s Disease), 330 Hydrocephalus, 330 Sinusitis, 332 9 Hematopoietic System, 336 Physiology of the Blood, 336 Diseases of Red Blood Cells, 337 Anemia, 337 Polycythemia, 342 Treatment of Polycythemias, 342 Diseases of White Blood Cells, 342 Leukemia, 342 Lymphoma, 344 Infectious Mononucleosis, 349 Diseases of Platelets (Bleeding Disorders), 349 Hemophilia, 350 Purpura (Thrombocytopenia), 350 10 Endocrine System, 354 Physiology of the Endocrine System, 354 Adrenal Glands, 355 Physiology of the Adrenal Glands, 355 Diseases of the Adrenal Cortex, 355 Diseases of the Adrenal Medulla, 360 Pituitary Gland, 364 Physiology of the Pituitary Gland, 364 Diseases of the Pituitary Gland, 364 Thyroid Gland, 367 Physiology of the Thyroid Gland, 367 Diseases of the Thyroid Gland, 367 Parathyroid Glands, 374 Physiology of the Parathyroid Glands, 374 Diseases of the Parathyroid Glands, 374 Diabetes Mellitus, 378 11 Reproductive System, 383 Infectious Diseases of Both Genders, 383 Syphilis, 383 Gonorrhea, 385

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CONTENTS Male Reproductive System, 386 Physiology of the Male Reproductive System, 386 Benign Prostatic Hyperplasia, 387 Carcinoma of the Prostate Gland, 388 Staging, 389 Undescended Testis (Cryptorchidism), 390 Testicular Torsion and Epididymitis, 391 Testicular Tumors, 393 Female Reproductive System, 394 Physiology of the Female Reproductive System, 394 Pelvic Inflammatory Disease, 396 Cysts and Tumors, 397 Ovarian Cysts and Tumors, 397 Dermoid Cyst (Teratoma), 400 Uterine Fibroids, 400 Endometrial Carcinoma, 402 Endometriosis, 403 Carcinoma of the Cervix, 404 Breast Lesions, 407 Breast Cancer, 407 Benign Breast Disease, 409

Imaging in Pregnancy, 414 Ectopic Pregnancy, 416 Trophoblastic Disease, 416 Female Infertility, 417 12 Miscellaneous Diseases, 419 Nutritional Diseases, 419 Vitamin Deficiencies, 419 Hypervitaminosis, 421 Protein–Calorie Malnutrition (Kwashiorkor), 422 Obesity, 422 Systemic Lupus Erythematosus, 423 Melanoma, 424 Muscular Dystrophy, 425 Hereditary Diseases, 426 Chromosomal Aberrations, 426 Genetic Amino Acid Disorders, 428 Answers to Review Questions, 432 Illustration Credits, 435 Appendix A: Prefixes/Suffixes/Roots, 439 Appendix B: Laboratory Values and Their Significance, 441 Glossary, 442 Index, 449

1 Introduction to Pathology OUTLINE Disease Inflammation Edema Ischemia and Infarction

Hemorrhage Alterations of Cell Growth Neoplasia Hereditary Diseases

Disorders of Immunity Infectious Disease Exposure Acquired Immunodeficiency Syndrome

epidemiology etiology grading granulation tissue hematogenous spread hematoma hemorrhage hereditary diseases hyperplasia iatrogenic idiopathic immune infarct inflammation ischemia lymphatic spread malignant metastasize morbidity mortality

mutations neoplasia nosocomial oncology permeable personal protective equipment prognosis pyogenic recessive sarcomas signs staging Standard Precautions symptoms syndrome toxoid Transmission-Based Precautions undifferentiated vaccine

KEY TERMS abscess acquired immunodeficiency syndrome (AIDS) active immunity anaphylactic anaplastic antibodies antigens asymptomatic atrophy autosomes bacteremia benign cancers carcinomas community acquired diagnosis dominant dysplasia edema

OBJECTIVES After reading this chapter, the reader will be able to: • Classify the more common diseases in terms of their attenuation of x-rays • Explain the changes in technical factors required for obtaining optimal quality radiographic images in patients with various underlying pathologic conditions • Define and describe all boldface terms in this chapter

• Differentiate inflammation, edema, infarction, hemorrhage, and neoplasia • Characterize the various alterations of cell growth • Describe the various immune reactions of the body • Describe AIDS and the precautions necessary when taking a radiograph of patients with AIDS or any patient with whom contact with any body fluid is possible (Standard Precautions)

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CHAPTER 1  Introduction to Pathology

DISEASE

RADIOGRAPHER NOTES

Pathology is the study of diseases that can cause abnormalities in the structure or function of various organ systems. In essence, a disease is the pattern of the body’s response to some form of injury that causes a deviation from or variation of normal conditions. Diseases may be hereditary or may result from a broad spectrum of traumatic, infectious, vascular, or metabolic processes manifesting as a set of characteristics known as signs and symptoms. Signs represent the measurable or objective manifestations of the disease process. The experiences the patient feels and describes are the symptoms, those (subjective) manifestations that are not measurable or observable. A patient showing no evidence of diseases is considered asymptomatic. Symptoms may reflect alterations of cell growth, as in neoplasia (tumors), or may even be caused by physicians and their treatment (iatrogenic). Imaging modalities are used to assist in making a diagnosis, the precise disease process affecting the patient. To best treat a disease process, it is important to discover its underlying cause, known as the etiology. If the underlying cause is unknown, the disease is termed idiopathic. Once the specific diagnosis and etiology are confirmed, the physician offers a prognosis, which describes the expected patient outcome. A condition characterized by a group of signs, symptoms, and disease processes may be categorized as a syndrome. Incidences of the development of infections at the acute care facility are called nosocomial, whereas infections that develop outside the healthcare facility are known as community acquired. This chapter discusses several basic reactions of the body that characterize the underlying mechanisms for the radiographic manifestations of most pathologic conditions. These processes are inflammation, edema, ischemia and infarction, hemorrhage, and alterations of cell growth leading to the development of neoplasms (tumors). In addition, this chapter deals with hereditary diseases and immune reactions, such as acquired immunodeficiency syndrome (AIDS).

Radiography of patients with underlying pathologic conditions can present problems for even the most experienced radiographers. Adjustments in patient position may be necessary to prevent excessive pain caused by the body’s response to trauma or certain disease processes. A change in routine projections may be indicated to visualize subtle alterations in the normal imaging appearance. Many disease processes also alter the density of the structures being radiographed and therefore require changes in technique. For example, extensive edema may require an increased technique, whereas severe atrophy may require a decreased technique. Unless the radiographer has access to previous images with recorded exposure factors, a standard technique chart should be used to determine the initial exposures. Any necessary adjustments can then be made on subsequent images. Box 1-1 lists the relative attenuation of x-rays that can be expected in advanced stages of various disease processes. In chest radiography, 110 to 125 kilovolts peak (kVp) is optimal; therefore, milliampere-second (mAs) factors should be adjusted to control density. In skeletal radiography, when bone quality changes are expected, the best exposure factor to change is the kilovolt peak (beam quality change for structural change). When bone quantity changes, the milliampere-second (mAs) value is the exposure factor to change to control density (beam quantity increases to ensure that enough radiation reaches the image receptor without changing the contrast). For example, in osteoporosis there is a decrease in bone quantity and quality; however, a decrease in kilovolts produces a higher-quality image. The normal kilovolt peak easily penetrates the diseased bone, producing a low-contrast image with loss of visibility of detail. As imaging progresses into the digital imaging arena, the same theories apply; however, the processing algorithm will control brightness (density) and contrast. The exposure index (number) will represent the over- or underexposure of the image. Certain diseases suppress the normal immune response. Immunocompromised patients (e.g., those with advanced leukemia) may require special care to prevent their acquiring a disease from the radiographer. Personal protective equipment (PPE) aids in preventing the spread of microorganisms to the patient and to the healthcare worker. The patient may have to be placed in protective isolation (or “reverse” isolation), and the radiographer may be required to put on a mask, gown, and gloves before approaching the patient. Diseases such as AIDS and hepatitis require that the radiographer wear rubber or latex gloves to be protected against exposure to blood and body fluids, which could contaminate any area near the patient. When examining a patient with AIDS who has a productive cough, the radiographer must wear a mask and possibly protective eye goggles if there is a need to be very close to the patient’s face. It is important to remember that many patients undergoing radiographic procedures have not been diagnosed, and thus all patients should be treated as though they may have a communicable disease. Therefore, whenever exposure to any type of body secretion or blood may occur, the healthcare worker should wear appropriate PPE.

Summary of Terms for Disease Term

Definition

Signs Symptoms

Measurable or objective manifestations Feelings that the patient describes— subjective manifestations Without subjective or objective manifestations Identification of disease process Study of the cause of the disease process Underlying cause is unknown Probable patient outcome Linked combination of signs and symptoms Disease caused by physician or treatment Infections contracted in the acute care facility Infections contracted in a public setting outside of the acute care facility

Asymptomatic Diagnosis Etiology Idiopathic Prognosis Syndrome Iatrogenic Nosocomial infections Communityacquired infections

CHAPTER 1  Introduction to Pathology

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BOX 1-1  Relative Attenuation of X-Rays in Advanced Stages of Diseases Skeletal System Additive (Increased Attenuation) Acromegaly Acute kyphosis Callus Charcot’s joint Chronic osteomyelitis (healed) Exostosis Hydrocephalus Marble bone Metastasis (osteosclerotic) Osteochondroma Osteoma Paget’s disease Proliferative arthritis Sclerosis Destructive (Decreased Attenuation) Active osteomyelitis Active tuberculosis Aseptic necrosis Atrophy (disease or disuse) Blastomycosis Carcinoma Coccidioidomycosis Degenerative arthritis Ewing’s tumor (in children) Fibrosarcoma Giant cell tumor Gout Hemangioma Hodgkin’s disease Hyperparathyroidism Leprosy Metastasis (osteolytic) Multiple myeloma Neuroblastoma New bone (fibrosis) Osteitis fibrosa cystica Osteoporosis/osteomalacia Radiation necrosis Solitary myeloma

Respiratory System Additive (Increased Attenuation) Actinomycosis Arrested tuberculosis (calcification) Atelectasis Bronchiectasis Edema Empyema Encapsulated abscess Hydropneumothorax Malignancy Miliary tuberculosis Pleural effusion Pneumoconiosis Anthracosis Asbestosis Calcinosis Siderosis Silicosis Pneumonia Syphilis Thoracoplasty Destructive (Decreased Attenuation) Early lung abscess Emphysema Pneumothorax Circulatory System Additive (Increased Attenuation) Aortic aneurysm Ascites Cirrhosis of the liver Enlarged heart Soft Tissue Additive (Increased Attenuation) Edema Destructive (Decreased Attenuation) Emaciation

Even though disease processes increase or decrease the attenuation of the x-rays, it is important to produce a quality image to demonstrate the change in attenuation. Excessive variation of the technical exposure factors may obscure the pathophysiologic changes due to the disease process. From Thompson TT: Cahoon’s formulating x-ray techniques, ed 9, Durham, NC, 1979, Duke University Press.

Inflammation Acute inflammation is the initial response of body tissues to local injury. The various types of injury include those caused by blunt or penetrating trauma, infectious organisms, and irritating chemical substances. Regardless of the underlying cause, the inflammatory response consists of four overlapping events that occur sequentially (Box 1-2). The earliest bodily response to local injury is dilation of arterioles, capillaries, and venules, leading to a dramatic increase in blood flow in and around the injury site. This hyperemia produces the heat and redness associated with

inflammation. As hyperemia develops, the venules and capillaries become abnormally permeable, allowing passage of protein-rich plasma across vessel walls into the interstitium. This inflammatory exudate in the tissues results in the swelling associated with inflammation, which produces pressure on sensitive nerve endings and causes pain. The protein-rich exudate of inflammation must be differentiated from a transudate, a low-protein fluid such as that seen in the pulmonary edema that develops in congestive heart failure. Very early in the inflammatory response, leukocytes (white blood cells, especially neutrophils and macrophages) of the

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CHAPTER 1  Introduction to Pathology

BOX 1-2  Events That Occur in

Inflammatory Response

1. Alterations in blood flow and vascular permeability 2. Migration of circulating white blood cells to the interstitium of the injured tissue 3. Phagocytosis and enzymatic digestion of dead cells and tissue elements 4. Repair of injury by regeneration of normal parenchymal cells or proliferation of granulation tissue and eventual scar formation

circulating blood migrate to the area of injury. These white blood cells cross the capillary walls into the injured tissues, where they engulf and enzymatically digest infecting organisms and cellular debris, a process called phagocytosis. The removal of necrotic debris and any injurious agents, such as bacteria, makes possible the repair of the injury that triggered the inflammatory response. In many tissues, such as the lung after pneumococcal pneumonia, regeneration of parenchymal cells permits reconstitution of normal anatomic structure and function. However, some tissues, such as the heart after myocardial infarction, cannot heal by regeneration. A fibrous scar replaces the area of destroyed tissue with granulation tissue. Granulation tissue refers to a combination of young developing capillaries and actively proliferating fibroblasts, which produce connective tissue fibers (collagen) that replace the dead tissue. Eventually, the strong connective tissue contracts to produce a fibrous scar. In the abdomen, such fibrous adhesions can narrow loops of intestine and result in an obstruction. The accumulation of excessive amounts of collagen (more common in African Americans) may produce a protruding, tumor-like scar known as a keloid. Unfortunately, surgery to remove a keloid is usually ineffective because the subsequent incision tends to heal in the same way. Many injuries heal by a combination of regeneration and scar tissue formation. An example is the response of the liver to repeated and persistent alcoholic injury; the result is cirrhosis, in which irregular lobules of regenerated liver cells are crisscrossed and surrounded by bands of scar tissue. Scar tissue formation consists of fibrous connective tissue, which can be divided into primary union (surgical incision) and secondary union (nonsurgical; gunshot wound). The five clinical signs of acute inflammation are rubor (redness), calor (heat), tumor (swelling), dolor (pain), and loss of function. The localized heat and redness result from increased blood flow in the microcirculation at the site of injury. The swelling occurs because the exudate increases the amount of interstitial fluid, resulting in pressure on nerve endings and thus pain, which results in a loss of function. Acute inflammation can also lead to systemic manifestations. Fever is especially common in inflammatory conditions associated with the spread of organisms into the bloodstream. The number of circulating white blood cells also increases (leukocytosis). Some bacterial organisms (e.g., staphylococci and streptococci) produce toxins that damage the tissues and incite an inflammatory response. The presence of pyogenic bacteria

leads to the production of a thick, yellow fluid called pus, which contains dead white blood cells, inflammatory exudate, and bacteria. A suppurative inflammation is one that is associated with pus formation. When a pyogenic infection occurs beneath the skin or in a solid organ, it produces an abscess, a localized, usually encapsulated, collection of pus. All pyogens, wherever they become implanted, have the ability to invade blood vessels to produce bacteremia, with the potential involvement of other organs and tissues in the body. A granulomatous inflammation manifests as a distinct pattern seen in relatively few diseases, including tuberculosis, syphilis, and sarcoidosis. A granuloma is a localized area of chronic inflammation, often with central necrosis. It is characterized by the accumulation of macrophages, some of which fuse to form multinucleated giant cells.

Summary of Terms for Inflammatory Process Term

Definition

Inflammation

Initial response of the tissue to local injury Allows fluids/cells to pass from one tissue to another tissue or location Fibrous scar replaces destroyed tissue Thick, yellow fluid called pus (dead white cells) Localized, usually encapsulated, collection of fluid Potential involvement of other organs and tissues in the body by organisms invading the blood vessels

Permeable membrane Granulation tissue Pyogenic bacteria Abscess Bacteremia

Edema Edema is the accumulation of abnormal amounts of fluid in the intercellular tissue spaces or body cavities. Localized edema results from an inflammatory reaction, whereas generalized edema occurs with pronounced swelling of subcutaneous tissues throughout the body (anasarca). Localized edema may result from inflammation, with the escape of protein-rich intravascular fluid into the extravascular tissue. It may also result from a local obstruction to lymphatic drainage; for example, in filariasis, a parasitic worm causes lymphatic obstruction, and the resulting localized edema is termed elephantiasis. Generalized edema occurs most frequently in patients with congestive heart failure, cirrhosis of the liver, and certain forms of renal disease. Because of the effect of gravity, generalized edema is usually most prominent in dependent portions of the body. Thus, ambulatory patients tend to accumulate fluid in tissues around the ankles and lower legs, whereas in hospitalized patients who are nonambulatory or sedentary, the edema fluid collects most prominently in the lower back, sacral areas, and lungs.

CHAPTER 1  Introduction to Pathology

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Extravascular fluid can also accumulate in serous cavities to produce pleural and pericardial effusions and peritoneal ascites. Edema may produce minimal clinical symptoms or be potentially fatal. If localized to the subcutaneous tissues, large amounts of edema may cause minimal functional impairment. In contrast, pulmonary edema, pericardial e­ ffusion, or edematous swelling of the brain may have dire consequences.

Summary of Terms for Edema Term

Definition

Edema

Accumulation of abnormal amounts of fluid in the intercellular tissue spaces or body cavities Generalized edema that occurs with pronounced swelling of subcutaneous tissues throughout the body Localized lymphatic obstruction resulting in localized edema

Anasarca

Elephantiasis

A

Ischemia and Infarction Ischemia refers to an interference with the blood supply to an organ or part of an organ, depriving the organ’s cells and tissues of oxygen and nutrients. Ischemia may be caused by a narrowing of arterial structures, as in atherosclerosis, or by thrombotic or embolic occlusion (Figure 1-1). Depending on several factors, occlusion of an artery or vein may have little or no effect on the involved tissue, or it may cause death of the tissue and even of the individual. A major determinant is the availability of an alternative or newly acquired route of blood supply (collateral vessels). Other factors include the rate of development of the occlusion, the vulnerability of the tissue to hypoxia, and the oxygen-carrying capacity of the blood. Slowly developing occlusions are less likely to cause tissue death (necrosis) because they provide an opportunity for the development of alternative pathways of flow. Ganglion cells of the nervous system and myocardial muscle cells undergo irreversible damage if deprived of their blood supply for 3 to 5 minutes. Anemic or cyanotic patients tolerate arterial insufficiency less well than normal individuals do, and thus occlusion of even a small vessel in such a patient may lead to death of tissue. An infarct is a localized area of ischemic necrosis within a tissue or organ produced by occlusion of either its a­ rterial supply or its venous drainage. The two most common clinical forms of infarction are myocardial and pulmonary. Almost all infarcts result from thrombotic or embolic occlusion. Infrequent causes include twisting of an organ (volvulus), compression of the blood supply of a loop of bowel in a hernia sac, or trapping of a viscus under a peritoneal adhesion. In cases in which ischemia continues to progress, resulting in an infarction, necrosis may occur as a result of lack of blood flow. This progressive situation can lead to a condition called gangrene. Severe arterial disease of the lower extremities may result in necrosis of several toes or a large segment of the foot, causing gangrene. A frequent presenting symptom in diabetic patients is ischemia of the foot, which may pro­ gress to infarction and result in gangrene.

B

FIGURE 1-1  Computed tomography (CT) scan of pulmonary embolism. (A) Filling defect in both the right and the left pulmonary arteries (saddle type), and (B) a blockage (filling defect) nearly complete on the right.

Infarctions tend to be especially severe because they occur more often in the patients least able to withstand them. Thus, infarcts tend to occur in elderly individuals with advanced atherosclerosis or impaired cardiac function and are more likely to occur after surgery or delivery.

Hemorrhage The term hemorrhage implies rupture of a blood vessel. Rupture of a large artery or vein is almost always caused by some form of injury, such as trauma, atherosclerosis, or inflammatory or neoplastic erosion of the vessel wall. Hemorrhage may be external, or the blood may be trapped within body tissues, resulting in an accumulation termed a hematoma (Figure 1-2). The accumulation of blood in a body cavity results in hemothorax, hemopericardium, hemoperitoneum, or hemarthrosis (blood in a joint).

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CHAPTER 1  Introduction to Pathology

Alterations of Cell Growth Changes in the number and size of cells, their differentiation, and their arrangement may develop in response to physiologic stimuli. Atrophy refers to a reduction in the size or number of cells in an organ or tissue, with a corresponding decrease in function. It must be distinguished from hypoplasia and aplasia, in which failure of normal development accounts for small size. An example is the disuse atrophy that occurs with immobilization of a limb by a plaster cast. The muscle mass of the encased limb reduces dramatically. Because the cast also removes the stress and strain from the enclosed bone

Summary of Terms for Alterations of Cell Growth Term

Definition

Atrophy

Reduction in the size or number of cells in an organ or tissue, with a corresponding decrease in function Increase in the size of the cells of a tissue or organ in response to a demand for increased function Increase in the number of cells in a tissue or organ Loss of uniformity of individual cells and their architectural orientation Ungoverned abnormal proliferation of cells Study of neoplasms (tumors) Growth that closely resembles the cells of origin in structure and function Neoplastic growth that invades and destroys adjacent structures Malignant neoplasms that travel to distant sites Malignant neoplasm of epithelial cell origin Undifferentiated cell growth—without form (bizarre) Highly malignant tumor originating from connective tissue Major route by which carcinoma metastasizes Malignant tumors that have invaded the circulatory system and travel as neoplastic emboli Assessment of aggressiveness or degree of malignancy (1) Extensiveness of tumor at the primary site (2) Presence or absence of metastases to lymph nodes and distant organs Study of determinants of disease events in given populations Rate that an illness or abnormality occurs Reflects the number of deaths by disease per population

Hypertrophy

FIGURE 1-2  Subdural hematoma. Concave appearance of increased attenuation on the left causing midline shift of the ventricles.

Minimal hemorrhages into the skin, mucous membranes, or serosal surfaces are called petechiae; slightly larger hemorrhages are termed purpura. A large (>1 to 2 cm) subcutaneous hematoma, or bruise, is called an ecchymosis. The significance of hemorrhage depends on the volume of blood loss, the rate of loss, and the site of the hemorrhage. Sudden losses of up to 20% of the blood volume or slow losses of even larger amounts may have little clinical significance. The site of the hemorrhage is critical. For example, an amount of bleeding that would have little clinical significance in the subcutaneous tissues may cause death when located in a vital portion of the brain. Large amounts of external bleeding lead to the chronic loss of iron from the body and anemia. In contrast, internal hemorrhages into body cavities, joints, or tissues permit the iron to be recaptured for the synthesis of hemoglobin and the development of normal red blood cells.

Hyperplasia Dysplasia Neoplasia Oncology Benign Malignant Metastasize Carcinoma Anaplastic Sarcoma Lymphatic spread Hematogenous spread

Summary of Terms for Blood Vessels

Grading

Term

Definition

Staging

Ischemia

Interference of blood supply to an organ; deprives cells and tissues of oxygen and nutrients Localized area of ischemic necrosis; produced by occlusion of either arterial supply or venous drainage Implies rupture of a blood vessel Accumulation of blood trapped within body tissues

Infarct

Hemorrhage Hematoma

Epidemiology Morbidity Mortality

CHAPTER 1  Introduction to Pathology that normally stimulates new bone formation, normal bone resorption continues unchecked and the loss of calcified bone can be detected on radiographs. In this situation, there is rapid recovery from the atrophic appearance when the cast is removed and normal function is resumed. Pathologic, irreversible atrophy may be caused by loss of innervation, by hormonal stimulation, or by decreased blood supply. For example, stenosis of a renal artery may cause atrophy of the kidney with shrinkage of individual nephrons and loss of interstitial tissue. Hypertrophy refers to an increase in the size of the cells of a tissue or organ in response to a demand for increased function. This must be distinguished from hyperplasia, an increase in the number of cells in a tissue or organ (Figure 1-3). Hypertrophy occurs most often in cells that cannot multiply, especially those in myocardial and peripheral striated muscle. Myocardial hypertrophy is necessary to maintain cardiac output despite increased peripheral resistance in patients with arterial hypertension or aortic valve disease. After the loss of a normal kidney, hypertrophy of the other kidney occurs in an attempt to continue adequate renal function. Examples of hyperplasia include: (1) proliferation of granulation tissue in the repair of injury and (2) the increased cellularity of bone marrow in patients with hemolytic anemia or after hemorrhage. Hyperplasia of the adrenal cortex is a response to increased adrenocorticotropic hormone (ACTH) secretion; hyperplasia of the thyroid gland occurs with increased thyrotropic hormone secretion by the pituitary gland. Dysplasia is a loss in the uniformity of individual cells and their architectural orientation; it is typically associated with prolonged chronic irritation or inflammation. Removal of the irritant may result in a return to normal, but often the tissue change persists, and it may evolve into a totally abnormal growth pattern. Thus, dysplasia is generally considered at least potentially premalignant—a borderline lesion that may heal or progress to cancer.

Neoplasia Neoplasia, from the Latin word for “new growth,” refers to an abnormal proliferation of cells that are no longer controlled by the factors that govern the growth of normal cells. Neoplastic cells act as parasites, competing with normal cells and tissues for their metabolic needs. Thus, tumor cells may flourish and the patient becomes weak and emaciated, a condition termed cachexia. Neoplasms are commonly referred to as tumors; indeed, the study of neoplasms is called oncology, derived from the Greek word oncos, meaning “tumor.” Although the word tumor originally referred to any swelling, which could also be produced by edema or hemorrhage in tissue, the word now refers almost exclusively to a neoplasm. Neoplasms are divided into benign and malignant categories on the basis of their potential clinical behavior. Benign tumors closely resemble their cells of origin in structure and function. They remain localized, without spreading to other sites, and thus can usually be surgically removed with resultant survival of the patient.

7

A

B

FIGURE 1-3  Infantile cortical hyperostosis (Caffey’s disease). Affected bones demonstrate cortical thickening with new periosteal bone formation bilaterally on the femurs (A) and tibias (B) (arrows).

Nevertheless, some benign tumors can have severe consequences because of their position or hormonal secretion. For example, a benign pituitary tumor can cause pressure atrophy and destruction of the surrounding gland, and a benign tumor of the islets of Langerhans in the pancreas can produce excessive amounts of insulin, resulting in possibly fatal low levels of blood glucose. Other potentially dangerous benign tumors include those arising in the brain or spinal cord, which may influence central nervous system function. Tumors of the trachea or esophagus may occlude the air supply or make it impossible to swallow. Malignant neoplasms invade and destroy adjacent structures and spread to distant sites (metastasize), causing death. Malignancies tend to be poorly differentiated so that it may be impossible to determine the organ from which they originate. Malignant tumors are collectively referred to as cancers. This term is derived from the Latin word for “crab,” possibly because the finger-like projections that extend into underlying tissue resemble crablike claws. All tumors, both benign and malignant, have two basic components: (1) the parenchyma (organ tissue), made up of proliferating neoplastic cells, and (2) the supporting stroma (supporting tissue), made up of connective tissue,

8

CHAPTER 1  Introduction to Pathology

FIGURE 1-4  Enchondroma. A lobulated area with increased bone density in the supra-acetabular region on the right side (arrow).

blood vessels, and possibly lymphatic vessels. The parenchyma of the neoplasm largely determines its biologic behavior and is the component that determines how the tumor is named. Most benign tumors consist of parenchymal cells that closely resemble the tissue of origin. Their names come from adding the suffix -oma to the cell type from which the tumor arose. For example, benign tumors of fibrous tissue are termed fibromas, whereas benign cartilaginous tumors are chondromas (Figure 1-4). The term adenoma is applied to benign epithelial neoplasms that grow in glandlike patterns. Benign tumors that form large cystic masses are called cystadenomas. Lipomas consist of soft fatty tissue, myomas are tumors of muscle, and angiomas are tumors composed of blood vessels. An epithelial tumor that grows as a projecting mass on the skin or from an inner mucous membrane (e.g., the gastrointestinal tract) is termed a papilloma or a polyp. Malignant neoplasms of epithelial cell origin are called carcinomas, from the Greek word karkinos, meaning “crab.” Carcinomas affect epithelial tissues, skin, and mucous membranes lining body cavities. Adenocarcinoma refers to malignancies of glandular tissues, such as the breast, liver, and pancreas, and of the cells lining the gastrointestinal tract. Squamous cell carcinoma denotes a cancer in which the tumor cells resemble stratified squamous epithelium, as in the lung and head and neck regions. At times, the tumor grows in such a bizarre pattern that it is termed undifferentiated or anaplastic (without form). Sarcomas are highly malignant tumors arising from connective tissues, such as bone, muscle, and cartilage. Although they are less common than carcinomas, sarcomas tend to spread more rapidly. Substantial evidence exists indicating that most tumors arise from a single cell (monoclonal origin). The rate of growth generally correlates inversely with the level of parenchymal differentiation. Thus, well-differentiated tumors tend

to grow slowly, whereas bizarre, undifferentiated neoplasms have a rapid growth rate. Although the cause of cancer is still unknown, many possible causative factors (carcinogens) have been implicated. Chemical carcinogens may cause structural alteration of the deoxyribonucleic acid (DNA) molecule (mutation), which may lead to the development of a neoplasm. Examples of chemical carcinogens include air and water pollution, cigarette smoke, asbestos, and a variety of other substances used in industry, food, cosmetics, and plastics. The development of specific types of cancer in certain families suggests a possible genetic predisposition. Excessive exposure to ultraviolet radiation (sunshine) may lead to the development of skin cancer. Survivors of the atom bomb who received huge doses of radiation have demonstrated a high incidence of leukemia. A greater-than-expected rate of leukemia was also seen in persons working with x-radiation before the need for proper protection was appreciated. The study of experimental animal tumors has offered convincing evidence that DNA and ribonucleic acid (RNA) viruses can induce neoplastic transformation. Viruses that invade normal cells may alter their genetic material, leading to the abnormal cell divisions and rapid growth observed in malignant tumors. The clinical symptoms of cancer vary with the site of malignancy. A blood-tinged stool, a change in bowel activity (e.g., intermittent constipation and diarrhea), or intestinal obstruction is suggestive of gastrointestinal malignancy. Difficulty in swallowing (dysphagia) or loss of appetite (anorexia), especially if accompanied by rapid weight loss, suggests a neoplasm in the esophagus or stomach. Hematuria may indicate kidney or bladder cancer, whereas difficulties in urination (e.g., urgency, a burning sensation, or an inability to start the stream of urine) in an elderly man may be a sign of prostate tumor. Hemoptysis (coughing up blood), a persistent cough, or hoarseness may suggest a neoplasm in the respiratory tract. Severe anemia may develop from internal bleeding or from malfunction of the bone marrow caused by growth of a malignant lesion in the skeleton. It should be stressed that these clinical symptoms may also be caused by benign disease. Nevertheless, because they may signal an underlying malignancy, they should be carefully investigated to exclude the presence of cancer. Pain is frequently not an early sign of cancer. Unfortunately, pain may be appreciated only when the malignancy has spread too extensively to be curable. Secondary infections are common and an increasing cause of death. Most cancer patients are immunologically compromised, either because of their original disease or as a result of irradiation or chemotherapy. In addition to having typical bacterial and viral infections, immunocompromised patients with malignancy are especially susceptible to unusual opportunistic infections, such as Pneumocystis jirovecii (formerly Pneumocystis carinii) pneumonia and cytomegalovirus. Some cancers that are still at a curable stage can be detected by screening procedures. Routine mammography

CHAPTER 1  Introduction to Pathology may identify nonpalpable breast cancer; a Papanicolaou (Pap) smear may show otherwise unsuspected cancer of the cervix. Surgical removal of these small tumors without metastatic spread offers an excellent prognosis. Malignant neoplasms disseminate to distant sites by one of three pathways: (1) seeding within body cavities, (2) lymphatic spread, and (3) hematogenous spread. Seeding (diffuse spread) of cancers occurs when neoplasms invade a natural body cavity. For example, a tumor of the gastrointestinal tract may penetrate the wall of the gut (visceral peritoneum), permitting metastases to enter the peritoneal cavity and implant at distant sites. A similar sequence may occur with lung cancers in the pleural cavity. Neoplasms of the central nervous system (medulloblastoma and ependymoma) may spread from the cerebral ventricles by means of the cerebrospinal fluid to reimplant on the meningeal surfaces within the brain or in the spinal cord. Lymphatic spread is the major metastatic route of carcinomas, especially those of the lung and breast. The pattern of lymph node involvement depends on the site of the primary neoplasm and the natural lymphatic pathways of drainage of that region. Carcinomas of the lung metastasize first to the regional bronchial lymph nodes and then to the tracheobronchial and hilar nodes. Carcinoma of the breast usually arises in the upper outer quadrant and first spreads to the axillary nodes. Medial breast lesions may drain through the chest wall to nodes along the internal mammary artery. The hematogenous spread of cancer is a complex process involving several steps. Tumor cells invade and penetrate blood vessels, traveling as neoplastic emboli in the circulation. These emboli of tumor cells are trapped in small vascular channels of distant organs, where they invade the wall of the arresting vessel and infiltrate and multiply in the adjacent tissue. The localization of hematogenous metastases tends to be determined by the vascular connections and anatomic relationships between the primary neoplasm and the metastatic sites. For example, carcinomas arising in abdominal organs, such as the gastrointestinal tract, tend to metastasize to the liver because of the flow of portal vein blood to that organ. Cancers arising in midline organs close to the vertebral column (e.g., prostate and thyroid) tend to embolize through the paravertebral venous plexus to seed the vertebral column. Neoplasms in organs drained by the inferior and superior vena cava, such as the kidney, tend to metastasize to the lung. However, several well-defined patterns of metastatic spread cannot be easily explained by vascular–anatomic relationships. Some examples are the tendency for carcinoma of the lung to involve the adrenal glands, simultaneous metastatic deposits in the brain and adrenal glands, and pituitary metastases occurring from breast carcinomas. The grading of a malignant tumor assesses aggressiveness, or degree of malignancy. The grade of a tumor usually indicates its biologic behavior and may allow prediction of its responsiveness to certain therapeutic agents. Staging refers to the extensiveness of a tumor at its primary site and

9

the presence or absence of metastases to lymph nodes and distant organs, such as the liver, lungs, and skeleton. The staging of a tumor aids in determining the most appropriate therapy. Well-localized tumors without evidence of metastases may be surgically removed. Fast-growing, undifferentiated tumors, such as those found in patients with Hodgkin’s disease, may respond best to radiation therapy. Cancer of the prostate responds to hormonal therapy, which consists of either the removal of the sources of male gonadal hormones that stimulate tumor growth or the administration of the female gonadal hormone (estrogen) that inhibits it. Chemotherapy uses one or a combination of cytotoxic substances that kill neoplastic cells, but these drugs may injure many normal cells and result in significant complications. Upon determination of the type of neoplastic involvement, a study of determinants is compiled for the specific disease in a given population, which is called epidemiology. Using epidemiology and the grading of the neoplasms then becomes part of establishing morbidity. Morbidity is the rate that an illness or abnormality occurs. Depending on the stage of the tumor, mortality is calculated by reviewing the population involved to statistically calculate the expected death rate. These factors will be taken into consideration when the best course of treatment for the patient is being determined.

HEREDITARY DISEASES Hereditary diseases pass from one generation to the next through the genetic information contained in the nucleus of each cell. They reflect an abnormality in the DNA, which provides the blueprint for protein synthesis in the cell. In many hereditary diseases, an error in a single protein molecule leads to enzyme defects; membrane receptor and transport system defects; alterations in the structure, function, or quantity of nonenzyme proteins; and unusual drug reactions. The most common hereditary abnormality is an enzyme deficiency. This leads to a metabolic block that results either in a decreased amount of a substance needed for normal function or in an accumulation of a metabolic intermediate that may cause injury. An example of the first mechanism is albinism, the absence of pigmentation resulting from an enzymatic deficiency that prevents the synthesis of the pigment melanin. An example of the second mechanism is phenylketonuria, in which the absence of an enzyme leads to the accumulation of toxic levels of the amino acid phenylalanine. A defect in the structure of the globin molecule leads to the development of the hemoglobinopathies, such as sickle cell disease and thalassemia. An example of a genetically determined adverse reaction to drugs is glucose 6-phosphate dehydrogenase deficiency, in which an insufficient amount of the enzyme results in a severe hemolytic anemia in patients receiving a common antimalarial drug. Despite our extensive knowledge of the biochemical basis of many genetic disorders, there are a large number of conditions for which the underlying mechanism is still

10

CHAPTER 1  Introduction to Pathology

unknown. This list includes neurofibromatosis, retinoblastoma, and familial colonic polyposis (see Chapter 5). Each human cell contains 46 chromosomes divided into 23 pairs. The chromosomes in turn contain thousands of genes, each of which is responsible for the synthesis of a single protein. Forty-four of the chromosomes are called autosomes; the other two are the X and Y chromosomes, which determine the sex of the person. A combination of XY chromosomes results in a male, whereas an XX configuration results in a female. Each person inherits half of his or her chromosomes from each parent. If the genes inherited from each parent are the same for a particular trait, the person is homozygous for that trait. If the genes differ (e.g., one for brown eyes and one for blue eyes), the person is heterozygous for that trait. Dominant genes always produce an effect regardless of whether the person is homozygous or heterozygous; recessive genes manifest themselves only when the person is homozygous for the trait. In determining eye color, brown is dominant, whereas blue is recessive. It must be remembered that although a recessive trait must have been contributed by both parents, the possibility exists that neither parent demonstrates that trait. For example, two parents, each with one gene for brown eyes and one gene for blue eyes, would show the dominant brown coloration, although they could each contribute a blue-eye gene to their offspring, who would manifest the recessive blue-eye trait. For some traits, the genes are codominant so that both are expressed. An example is the AB blood type, in which the gene for factor A is inherited from one parent and that for factor B is inherited from the other. Mutations are alterations in the DNA structure that may become permanent hereditary changes if they affect the gonadal cells. Mutations may result from radiation, chemicals, or viruses. They may have minimal effect and be virtually undetectable or may be so serious that they are incompatible with life, causing the death of a fetus and spontaneous abortion. Autosomal dominant disorders are transmitted from one generation to the next. These disorders affect females and males, and both can transmit the condition. When an affected person marries an unaffected person, half the children (on average) will have the disease. The clinical manifestations of autosomal dominant disorders can be modified by reduced penetrance and variable expressivity. Reduced penetrance means that not everyone who has the gene will demonstrate the trait; variable expressivity refers to the fact that a dominant gene may manifest somewhat differently in different individuals (Figure 1-5) (e.g., polydactyly may be expressed in the toes or in the fingers as one or more extra digits). Examples of autosomal dominant disorders include achondroplasia (see Chapter 4), neurofibromatosis, Marfan’s syndrome (see Chapter 12), and familial hypercholesterolemia. Autosomal recessive disorders result only when a person is homozygous for the defective gene. The trait does not usually affect the parents, although siblings may show the disease. On

FIGURE 1-5  Polydactyly. Right foot image with seven metatarsals and eight digits.

average, siblings have a one-in-four chance of being affected; two out of four will be carriers of the gene, and one will be normal. Recessive genes appear more frequently in a family, and close intermarriage (as between first cousins) increases the risk of the particular disease. Unlike in autosomal dominant diseases, the expression of the defect tends to be uniform in autosomal recessive diseases and the age of onset is frequently early in life. Examples of autosomal recessive disorders are phenylketonuria (see Chapter 12), cystic fibrosis (see Chapter 3), galactosemia, glycogen and lipid storage diseases (see Chapter 12), Tay–Sachs disease, and sickle cell anemia (see Chapter 9). Sex-linked disorders generally result from defective genes on the X chromosome because the Y chromosome is small and carries very few genes. Most of these conditions are transmitted by heterozygous female carriers virtually only to sons, who have only the single, affected X chromosome. Sons of a heterozygous woman have a one-in-two chance of receiving the mutant gene. An affected man does not transmit the disorder to his sons, but all his daughters carry the genetic trait. In rare cases, a female may have the sex-linked disease if she is homozygous for the recessive gene. Virtually all sex-linked disorders are recessive. The most common example of a sexlinked disorder is color blindness. Other conditions are glucose 6-phosphate dehydrogenase deficiency and some types of hemophilia (see Chapter 9) and muscular dystrophy (see Chapter 12).

CHAPTER 1  Introduction to Pathology Summary of Terms for Hereditary Diseases Term

Definition

Hereditary process

Genetic information contained in the nucleus of each cell passed to the next generation 44 chromosomes other than X and Y Always produces an effect Manifests when a person is homozygous for the trait Alteration in the DNA structures that may become permanent hereditary change

Autosomes Dominant gene Recessive gene Mutation

DISORDERS OF IMMUNITY The immune reaction of the body provides a powerful defense against invading organisms by allowing it to recognize foreign substances (antigens), such as bacteria, viruses, fungi, and toxins, and to produce antibodies to counteract them. The antibody binds together with the antigen to make the antigen harmless. Once antibodies have been produced, a person becomes immune to the antigen. Antibodies, or immunoglobulins, form in lymphoid tissue, primarily in the lymph nodes, thymus gland, and spleen. Although an infant has some immunity at birth, most immunity is acquired either naturally by exposure to a disease or artificially by immunization. There are two types of artificial immunity: active and passive. In active immunity, a person forms antibodies to counteract an antigen in the form of a vaccine or a toxoid. A vaccine consists of a low dose of dead or deactivated bacteria or viruses. Although these organisms cannot cause disease, they are foreign proteins containing antigens that stimulate the body to produce antibodies against them. A toxoid is a chemically altered toxin, the poisonous material produced by a pathogenic organism. As with a vaccine, the toxin cannot cause disease but does trigger the development of antibodies. Examples of active immunity are the vaccines given to prevent smallpox, polio, measles, tetanus, and diphtheria. Active immunity persists for a long time, although a relatively long time is required to build up immunity, and a booster shot frequently gives a stronger effect. Passive immunity refers to the administration of a dose of preformed antibodies from the immune serum of an animal, usually a horse. This type of immunity acts immediately but lasts for a relatively short time. It is used in situations in which a person is exposed to a serious disease (hepatitis, rabies, and tetanus) but has no immunity against it and thus requires an immediate supply of antibodies to prevent a possibly fatal infection. Several fundamental mechanisms of immunologic responses to antigens exist. The first type is a rapidly occurring reaction in which antigens are attacked by antibodies previously bound to the surface of mast cells. The

11

mast cells release histamine, which causes a local increase in vascular permeability and smooth muscle contraction. Disorders resulting from localized reactions of this type (which probably have a genetically determined predisposition) include hay fever, asthma, and gastrointestinal allergies. Generalized, or systemic, anaphylactic reactions are characterized by hypotension and vascular collapse (shock) with urticaria (hives), bronchiolar spasm, and laryngeal edema. This reaction causes sudden death in patients who are hypersensitive (“allergic”) to the sting of bees, wasps, and other insects and to medications, such as penicillin and the iodinated contrast materials used in radiology. In the second type of immune reaction, called a cytotoxic reaction, either the antigen is a component of a cell or it attaches to the wall of red blood cells, white blood cells, platelets, or vascular endothelial cells. The reaction with an antibody leads to cell destruction by lysis or phagocytosis. Examples of a cytotoxic immune reaction include the transfusion reaction occurring after the administration of ABO-incompatible blood, and erythroblastosis fetalis, the hemolytic anemia of the Rh-positive newborn whose Rh-negative mother has produced anti-Rh antibodies. The third type of immune reaction, a delayed reaction, occurs in an individual previously sensitized to an antigen. As an example, the first time a person touches poison ivy, no reaction occurs. However, on the next exposure to poison ivy, antibodies are present to attack the antigen, and the patient develops the typical rash and irritation. A similar process produces a reaction to tuberculosis, leprosy, many fungal diseases, and other infections. This process also represents the principal component of rejection in organ transplants.

INFECTIOUS DISEASE EXPOSURE Working in the healthcare environment means that exposure to infectious microorganisms will occur. To minimize exposure, all healthcare workers should follow the Centers for Disease Control and Prevention’s (CDC) Standard Precautions. Exposure to blood-borne pathogens such as human immunodeficiency virus (HIV) and hepatitis B virus (HBV) can be minimized for all persons involved with the use of the appropriate personal protective equipment (PPE). The CDC recommends that all such persons be considered potentially infected and that Standard Precautions be applied when they are delivering health services to every patient. In cases of highly transmissible pathogens, additional precautions are necessary; Transmission-Based Precautions should be used for persons with pathogens transmissible by contact, droplet, or through air (airborne). Each healthcare facility is responsible for administering the precautions; educating, training, and monitoring its employees; and providing a protective environment. Every healthcare worker must take personal responsibility to help contain the infectious process in the work environment by following CDC standards.

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CHAPTER 1  Introduction to Pathology

Summary of Terms for Immunity Disorders Term

Definition

Antigens

Foreign substance that evokes an immune response Immunoglobulins responding to the antigens to make them harmless Protected against antigens; antibodies binding with antigens to make them harmless Forming antibodies to counteract an antigen by way of vaccine or toxoid Contact with dead or deactivated microorganisms to form antibodies Treated toxin with antigenic power to produce immunity by creating antibodies Hypersensitive reaction resulting in a histamine release Protection used when delivering healthcare services to any person PPE—gowns, gloves, masks, shoe covers, and eye protection used to prevent transmission of potential infectious agents Additional protective equipment to prevent the spread of highly infectious pathogens through contact, droplet, or airborne transmission

Antibodies Immune

Active immunity

Vaccine

Toxoid

Anaphylactic reaction Standard Precautions Personal protective equipment

TransmissionBased Precautions

ACQUIRED IMMUNODEFICIENCY SYNDROME Acquired immunodeficiency syndrome (AIDS), which most commonly affects young homosexual men and intravenous drug abusers, is characterized by a profound and sustained impairment of cellular immunity that results in recurrent or sequential opportunistic infections and a particularly aggressive form of Kaposi’s sarcoma. AIDS has also been reported in a substantial number of hemophiliac patients, in recipients of transfusions, and increasingly in heterosexual partners of affected individuals. AIDS is attributable to infection with retroviruses (RNA viruses) known as human immunodeficiency viruses (HIV). This immune deficiency predominantly involves the lungs, gastrointestinal tract, and central nervous system. Pulmonary infections are extremely common in patients with AIDS and are frequently caused by organisms that only rarely produce disease in individuals with normal immune systems. Approximately 60% of AIDS victims experience one or more attacks of P. jirovecii pneumonia, which is characterized by a sudden onset, a rapid progression to diffuse lung involvement, and a considerable delay in resolution. The fungus cannot be cultured, and the disease is usually fatal if untreated. An open-lung biopsy is often necessary to make the diagnosis if a sputum examination reveals no organisms in a patient in whom this disease is suspected.

FIGURE 1-6  Kaposi’s sarcoma. Small bowel study shows multiple intramural nodules (predominantly involving the jejunum) that distort the mucosal pattern and produce contour defects and intraluminal lucencies.

Gastrointestinal manifestations of AIDS include a variety of sexually transmitted diseases involving the rectum and colon, infectious processes (e.g., shigellosis, amebiasis, candidiasis, and giardiasis), and alimentary tract dissemination (spread) of Kaposi’s sarcoma. Kaposi’s sarcoma, a systemic disease, characteristically affects the skin and causes an ulcerated hemorrhagic dermatitis. Metastases to the small bowel, which are relatively common, consist of multiple reddish or bluish red nodules that intrude into the lumen of the bowel (Figure 1-6). Similar lesions can develop throughout the gastrointestinal tract. Central ulceration of the metastases causes gastrointestinal bleeding and a characteristic radiographic appearance of multiple “bull’s-eye” lesions simulating metastatic melanoma. Approximately 40% of all AIDS victims have neurologic symptoms, most commonly progressive dementia. Patients with mass lesions of the brain commonly have focal neurologic symptoms and signs. Imaging appearance. The typical early radiographic finding of P. jirovecii pneumonia is a hazy, perihilar, granular infiltrate that spreads to the periphery and appears predominantly interstitial. In later stages, the pattern progresses to patchy areas of air-space consolidation with air bronchograms, indicating the alveolar nature of the process (Figure 1-7). The radiographic appearance may closely resemble that of pulmonary edema or bacterial pneumonia. Magnetic resonance imaging (MRI) best demonstrates the multiple manifestations of AIDS in the central nervous system, where areas of increased signal intensity can be seen on T2-weighted images. Atypical brain abscesses and meningeal infection often occur, most commonly related to toxoplasmosis, cryptococcosis, cytomegalovirus, and herpesvirus

13

CHAPTER 1  Introduction to Pathology

(Figure 1-8). Increasing evidence indicates that cerebral infections may manifest from the HIV itself. Patients with AIDS also have a high incidence of lymphoma involving the central nervous system. Treatment. Although much research has been initiated, no cure for AIDS has been found. Currently, treatment assists in maintaining quality of life and managing symptoms as they manifest. Antiviral drugs help suppress the HIV infection. A healthy lifestyle free of stress, alcohol, and illegal drugs is recommended. An HIV carrier should avoid infections if possible because they may accelerate the HIV process.

FIGURE 1-7  Pneumocystis jirovecii pneumonia. Diffuse bilateral air-space consolidation is suggestive of severe bacterial pneumonia or pulmonary edema.

A

B

FIGURE 1-8  Neurologic manifestations of AIDS. (A) Computed tomography (CT) scan shows multiple ring-enhancing lesions caused by cryptococcal brain abscesses. (B) MRI, after intravenous administration of contrast medium, demonstrates multiple enhancing abscesses caused by toxoplasmosis.

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CHAPTER 1  Introduction to Pathology

  REVIEW QUESTIONS 1. The accumulation of abnormal amounts of fluid in the spaces between cells or in body cavities is termed _________________. 2. _________________ is the process by which white blood cells surround and digest infectious organisms. 3. A tumor-like scar is referred to as a(n) _______________. 4. Inflammation with pus formation is termed _________________. 5. An interruption in the blood supply to an organ or body part is referred to as _________________. 6. A localized area of ischemic necrosis in an organ or tissue is termed a(n) _________________. 7. A swelling caused by bleeding into an enclosed area is termed _________________. 8. A decrease in function of an organ or tissue because of a reduction in the size or number of cells is termed _________________. 9. The term _________________ means new growth. 10. The term for benign epithelial neoplasms that have a glandlike pattern is _________________. 11. The study of determinants of disease events in given populations is _________________.

12. Statistically, _________________ reflects the number of deaths by disease per population. 13. The rate that an illness or abnormality occurs is called _________________. 14. Gowns, gloves, masks, shoe covers, and eye protection used to prevent transmission of potential infectious agents are _________________. 15. _________________ determines the additional protective equipment needed to prevent the spread of highly infectious pathogens through contact, droplet, or airborne transmission. 16. The cause of the disease process is called _________________. 17. A(n) _________________ is the combination of signs and symptoms used to determine the disease process. 18. When a combination of signs, symptoms, and disease processes are linked, it is known as a(n)_________________. 19. _________________ is when a patient does not show any evidence of disease. 20. The expected outcome of a disease process is _________________.

2 Specialized Imaging Techniques OUTLINE Diagnostic Imaging Modalities Imaging Features Mammography Ultrasound Computed Tomography

Magnetic Resonance Imaging Nuclear Medicine Single-Photon Emission Computed Tomography Positron Emission Tomography

Fusion Imaging

KEY TERMS anechoic annihilation collimator computed tomography (CT) CT number diffusion imaging direct fusion fat suppression functional MRI (fMRI) gamma camera helical

hyperechoic hypoechoic imaging features integrated imaging isoechoic magnetic resonance imaging (MRI) mammography nuclear medicine perfusion imaging positron emission tomography (PET)

radiofrequency (RF) pulse radiopharmaceutical single-photon emission computed tomography (SPECT) T1-weighted images T2-weighted images ultrasound virtual reality volume-rendered imaging

OBJECTIVES After reading this chapter, the reader will be able to: • Define the imaging features most commonly used by radiologists to indicate pathophysiology changes • Differentiate screening and diagnostic mammography imaging protocols and how the protocols are used to demonstrate pathology • Describe the theory of image production with ultrasound and why this modality becomes the optimal choice to demonstrate pathologic conditions • Describe the theory of image production with computed tomography (CT) and the body structures best demonstrated

• Briefly describe the theory of image production with magnetic resonance imaging (MRI) and the different sequences used to demonstrate specific tissue • Describe the theory of image production with nuclear medicine, single-photon emission computed tomography (SPECT), and positron emission tomography (PET) • Identify the fusion imaging techniques required to produce optimal quality images in patients with various underlying pathologic conditions • Define and describe all boldface terms in this chapter

DIAGNOSTIC IMAGING MODALITIES As the world of technology advances, medical imaging modalities have become more technical. This change requires the radiographer to have a broader and more specific skill set to produce quality images. An example of this trend in diagnostic imaging is the expansion of the department with the development of specific x-ray tubes to produce high-quality mammographic images of the breast.

The first of these new modalities was ultrasound, which was capable of producing images without the use of ionizing radiation, providing a diagnostic tool to view soft tissues, especially in the fetus. In the early to mid-1970s, computed axial tomography (now known as CT) provided revolutionary new images of the brain that demonstrated the bone structure, white and gray matter, and the fluid-filled ventricles. Eventually, CT eliminated the need for pneumoencephalography and replaced many cerebral angiograms. Scientists integrated

15

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CHAPTER 2  Specialized Imaging Techniques

the use of strong magnets and radiofrequencies to provide another mode of producing images without the use of ionizing ­radiation—nuclear magnetic resonance (now known as magnetic resonance imaging). MRI offers clinicians images with high soft tissue resolution and the ability to visualize structural and functional tissue. CT and MRI now provide diagnosticians with three-dimensional (3D) (axial, sagittal, and coronal) images and offer a way to separate overlapping anatomic structures. With continuing research, nuclear medicine expanded its role by adding movement and a computer that allowed more than anterior and posterior projections, resulting in the development of single-­photon emission computed tomography. Additional research developments in radiopharmaceuticals led to the creation of a positron-emitting radionuclide, which resulted in the newest modality—positron emission tomography. Now the concept of multiplanar imaging and gamma camera movement (tomography) has provided healthcare with two new perspectives in molecular imaging. Computerized technology has become prevalent in imaging today. Imaging modalities with special software can now be integrated to create a fused image (superimposition of images from two different modalities). PET/CT is the most prominent hybrid equipment available today. As computed technology continues to become more complex, the modalities of today’s imaging department will also become more complicated. However, these positive changes result in images that are more precise and have greater sensitivity. This offers the radiologist opportunity to make a quicker, more accurate diagnosis for the patient.

Imaging Features When radiologists interpret images, they use a common terminology called imaging features, imaging descriptors that the technologist should become familiar with to better understand the pathophysiologic changes reflected in the diagnostic image. Common features or descriptors include location, size, density, structure, shape, demarcation, perfusion, and integration. The location descriptor indicates the site where the changes in the anatomic features are evident, whereas the size descriptor refers to the measurements of those changes on the image. The tissue density and structure describe the abnormal appearance in comparison with what is expected as normal. Shape and border (demarcation) describe anatomic structure changes and involvement. Perfusion of abnormal tissue relates to its degree of vascularity, which may be of value in distinguishing between cystic and solid-tissue lesions. Depending on the type of pathologic process, the tissue changes may be described as being space-occupying or integrated in the anatomic structure. Imaging features and descriptors are essentially a common language used by radiologists in interpreting images and conveying this information to referring physicians reviewing them. Each specific diagnostic modality utilizes a series of imaging descriptors that may have to be modified for it.

Summary of Imaging Descriptors Term

Definition

Where

RADIOGRAPHER NOTES A medical radiographer is one of the patient’s healthcare team, providing care, diagnosis, and treatment, especially in the diagnostic imaging department. The role of the radiographer as a team member is to produce the best quality images for diagnosis. Not only radiologists and physicians view the images; technologists using other imaging modalities—such as mammography, ultrasound, CT, MRI, nuclear medicine, SPECT, and PET—view these images as a basis for producing studies in their respective modalities. For the healthcare team, communication is especially important. To communicate effectively, the radiographer may need to gather information from the patient (patient history). Once the added information is recorded, the technologist may confer with the radiologist to ensure that the correct examination has been ordered. In some cases, even though the examination is correct, it also would be beneficial if further history were gathered or additional image projections were taken to provide supplementary information. The better radiographers understand their role in imaging, the more adept they will be at producing the correct images for the specific pathophysiologic condition of the patient. To best demonstrate the pathology, all imaging technologists must do their part to provide added information. The imaging team is responsible for providing the best images to complement one another. The collection of images from all modalities aids the diagnostician in making the most accurate diagnosis.

Location, lateralization, relative position to organs and vessels Size Diameter or width and length (millimeters or centimeters) Density Relative to surrounding tissue (isodense, hyperdense, or hypodense; radiolucent or radiopaque) Structure Heterogeneous (septate) or homogeneous (fluids) Shape Tubular (vessels or muscles) Nodular (tumor or lymph nodes) Reticular (resembling a net) Striate or diffuse (streaked or widely spread) Demarcation Sharply marginated (more likely benign) Indistinctly marginated (infiltration into surrounding tissue—inflammation or malignancy) Perfusion Peripheral, homogeneous, or heterogeneous enhancement Integration Space-occupying effect

Mammography Most modern imaging departments have a separate area where breast imaging procedures are performed. The most common imaging technique for diagnosing breast cancer is full-field digital mammography (FFDM). Some centers still use the conventional screen-film imaging, which employs a specially designed x-ray screen that permits the proper exposure of film by many

17

CHAPTER 2  Specialized Imaging Techniques fewer x-rays than would otherwise be necessary. This procedure produces a conventional black-and-white image at a very low radiation dose. Full-field digital mammography relies on radiation captured by multiple cells that convert the radiation energy to electrical energy to produce a numerical value (i.e., a digitized image). The advantages of digital mammography are faster image acquisition with lower dose (shorter exposure), increased contrast resolution with the ability to manipulate images to visualize specific areas of interest, decreased need to repeat studies, and the ease of sharing images with other professionals. Screening mammography consists of two images of each breast, the craniocaudal and mediolateral oblique projections. For a woman with a palpable nodule, the first choice may be a diagnostic mammogram, which includes an additional 90-degree mediolateral projection. When screening mammography demonstrates a suspicious area or a definite abnormality, additional images, such as coned-down or magnification projections, can be completed to compliment the study. In some cases, ultrasound supplements mammography images by demonstrating the lesion to be fluid filled (cystic) or solid.

different amounts depending on the acoustic properties of the tissues through which they travel. The crystal mounted in a transducer sends the signal and also acts as a receiver to record echoes reflected back from the body whenever the sound wave strikes an interface between two tissues that have different acoustic properties. The transducer records the tiny changes of the signal’s pitch and direction. A water-tissue interface can produce strong reflections (echoes), whereas a solid tissue mass that contains small differences in composition can cause weak reflections. The display of the ultrasound image on an imaging monitor shows both the intensity level of the echoes and the position in the body from which they were scanned. Ultrasound images may be displayed as static grayscale images or as multiple (video) images that permit movement to be viewed in real time. Color display on a sonogram is used to detect motion (specifically, blood flow). Depending on the equipment used, the interactions of the tissue with the sound wave determine how the tissue or organ is visualized and described. In general, fluid-filled structures have intense echoes at their borders, no internal echoes, and good transmission of the sound waves. Anechoic tissue or structures (which are echo free, or lacking a signal) transmit sound waves easily and appear as the dark region on the image; examples are the gallbladder and a distended urinary bladder. Solid structures (e.g., liver and spleen) produce internal echoes of variable intensity. The terms hyperechoic and hypoechoic are used to make comparisons of echo intensities between adjacent structures. For example, the normal liver can be described as being hyperechoic to the normal renal cortex because the hepatic parenchymal tissue appears as a lighter shade of gray. Conversely, because the normal renal cortex appears as a darker shade of gray than the normal liver parenchyma, it can be described as being hypoechoic to the liver. The term isoechoic is used to describe two structures that have the same echogenicity even though the tissue may not be the same; for example, liver tissue is often isoechoic to the spleen. Complex tissue types have both anechoic and echogenic areas (Figure 2-2).

Summary of Imaging for Mammography—Anatomic Imaging Image creation Image receptor Imaging descriptors

Ionizing radiation—x-ray attenuation of breast tissue Digital plate or analog system Same as used for general x-ray

Ultrasound Ultrasound (also called ultrasonography) is a widely accepted cross-sectional imaging technique because of its low cost, availability, and ability to differentiate cystic (gallbladder), solid (liver), and complex (liver tumor) tissue. A noninvasive imaging modality, ultrasound uses high-­frequency sound waves produced by electrical stimulation of a specialized crystal (Figure 2-1). When the high-frequency sound waves pass through the body, their intensity is reduced by

A

GB h CBD V

FIGURE 2-1  Ultrasound images of normal abdomens. (A) Right atrium of the heart (RA), the inferior vena cava (marked for measurement), and the hepatic vein joining the inferior vena cava. (B) Gallbladder (GB), common bile duct (CBD), portal vein (P), hepatic vein (h), and inferior vena cava (V).

P

B

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CHAPTER 2  Specialized Imaging Techniques

A A

B

FIGURE 2-3  Sonogram of the abdomen of a woman with a multiple pregnancy. Cranial architecture is normal in fetus A and abnormal in fetus B, a finding that documented demise of fetus B (and also fetus C, which is not imaged). B

FIGURE 2-2  Ultrasound images of the abdomen. (A) Transverse right kidney demonstrates a hyperechoic area (white) within the mass caused by renal cell carcinoma. (B) Gallbladder (GB) and aorta (AO) are hypoechoic compared with the pancreas. Focal masses (arrows) are isoechoic (i.e., similar in density) to the adjacent pancreatic tissue.

The major advantage of ultrasound is its safety. There has been no evidence of any adverse effect on human tissues at the intensity level currently used for diagnostic procedures. Therefore, ultrasound is the modality of choice for examinations of children and pregnant women in whom a potential danger exists from the radiation exposure involved with other imaging studies. Ultrasound is by far the best technique for evaluating fetal age and placenta placement, congenital anomalies, and complications of pregnancy (Figure 2-3). Abdominal ultrasound is used extensively to evaluate the intraperitoneal and retroperitoneal structures, to detect abdominal and pelvic abscesses, and to diagnose obstruction of the biliary and urinary tracts. Pelvic ultrasound images of the prostate gland aid in the detection and accurate staging of neoplasms. Pelvic imaging is performed via a transabdominal (through the abdominal wall), transvaginal (through the vagina), or transrectal (through the rectum) approach. Vascular or color-flow Doppler studies assess the patency of major blood vessels, demonstrating obstructions (stenoses), blood clots, plaques, and emboli. The color-flow duplex system, in which conventional real-time imaging is

C

FIGURE 2-4  Ultrasound image of a focal area of breast tissue. The sonogram shows an anechoic mass (C) with a well-defined back wall and distal enhancement (arrows).

integrated with Doppler imaging (to produce quantitative data) and with color, depicts motion and the direction and velocity of blood flow. The color and intensity represent the direction of flow and the velocity, respectively (e.g., in the carotid artery). Other uses of ultrasound include breast imaging (to differentiate solid from cystic masses) (Figure 2-4), musculoskeletal imaging (to detect problems with tendons, muscles, and joints and also soft tissue fluid collections or masses) (Figure 2-5), and as an imaging guide for invasive procedures (biopsies, aspirations, and drain placement) (Figure 2-6). Ultrasound is a quick, inexpensive procedure for evaluating postoperative complications, although it may be difficult to perform in some patients because of overlying dressings, retention sutures, drains, and open wounds,

19

CHAPTER 2  Specialized Imaging Techniques

A

FIGURE 2-5  Ultrasound image of a wrist demonstrating the musculoskeletal architecture. A cystic structure (15 × 5 mm) can be seen near the dorsal aspect of base of the fourth and fifth metacarpals.

which may prevent the transducer from being in direct contact with the skin. In children with open fontanelles, ultrasound can image the intracranial structures. High-­ resolution, real-time ultrasound systems can assist surgeons during operative procedures. This technique has been applied to the neurosurgical localization of brain and spine neoplasms, to the evaluation of intraventricular shunt tube placement, to the localization of renal calculi, and to surgical procedures involving the hepatobiliary system and pancreas. The role of ultrasound imaging has expanded as a result of the availability of multifrequency transducers (2–15 MHz) and advances in software (signal-processing) technology. The resultant higher-resolution images are used in musculoskeletal, breast, and small-parts imaging. The latest technologies include harmonic imaging (which involves a broad band of low frequencies and can suppress reflection from surrounding tissue) to reduce image noise and artifact, real-time compound imaging (a combination of multiple lines of sight that increases image clarity and provides more diagnostic information), and contrast agents (microbubble echo-enhancing agents) that increase vasculature definition. Harmonic imaging produces diminished noise images, increasing the resolution in a hypersthenic patient so that patient size does not prevent obtaining diagnostic images. Contrast agents, injectable low-solubility gas bubbles (3 cm CTA—aneurysm extent and size, evidence of leak or rupture by retroperitoneal hematoma MRA—same as CTA, but used when iodinated contrast agents are contraindicated PA chest—widened mediastinum; deviation of NG tube to right; apical pleural cap CTA/aortography—demonstrates tear and hemorrhage PA chest—widening of aortic shadow, which may be irregular CT—double-barrel channel with linear filling defect within lumen (intimal flap) MRI—intimal flap causes medium-intensity signal separating true and false lumina; blood flow causes signal void TEE—demonstrates intimal tear, extension of dissection and pleural effusion Aortography—extent of true and false lumina Radiograph—calcification demonstrating “hardening” of the artery Color Doppler—demonstrates plaque and degree of luminal stenosis MRA—two-dimensional time-of-flight view demonstrates narrowing and flow changes in infrapopliteal vessels; 3D images demonstrate narrow occlusions as signal absences Arteriography—extent of occlusion, degree of collateral circulation, and distal vessel condition

Diuretics Digoxin

Treatment of cause of edema

Surgical repair Proximal or continuous dissection— immediate surgical repair Intervention—fenestration and stenting Other dissections—medical management PTA with or without stent placement Surgical arterial bypass

Interventional catheter removal Surgical removal Medical treatment to reduce thrombus or emboli

IVUS, Intravascular ultrasound; NG, nasogastric; NM, nuclear medicine; PTCA, percutaneous transluminal coronary angioplasty; SPECT, single-photon emission computed topography; US, ultrasound.

CHAPTER 7  Cardiovascular System

Disorder Coronary artery disease

274

Summary of Findings for Acquired Vascular Disease

CHAPTER 7  Cardiovascular System

VALVULAR DISEASE The valves of the heart permit blood to flow in only one direction through the heart. There are four heart valves. As previously described, the tricuspid valve separates the right atrium and the right ventricle, and the mitral valve separates the left atrium and the left ventricle. These two atrioventricular valves must open for the heart chambers to fill. The pulmonary valve lies between the right ventricle and the pulmonary artery, and the aortic valve is situated between the left ventricle and the aorta. When any of these valves is closed, the heart chamber fills with blood; when the valve opens, blood can move forward and leave the chamber. The malfunction of a heart valve alters the normal blood flow through the heart. Too small an opening (stenosis) does not permit sufficient blood flow. In contrast, too large an opening or failure of the valve to properly close permits backflow of blood (regurgitation) and the condition of valvular insufficiency. Both stenosis and insufficiency of valves cause heart murmurs with characteristic sounds that indicate the nature of the defect. Two-dimensional and Doppler echocardiography have become the modalities of choice to demonstrate valvular diseases. Although valvular heart disease once invariably forced a patient to restrict activity and was associated with a limited life span, surgical reconstruction or replacement of a diseased valve (Figure 7-48) can offer a patient the prospect of a normal life.

Rheumatic Heart Disease Rheumatic fever is an autoimmune disease that results from a reaction of the patient’s antibodies against antigens from

275

a previous streptococcal infection. The disease is much less common today because of the frequent use of antibiotics to treat streptococcal throat or ear infections. The symptoms of rheumatic fever (fever, inflamed and painful joints, and rash) typically develop several weeks after the streptococcal infection. The major damage of rheumatic fever is to the valves of the heart, most frequently the mitral and aortic valves. Indeed, it is the major cause of acquired cardiac valvular disease. The allergic response causes inflammation of the valves. Deposits of blood platelets and fibrin from blood flowing over the valve produce small nodules (vegetations) along the margin of the valve cusps. The thickened valves may stick together so that the valvular opening remains permanently narrowed (stenosis) rather than opening properly when blood flows through. In contrast, fibrous scarring may cause retraction of the valve cusps so that the cusps are unable to meet when the valve tries to close; this is insufficiency, and blood leaks through the valve when it should be closed. Doppler echocardiography is used to best identify and quantify the insufficiencies and determine the degree of ventricular dysfunction. Treatment. Prevention of rheumatic fever and subsequent heart disease by treatment of the streptococcal infection with a full course of antibiotic therapy is the best approach. If the infection progresses into rheumatic heart disease, antibiotics, anti-inflammatory drugs, and restricted activity are the appropriate interventions.

Mitral Stenosis Stenosis of the mitral valve, almost always a complication of rheumatic disease, results from diffuse thickening of the valve by fibrous tissue, calcific deposits, or both.

A

B

FIGURE 7-48  Prosthetic aortic and mitral valves. Frontal (A) and lateral (B) projections of the chest show an anteromedially located prosthetic aortic valve (A) and a posterolaterally situated prosthetic mitral valve (M).

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CHAPTER 7  Cardiovascular System

Imaging appearance. The obstruction of blood flow from the left atrium into the left ventricle during diastole causes increased pressure in the left atrium and enlargement of this chamber (Figure 7-49). The enlarged left atrium produces a characteristic anterior impression on and posterior displacement of the barium-filled esophagus that is best seen on lateral and right anterior oblique projections. Other radiographic signs of left atrial enlargement include posterior displacement of the left mainstem bronchus, widening of the tracheal bifurcation (carina), and a characteristic “double-contour” configuration caused by the projection of the enlarged left atrium through the normal right atrial silhouette. The increased left atrial pressure is transmitted to the pulmonary veins and produces the appearance of chronic venous congestion. Calcification of the mitral valve or left atrial wall (Figure 7-50), best demonstrated by fluoroscopy, can develop in patients with long-standing severe mitral stenosis. A thrombus may form in the dilated left atrium and be the source of emboli to the brain or elsewhere in the systemic circulation. Echocardiography is the most sensitive and most specific, noninvasive method for diagnosing mitral stenosis (Figure 7-51). Echocardiography demonstrates chamber enlargement or wall thickening and permits measurement of the valvular orifices. Cine MRI has now been used to demonstrate and quantitate the abnormal pattern of flow between the left atrium and the left ventricle in mitral stenosis without the use of contrast agents.

the chordae tendineae or by the dysfunction of the papillary muscles that are attached to the underside of the valve cusps and normally prevent them from swinging up into the atrium when the ventricles contract. Regurgitation of blood into the left atrium during ventricular systole causes overfilling and

Mitral Insufficiency

FIGURE 7-50  Left atrial calcification in mitral stenosis. Lateral projection with barium in the esophagus shows enlargement of the left atrium and calcification of the wall of its chamber (arrows).

Although most often caused by rheumatic heart disease, mitral insufficiency may also be caused by the rupture of

A

B

FIGURE 7-49  Mitral stenosis. Frontal (A) and lateral (B) projections of the chest demonstrate cardiomegaly with enlargement of the right ventricle and left atrium. Right ventricular enlargement causes obliteration of the retrosternal air space, whereas left atrial enlargement produces convexity of the upper left border of the heart (arrow).

277

CHAPTER 7  Cardiovascular System dilation of this chamber, which lead to a decrease in ventricular stroke volume and cardiac output. In most cases, the left atrium is considerably larger in mitral insufficiency than in mitral stenosis (Figure 7-52); occasionally, an enormous left atrium can form both the

right and the left borders of the heart on frontal projections. An increased volume of blood flowing from the dilated left atrium to the left ventricle in diastole increases the left ventricular workload and leads to dilation and hypertrophy of this chamber. CHF, pulmonary congestion, and pulmonary hypertension may result, causing downward displacement of the cardiac apex and rounding of the lower left border of the heart.

Treatment of Mitral Stenosis and Mitral Insufficiency Surgical valvular replacement or correction of the stenosis may be performed to correct flow insufficiency. CHF resulting from stenosis or insufficiency may require treatment.

Aortic Stenosis

FIGURE 7-51  Echocardiogram of mitral stenosis. There is thickening of the mitral valve with decreased slope (arrows).

Aortic stenosis may be caused by rheumatic heart disease, a congenital valvular deformity (especially of a bicuspid valve), or a degenerative process of aging (idiopathic calcific stenosis). The obstruction to left ventricular outflow in aortic stenosis increases the workload of the left ventricle. Imaging appearance. Initially, this condition causes left ventricular hypertrophy without dilation, which produces only some rounding of the cardiac apex on frontal chest radiographs and slight backward displacement on lateral projections. The overall size of the heart remains within normal limits until left ventricular failure develops. Significant aortic stenosis is usually associated with lateral bulging (poststenotic dilation) of the ascending aorta caused by the jet of blood forced under high pressure through the narrowed valve (Figure 7-53). Aortic valve calcification, best demonstrated on fluoroscopic examination, is

A

B

FIGURE 7-52  Mitral insufficiency. Frontal (A) and lateral (B) projections of the chest demonstrate gross cardiomegaly with enlargement of the left atrium and left ventricle. Note the striking double-contour configuration (arrows) on the frontal image and elevation of the left mainstem bronchus (arrows) on the lateral image, characteristic signs of left atrial enlargement.

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CHAPTER 7  Cardiovascular System

a common finding and indicates that the aortic stenosis is severe (Figure 7-54).

Aortic Insufficiency Although most commonly caused by rheumatic heart disease, aortic insufficiency may be attributable to syphilis, infective endocarditis, dissecting aneurysm, or Marfan’s syndrome. Reflux of blood from the aorta during diastole causes volume overloading of the left ventricle and dilation of this chamber. Imaging appearance. Aortic insufficiency causes downward, lateral, and posterior displacement of the cardiac apex (Figure 7-55). Pronounced left ventricular dilation causes relative mitral insufficiency, which leads to left atrial enlargement and signs of pulmonary edema.

may be normal or may demonstrate evidence of previous valvular heart disease or CHF. Echocardiography is the only noninvasive procedure that can detect the valvular vegetations that are the hallmark of infective endocarditis. On the echocardiogram, these vegetations appear as masses of shaggy echoes producing an irregular thickening of the affected valves (Figure 7-56). Electron-beam CT demonstrates the vegetations and the valvular calcifications, distorted orifices, and possible aneurysms.

Treatment of Aortic Stenosis and Aortic Insufficiency CHF should be treated if the patient is symptomatic. Surgical valvular replacement or repair to correct stenosis can reestablish correct pressures and flow.

Infective Endocarditis Infective endocarditis refers to the formation of nodules or vegetations on heart valves by deposits of bacteria or fungi. Unlike the smaller nodules in rheumatic fever, the vegetations of infective endocarditis are filled with bacteria and tend to break apart easily (they are friable) to enter the bloodstream and form septic emboli that travel to the brain, kidney, lung, or other vital organs. Emboli lodging in the skin may cause rupture of small blood vessels and characteristic tiny hemorrhagic red spots (petechiae). Imaging appearance. Plain radiography is of little value in patients with infective endocarditis. The cardiac silhouette

FIGURE 7-54  Aortic stenosis. Calcification in three leaflets of the aortic valve (arrows).

A

B

FIGURE 7-53  Aortic stenosis. (A) Frontal projection shows downward displacement of the cardiac apex with poststenotic dilation of the ascending aorta (arrowheads). The aortic knob and descending aorta (arrows) are normal. (B) On lateral projection in another patient, bulging of the lower half of the posterior cardiac silhouette causes a broad indentation on the barium-filled esophagus (arrows).

CHAPTER 7  Cardiovascular System

FIGURE 7-55  Aortic insufficiency. Frontal chest radiograph shows left ventricular enlargement with downward and lateral displacement of the cardiac apex. Notice that the cardiac shadow extends below the dome of the left hemidiaphragm (small arrow). The ascending aorta is strikingly dilated (large arrows), suggestive of some underlying aortic stenosis.

279

FIGURE 7-56  Infective endocarditis. Echocardiogram demon­ strates vegetations as masses of shaggy echoes producing irregular thickening of the aortic valve (arrows).

Summary of Findings for Valvular Disease Disorder

Location

Imaging Appearance

Treatment

Rheumatic heart disease

Most frequently in mitral and aortic valves

Doppler echocardiography—quantify valvular insufficiencies

Prevention—antibiotics for streptococcal infections Therapy—antibiotics, anti-­ inflammatory drugs, and restricted activity

Mitral stenosis

Mitral valve

Mitral insufficiency

Valve dysfunction, rupture, or muscular dysfunction Obstruction of flow exiting the heart

PA chest—left atrium enlargement Lateral, RAO—posterior displacement of esophagus, posterior displacement of left main bronchus, calcification of valves Echocardiography—chamber enlargement, wall thickness, and size of valvular orifices Cine MRI—demonstrates and quantitates abnormal flow pattern PA chest—cardiomegaly—enlarged left atrium and left ventricle

Aortic stenosis

Aortic insufficiency Infective endocarditis

Reflux of blood, causing volume overload of left ventricle Nodules on heart valves

Surgical—valvular replacement, correction of stenosis Treat for CHF if needed

PA chest—enlargement of left ventricle; rounding of cardiac apex Posterior displacement of cardiac apex in lateral projection Lateral—posterior displacement of a cardiac apex; bulging of ascending aorta Aortic valve calcification PA chest—cardiac apex—inferior, lateral, and posterior displacement Echocardiography—shaggy echoes produced by irregular thickening of affected valves Electron-beam CT—vegetations in valve, valvular calcifications, distorted orifices

PA chest, Posteroanterior image of the chest; RAO, right anterior oblique.

Bacterial—treatment with antibiotics Surgically replace severely damaged valves

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CHAPTER 7  Cardiovascular System

Treatment. Antibiotics are taken until there is complete eradication of the bacterial infections. Severely damaged valves must be surgically replaced with artificial valves.

PERICARDIAL EFFUSION Pericardial effusion refers to the accumulation of fluid within the pericardial space surrounding the heart. The effusion may result from bacteria, viruses, or neoplastic involvement. In some cases, the cause cannot be determined (idiopathic pericardial effusion). Rapid accumulation of effusion interferes

FIGURE 7-57  Pericardial effusion. Globular enlargement of the cardiac silhouette.

with cardiac function because of an increase in pericardial pressure. A slow accumulation of fluid allows the pericardium to expand so that the pericardial pressure usually remains within the normal range. Imaging appearance. Echocardiography is the most effective imaging technique for demonstrating pericardial effusions and has largely replaced other methods. With this modality, a pericardial effusion is seen as a posterior sonolucent collection, and as little as 50 mL of fluid can be detected as an echofree space between the visceral and parietal pericardium. On plain chest radiographs, on the other hand, at least 200 mL of fluid must be present before it is possible to detect an effusion, which appears as an enlargement of the cardiac silhouette (Figure 7-57). Rapid enlargement of the cardiac silhouette, especially in the absence of pulmonary vascular engorgement indicating CHF, is highly suggestive of pericardial effusion. Angiocardiography, intravenous carbon dioxide injection, and a pericardial tap with air injection have been used in the past to demonstrate pericardial effusion by showing an excessive distance (>5 mm) between the contrast agent– or airfilled atrium and the outer border of the cardiac silhouette. CT can detect loculated pericardial effusions as small as 50 mL (Figure 7-58), whereas MRI may be able to characterize the fluid as serous or hemorrhagic by characteristic changes in the signal intensity and identify an accumulation of as little as 30 mL. Gated MRI (Figure 7-59) demonstrates a pericardial effusion as a region of decreased signal intensity between the myocardium and the fat on the surface of the parietal pericardium (which is usually invisible when it is in direct contact with the heart). However, echocardiography has effectively replaced these invasive techniques (Figure 7-60).

B

A

FIGURE 7-58  CT scans demonstrating peri­cardial effusion. (A) The heart is seen with a dark halo surrounded by fluid. (B) A CT-guided catheter was placed in this patient for drainage (arrow).

Summary of Findings for Pericardial Effusion Disorder Pericardial effusion

Location Increased fluid accumulation in pericardial sac

PA chest, Posteroanterior image of the chest.

Imaging Appearance PA chest—enlargement of cardiac silhouette Echocardiography—posterior sonolucent fluid collection CT—loculated fluid accumulations MRI—differentiates serous from hemor­rhagic fluid as a decreased signal intensity

Treatment Pericardiocentesis Pericardiectomy Administration of drugs into pericardial sac

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CHAPTER 7  Cardiovascular System A

A

S

L AR

R

PL

B

FIGURE 7-59  MRI of pericardial effusion. Transverse (A) and sagittal (B) images demonstrate the pericardium (arrows) displaced away from the heart by a huge pericardial effusion that has a very low signal intensity.

f RV

RA

LV

LA

f

FIGURE 7-60  Pericardial effusion. Echocardiogram demonstrates an apical four-chamber heart image with fluid around the heart (f) producing back-wall enhancement (arrow). LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

Treatment. The treatment depends on the cause. Pericardiocentesis is performed to remove fluid buildup, and insertion of a drain may be required. If the pericardial effusion recurs, a pericardiectomy may be necessary. An interventional technique includes administration of drugs into the pericardial sac.

VENOUS DISEASE Deep Venous Thrombosis DVT, which primarily involves the lower extremities, is the major source of potentially fatal pulmonary embolism. Precipitating factors in the development of venous thrombosis include trauma, bacterial infection, prolonged bed rest, and oral contraceptives. At times, DVT may be the earliest symptom of an unsuspected malignancy of the pancreas, lung, or gastrointestinal system. Imaging appearance. A precise diagnosis of DVT requires contrast venography, which can demonstrate the major

venous channels and their tributaries from the foot to the inferior vena cava. During venography, the patient’s leg should not be massaged to decrease edema. If DVT exists, the pressure applied could cause a thrombus to break free, becoming an embolus. The identification of a constant filling defect, representing the actual thrombus, is conclusive evidence of DVT (Figure 7-61). Venographic findings that are highly suggestive of, although not conclusive for, the diagnosis of DVT include the abrupt ending of the opaque column in a vein, the nonfilling of one or more veins that are normally opacified, and extensive collateral venous circulation. Because venography is an invasive technique, other modalities have been developed for detecting DVT. Duplex color Doppler ultrasound, which demonstrates changes in the velocity of venous blood flow with 95% accuracy, is now the preferred initial imaging modality. It is of special value in demonstrating thrombotic occlusion of major venous pathways in the popliteal and femoral regions. Ultrasound demonstrates lack of compressibility of the vein, an indication of the presence of a thrombus (Figure 7-62). Color Doppler allows visualization of the intraluminal thrombus itself and the characteristic changes in spontaneous flow that occur because of obstruction. However, abnormal Doppler ultrasound findings are not specific for thrombosis because similar changes in venous blood flow may be caused by CHF, extensive leg edema, local soft tissue masses, and decreased inflow of arterial blood into the extremity. Treatment. An anticoagulant drug is prescribed to prevent the formation of more thrombi. The patient receives an intravenous thrombolytic agent to lyse the already formed clot. For DVT involving the lower extremity, many authorities recommend bed rest to reduce the possibility of emboli.

Varicose Veins Varicose veins are dilated, elongated, and tortuous vessels that most commonly involve the superficial veins of the leg just under the skin (Figure 7-63). If the venous dilation becomes extreme, the valves that normally prevent backflow of blood

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A

B

FIGURE 7-61  DVT. (A) Initial contrast venogram demonstrates early nonocclusive thrombus extending from the valve cusp. Arrow points to the thrombus tail, the portion most likely to embolize. (B) Subsequent contrast venogram demonstrates growth and proximal extension of the thrombus, which has resulted in occlusion of the popliteal vein at the adductor hiatus.

A

B

FIGURE 7-62  Doppler image of DVT. The left leg was swollen with some discoloration. The deep venous system shows abnormal intraluminal echoes involving the distal superficial femoral vein (A) and the popliteal vein (B); both areas show no compressibility, a finding consistent with a diagnosis of thrombosis.

FIGURE 7-63  Varicose veins. Lower extremity venogram shows multiple tortuous, dilated venous structures.

CHAPTER 7  Cardiovascular System due to gravity become incompetent and cease to function, thus increasing the volume of blood in these slow-flowing vessels. Although heredity plays some role in the development of varicose veins, the underlying cause is increased pressure in an affected vein. Varicose veins can be an occupational hazard for people who stand or sit for long periods. Normally, the action of leg muscles helps move blood upward toward the heart from one venous valve to the next. If this “milking action” of the muscles is absent, the blood puts pressure on the closed valves and the thin walls of the veins, resulting in venous dilation, incompetence of the valves, and stasis of blood in the stagnant lower extremity veins. Increased pressure on a vein can also be attributable to a pregnant uterus or a pelvic tumor. Stasis of blood within varicose veins may lead to the development of phleboliths, calcified clots within a vein that appear radiographically as rounded densities, which often contain lucent centers (Figure 7-64). Chronic venous stasis may also lead to periosteal new bone formation along the tibial and fibular shafts and the development of plaquelike calcifications in the chronically congested subcutaneous tissues. The poor venous flow can lead to the development of superficial ulcers, and the distended veins can rupture, causing hemorrhage into the surrounding tissues. Imaging appearance. Although the diagnosis of varicose veins is primarily based on the clinical observation of the multiple bluish nodules just under the skin, venography is of value in demonstrating the patency of the deep venous system and the degree of collateral circulation from the superficial to the deep veins, especially if surgical intervention (tying off and removing the superficial veins) is being considered. After the application of a tourniquet to occlude superficial flow, the peripheral injection of contrast material opacifies the deep venous system. Filling of the superficial veins indicates that the perforating veins above the level of the tourniquet are incompetent. Treatment. Treatment consists of various ways to decrease the pressure in the lower extremities. If the varices are related to excess weight, weight reduction helps alleviate symptoms; if they are related to standing all day, then elevating the legs to

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assist blood flow return is recommended. Support hose and exercise to strengthen contractibility of the leg muscles may also aid in blood flow return. When nonsurgical treatment is not successful, vein stripping or cauterization may be performed.

FIGURE 7-64  Varicose veins. Multiple round and oval calcifications in soft tissues (phleboliths) represent calcified thrombi, some of which have characteristic lucent centers (black arrows). Extensive new bone formation along the medial aspect of the tibial shaft (white arrows) is caused by long-standing venous stasis.

Summary of Findings for Venous Disease Disorder

Location

Imaging Appearance

Treatment

Deep venous thrombosis

Primarily involves the lower extremities

Anticoagulants to prevent new thrombus formation Thrombolytic to lyse clot Bed rest to decrease possible emboli

Varicose veins

Commonly involve superficial veins of the leg

Venography—constant filling defect or abrupt ending of the opaque column in a vein; nonfilling of one or more veins; extensive collateral venous circulation Color Doppler—visualization of thrombus and flow changes due to obstruction Venography—demonstrates patency of the deep venous system and degree of collateral circulation from the superficial to deep veins

Therapeutic—weight reduction; elevation of legs; support hose and exercise Surgical—vein stripping or cauterization; removal of superficial veins

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  REVIEW QUESTIONS 1. Heart rate is controlled by the _________________ nervous system. a. psychogenic b. central c. peripheral d. autonomic 2. The _________________ valve is located between the left atrium and the left ventricle, whereas the _________________ valve is located between the right atrium and the right ventricle. 1. tricuspid 2. mitral 3. pulmonary 4. aortic a. 2, 1 b. 3, 1 c. 4, 1 d. 1, 2 3. The general circulation of the body is termed the _________________ circulation. a. pulmonary b. systemic c. general d. autonomic 4. The contracting phase of the heart is termed _________________, whereas the relaxation phase is termed _________________. 1. autonomic 2. diastole 3. systemic 4. systole a. 1, 3 b. 2, 4 c. 2, 3 d. 4, 2 5. Contraction of which chamber of the heart forces oxygenated blood into the aorta? a. right atrium b. right ventricle c. left atrium d. left ventricle 6. Oxygenated blood reaches the heart muscle by way of the _________________ and _________________. 1. right coronary artery 2. left coronary artery 3. left coronary vein 4. right coronary vein a. 1, 3 b. 4, 1 c. 2, 1 d. 2, 3 7. The heart has a specialized pacemaker named the _________________. a. bundle of His b. sinoatrial node

c. Purkinje fibers d. atrioventricular node 8. Which of the following factors leads to coronary artery disease? a. lack of exercise b. obesity, hypertension c. smoking, high-cholesterol diet d. all of above 9. Temporary oxygen insufficiency to the heart muscle causes severe chest pain termed _________________. a. angina pectoris b. myocardial occlusion c. myocardial pectoris d. angina occlusion 10. Arterial disease caused by fatty deposits on the inner arterial wall is termed _________________. a. arteriosclerosis b. myocardial infarction c. aneurysm d. myocardial ischemia 11. What radiographic procedure is used to determine the presence of coronary artery disease? a. angioplasty b. chest image c. coronary arteriogram d. CT 12. The procedure in which a balloon is used to dilate narrowed coronary arteries is named _________________. a. aortocoronary bypass b. coronary arteriography c. percutaneous transluminal angioplasty d. fluoroscopy 13. Which term refers to an inability of the heart to propel blood at a sufficient rate and volume? a. congestive heart failure b. pulmonary edema c. valvular disease d. valvular stenosis 14. An elevation of the pulmonary venous pressure is the most common cause of _________________. a. congestive heart failure b. pulmonary edema c. valvular disease d. valvular stenosis 15. The leading cause of strokes and CHF is ________ _________. a. hypertension b. low blood pressure c. hypotension d. cor pulmonale 16. A localized bulging or dilation of an artery is termed _________________. a. edema b. effusion c. aneurysm d. fat emboli

CHAPTER 7  Cardiovascular System 17. What is the modality of choice for demonstration of an abdominal aortic aneurysm? a. MRI b. ultrasonography c. CT d. plain image radiography 18. A congenital narrowing or constriction of the thoracic aorta is referred to as _________________. a. embolism b. plaque c. coarctation d. tetralogy 19. The _________________ of the heart is/are the major site of damage from rheumatic fever. a. myocardium b. valves c. septum d. endocardium 20. The most sensitive and specific noninvasive method of diagnosing mitral stenosis is _________________. a. ultrasonography b. echocardiography c. cardiac arteriography d. CT

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21. The accumulation of fluid within the pericardial space surrounding the heart is termed _________________. a. pericardial thrombosis b. pericardial effusion c. pulmonary edema d. pulmonary effusion 22. The invasive procedure for determining deep venous thrombosis is _________________. a. Doppler ultrasound b. venography c. CT d. arteriography 23. The most accurate screening procedure for assessing renovascular lesions is _________________. a. Doppler ultrasound b. venography c. CT d. arteriography 24. A potentially life-threatening condition that usually begins as a tear in the intima above the aortic valve is an _________________. a. aortic stenosis b. aortic coarctation c. aortic thrombosis d. aortic dissection

8 Nervous System OUTLINE Physiology of the Nervous System Infections of the Central Nervous System Meningitis Encephalitis Brain Abscess Subdural Empyema Epidural Empyema Treatment of Subdural and ­Epidural Empyemas Osteomyelitis of the Skull Tumors of the Central Nervous System Glioma Meningioma Acoustic Neuroma Pituitary Adenoma Craniopharyngioma

Pineal Tumors Chordoma Metastatic Carcinoma Traumatic Processes of the Brain and Skull Skull Fracture Epidural Hematoma Subdural Hematoma Cerebral Contusion Intracerebral Hematoma Subarachnoid Hemorrhage Carotid Artery Injury Facial Fractures

Vascular Disease of the Central Nervous System

Transient Ischemic Attacks Intraparenchymal Hemorrhage Subarachnoid Hemorrhage Multiple Sclerosis Epilepsy and Convulsive Disorders Degenerative Diseases Normal Aging Alzheimer’s Disease Huntington’s Disease Parkinson’s Disease Cerebellar Atrophy Amyotrophic Lateral Sclerosis (Lou Gehrig’s Disease) Hydrocephalus Sinusitis

Cerebrovascular Disease Stroke Syndrome

KEY TERMS arachnoid membrane arachnoid villi astrocytomas autonomic nervous system bacterial meningitis basal ganglia blowout fracture central nervous system (CNS) cerebellum cerebrovascular disease cerebrum choroid plexuses chromophobe adenomas communicating hydrocephalus corpus callosum cortex depressed fractures diastatic fracture diencephalon dura mater dysarthria

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ependymomas fissures glioblastomas gliomas grand mal gyri hemiparesis hemiplegia hypothalamus linear skull fracture mandibular fractures medulla medulloblastomas meninges meningitis midbrain myelin sheath nasal bone fractures neuron noncommunicating (obstructive) hydrocephalus

normal-pressure hydrocephalus oligodendrocytomas peripheral nervous system (PNS) petit mal pia mater pituitary adenomas pons reflex arc releasing hormones somatic nervous system stroke subarachnoid space sulci synapse thalamus tripod fracture vermis viral meningitis zygomatic arch fractures

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OBJECTIVES After reading this chapter, the reader will be able to: • Define and describe all boldface terms in this chapter • Describe the physiology of the nervous system • Identify anatomic structures on both diagrams and radiographs of the skull and nervous system

• Differentiate the various pathologic conditions affecting the skull and nervous system, and their radiographic manifestations

RADIOGRAPHER NOTES Proper positioning is critical in skull and spine radiography to ensure bilateral symmetry and to permit an evaluation of the complex anatomy and structural relationships. The demonstration of asymmetry or a shift in the normal location of a structure in a patient who is positioned correctly may be indicative of an underlying pathologic condition. Proper positioning and correct angulation of the central ray may allow visualization of otherwise superimposed structures. When evaluating anatomic areas such as the sinuses or facial bones, it is often necessary to place the patient in the erect position (either standing or sitting) and to use a horizontal beam to demonstrate an air–fluid level indicative of underlying inflammatory disease or fracture. If the patient’s condition prohibits placement in an erect position, air–fluid levels can be demonstrated only by obtaining a cross-table lateral projection using a horizontal beam with the patient in a dorsal decubitus position. Exposure factors should produce a scale of contrast that provides maximal detail (definition), especially when imaging vascular structures and when looking for subtle changes in bone density, such as those resulting from fractures of the skull or spine. Advanced stages of certain pathologic conditions may require changes in technique to maintain the proper level of density, contrast, and visibility of detail (see Box 1-1 in Chapter 1). If contrast material is used, the kilovolts-peak level must remain

PHYSIOLOGY OF THE NERVOUS SYSTEM The divisions of the nervous system can be classified by location or by the type of tissue supplied by the nerve cells in the division. The central nervous system (CNS) consists of the brain and spinal cord. The remaining neural structures, including 12 pairs of cranial nerves, 31 pairs of spinal nerves, autonomic nerves, and ganglia, make up the peripheral nervous system (PNS). The PNS consists of afferent and efferent neurons. Afferent (sensory) neurons conduct impulses from peripheral receptors to the CNS. Efferent (motor) neurons conduct impulses away from the CNS to the peripheral effectors. The somatic nervous system supplies the striated skeletal muscles, whereas the autonomic nervous system supplies smooth muscle, cardiac muscle, and glandular epithelial tissue. The basic unit of the nervous system is the neuron, or nerve cell (Figure 8-1). A neuron consists of a cell body and two types of long, threadlike extensions. A single axon leads from the nerve cell body, and one or more dendrites lead

in the low to mid-range (70–85 kVp) to provide enough radiographic contrast to properly show the contrast-filled vessels. In digital imaging, the technologist must process the digital image to provide the greatest contrast resolution by selecting the proper processing algorithm. The administration of radiographic contrast material is an essential component of many examinations of the skull and nervous system. Therefore, it is essential that the radiographer be familiar with the use of these agents and be extremely alert to the development of possible allergic reactions. Currently, the radiographic scope of practice includes venous access and pharmacology of contrast agents. Some facilities may require the radiographer to inject agents intravenously, especially for computed tomography (CT) and magnetic resonance imaging (MRI). After contrast administration, the radiographer is often left alone in the room with the patient and must be able to immediately recognize an allergic reaction to contrast material and be able to initiate and maintain basic life-support techniques until advanced life-support personnel have arrived. Although departmental policy varies, it is usually the radiographer’s responsibility to assist during resuscitation procedures. Therefore, it is essential that the radiographer be familiar with the contents of the emergency cart and be responsible for ensuring that the cart is completely stocked with all appropriate medications.

toward it. Axons are insulated by a fatty covering called the myelin sheath, which increases the rate of transmission of nervous impulses. Deterioration of this fatty myelin sheath (demyelination) is a characteristic abnormality in multiple sclerosis. In involuntary reactions, the impulse conduction route to and from the CNS is termed a reflex arc. Voluntary actions are commonly a reaction due to stimulation of a combination of sensors. The basic reflex arc consists of an afferent, or sensory, neuron, which conducts impulses to the CNS from the periphery; and an efferent, or motor, neuron, which conducts impulses from the CNS to peripheral effectors (muscles or glandular tissue). Impulses pass from one neuron to another at a junction called the synapse. Transmission at the synapse is a chemical reaction in which the termini of the axon release a neurotransmitter substance that produces an electrical impulse in the dendrites of the next axon. Once the neurotransmitter has accomplished its task, its activity rapidly terminates so that subsequent impulses pass along this same route.

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Dendrite Golgi apparatus

Endoplasmic reticulum Mitochondrion Cell body (soma)

Dendrites Nucleus Axon hillock

Axon

Schwann cell

Myelin sheath

Cell body

Axon collateral

Axon hillock

Node of Ranvier

Axon

Synaptic knobs

Telodendria

FIGURE 8-1  Structure of a neuron.

The largest part of the brain is the cerebrum, which consists of two cerebral hemispheres (Figure 8-2). The surface of the cerebrum is highly convoluted with elevations called gyri and shallow grooves called sulci. Deeper grooves called fissures divide each cerebral hemisphere into lobes. The outer portion of the cerebrum, termed the cortex, consists of a thin layer of gray matter where the nerve cell bodies are concentrated. The inner area consists of white matter, which is composed of the nerve fiber tracts.

The cerebral cortex is responsible for receiving sensory information from all parts of the body and for triggering impulses that govern all motor activity. Just posterior to the central sulcus, the cerebral cortex has specialized areas to receive and precisely localize sensory information from the PNS. Visual impulses are transmitted to the posterior portion of the brain; olfactory (smell) and auditory impulses are received in the lateral portions. The primary motor cortex is just anterior to the central sulcus. Because efferent motor

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CHAPTER 8  Nervous System Cerebrum

Cerebrum Cerebellum Diencephalon Midbrain Pons Medulla oblongata

Thalamus Diencephalon

Pineal body Hypothalamus Midbrain

Brainstem

Pons

Cerebellum

Medulla oblongata

FIGURE 8-2  Divisions of the brain.

fibers cross over from one side of the body to the other at the level of the medulla and spinal cord, stimulation on one side of the cerebral cortex causes contraction of muscles on the opposite side of the body. The premotor cortex, which lies anterior to the primary motor cortex, controls movements of muscles by stimulating groups of muscles that work together. This region also contains the portion of the brain responsible for speech, which is usually on the left side in right-handed people. In addition, the cerebral cortex is the site of all higher functions, including memory and creative thought. The two cerebral hemispheres are connected by a mass of white matter called the corpus callosum. These extensive bundles of nerve fibers lie in the midline just above the roofs of the lateral ventricles. Deep within the white matter are a few islands of gray matter that are collectively called the basal ganglia. These structures help control position and automatic movements and consist of the caudate nuclei, the globus pallidus, and the putamen. Between the cerebrum and spinal cord lies the brainstem, which is composed of (from top down) the midbrain (mesencephalon), the pons, and the medulla (see Figure 8-2). In addition to performing sensory, motor, and reflex functions, the brainstem contains the nuclei of the 12 cranial nerves and the vital centers controlling cardiac, vasomotor, and respiratory function. Centers in the medulla are responsible for such nonvital reflexes as vomiting, coughing, sneezing, hiccupping, and swallowing.

The cerebellum, the second largest part of the brain, is located just below the posterior portion of the cerebrum (see Figure 8-2). It is composed of two large lateral masses: the cerebellar hemispheres and a central section (vermis) that resembles a worm coiled on itself. The cerebellum acts with the cerebral cortex to produce skilled movements by coordinating the activities of groups of muscles. It coordinates skeletal muscles used in maintaining equilibrium and posture by functioning below the level of consciousness to make movements smooth rather than jerky, steady rather than trembling, and efficient and coordinated rather than ineffective and awkward. Therefore, cerebellar disease produces such characteristic symptoms as ataxia (muscle incoordination), tremors, and disturbances of gait and equilibrium. The diencephalon lies between the cerebrum and the midbrain (see Figure 8-2). It consists of several structures located around the third ventricle, primarily the thalamus and hypothalamus. The thalamus primarily functions as a relay station that receives and processes sensory information of almost all kinds of sensory impulses before sending this information on to the cerebral cortex. The tiny hypothalamus is an extremely complex structure that functions as a link between the mind and body and is the site of “pleasure” or “reward” centers for such primary drives as eating, drinking, and mating. It plays a major role in regulating the body’s internal environment by coordinating the activities of the autonomic nervous system and secreting the releasing hormones that control the secretion of hormones by the anterior and posterior portions of

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CHAPTER 8  Nervous System Gray matter White matter

Ventral root Dorsal root

Dorsal root ganglion

Arachnoid Dura mater

Pia mater

Sympathetic chain Autonomic (sympathetic) ganglion

Spinal nerve

Pia mater

Rami communicantes Arachnoid mater

Ventral root

Sympathetic ganglion

Ventral ramus Dorsal ramus

Dura mater Spinal cord

Dorsal root ganglion

Adipose tissue in epidural space

Denticulate ligament

FIGURE 8-3  Structures covering the central nervous system.

the pituitary gland. The hypothalamus is also important in helping to maintain a normal body temperature and in keeping the individual in a waking state. The spinal cord lies within the vertebral column and extends from its junction with the brainstem at the foramen magnum to approximately the lower border of the first lumbar vertebra. It consists of an inner core of gray matter surrounded by white matter tracts. The basic function of the spinal cord is to conduct impulses up the cord to the brain (ascending tracts) and down the cord from the brain to spinal nerves (descending tracts). It also serves as the center for spinal reflexes and involuntary responses, such as the knee jerk (patellar reflex). The delicate, yet vital, brain and spinal cord are protected by two layers of coverings. The outer bony coverings are the cranial bones of the skull encasing the brain and the vertebrae surrounding the spinal cord. The inner coverings consist of three distinct layers of meninges (Figure 8-3). The innermost layer adhering to the outer surface of the brain and spinal cord is the transparent pia mater, and the tough outermost covering is termed the dura mater. Between these layers is the delicate, cobweb-like arachnoid membrane. Inflammation of these three protective layers is called meningitis. Three extensions of the dura mater separate portions of the brain. The falx cerebri projects downward into the longitudinal fissure to separate the cerebral hemispheres. Similarly, the falx cerebelli separates the two cerebellar hemispheres. The tentorium cerebelli forms a tentlike covering over the cerebellum that separates it from the occipital lobe of the cerebrum. In addition to bony and membranous coverings, the brain and spinal cord are further protected by a cushion of fluid both around them and within them. The ventricles are four spaces within the brain that contain cerebrospinal fluid (CSF). There are two large lateral ventricles, one located in

each cerebral hemisphere. The slitlike third ventricle lies between the right and left thalamus. The anterior parts of the lateral ventricles (frontal horns) are connected by a Y-shaped canal that extends downward to open into the upper part of the third ventricle at the foramen of Monro. The fourth ventricle is a diamond-shaped space between the cerebellum posteriorly and the medulla and pons anteriorly. It is continuous inferiorly with the central canal of the spinal cord. The third and fourth ventricles are connected by the aqueduct of Sylvius (cerebral aqueduct), a narrow canal that runs through the posterior part of the midbrain. CSF is formed by the filtration of plasma from blood in the choroid plexuses, networks of capillaries that project from the pia mater into the lateral ventricles and into the roofs of the third and fourth ventricles. After flowing through the ventricular system, the fluid circulates in the subarachnoid space (between the pia mater and the arachnoid) around the brain and spinal cord before being absorbed into venous blood through arachnoid villi. Obstruction of CSF circulation results in hydrocephalus.

INFECTIONS OF THE CENTRAL NERVOUS SYSTEM The incidence of infectious diseases of the CNS has decreased with the widespread availability of antibiotics. Nevertheless, bacterial, fungal, viral, and protozoal organisms can infect the brain parenchyma, meningeal linings, and bones of the skull.

Meningitis Meningitis is an acute inflammation of the pia mater and arachnoid, two of the membranes covering the brain and spinal cord. Infecting organisms can reach the meninges from a middle ear, the upper respiratory tract, or a frontal sinus

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Although MRI and CT are best for evaluating acute bac­ terial meningitis, plain images of the sinuses and skull can demonstrate cranial osteomyelitis, paranasal sinusitis, or a skull fracture as the underlying cause of meningitis. In approximately 50% of patients, chest radiographs may show a silent area of pneumonia or a lung abscess. Contrastenhanced MRI is the most sensitive modality for demonstrating enhancement of the two innermost layers of the meninges (pia mater and arachnoid membrane) and subarachnoid distention with interhemispheric widening that is consistent with early findings in severe meningitis. On T2-weighted MR images, edema produces cortical hyperintensities. Treatment. A sample of CSF is collected for culture, and when the organism is identified, specific antibiotics are given to eradicate the bacteria. Even before these results are available, treatment with a broad-spectrum antibiotic is begun to prevent morbidity. If secondary encephalitis develops, the patient receives antiviral drugs. Any increased intracranial pressure is appropriately treated.

Encephalitis FIGURE 8-4  Meningitis. Subarachnoid enhancement in the basal cisterns and left sylvian fissure in a patient with ­cysticercosis.

infection, or they can be spread through the bloodstream (hematogenously) from an infection in the lungs or other site. Bacterial meningitis (pyogenic) is most commonly caused by Haemophilus influenzae in neonates and young children and by meningococci and pneumococci in adolescents and adults. Viral meningitis may be caused by mumps, poliovirus, and occasionally herpes simplex. A chronic form of meningitis can be caused by tuberculous infection. Bacterial meningitis is the most common form. The bacteria release toxins that destroy the meningeal cells, thus stimulating immune and inflammatory reactions. Imaging appearance. Although the meninges initially demonstrate vascular congestion, edema, and minute hemorrhages, the underlying brain remains intact. MRI and CT scans are normal during most acute episodes of meningitis and remain normal if appropriate therapy is promptly instituted. If the infection extends to involve the cortex of the brain and the ependymal lining of the ventricles, contrast studies may show characteristic meningeal enhancement in the basal cisterns, interhemispheric fissure, and choroid plexus (Figure 8-4). Diffuse brain swelling may symmetrically compress the lateral and third ventricles. MRI and CT are also of value in the early detection of such complications of acute meningitis as arterial or venous vasculitis or thrombosis with infarction, hydrocephalus caused by adhesions or thickening of the arachnoid at the base of the brain, subdural effusion or empyema, and brain abscess. A spinal tap is necessary to determine the cause of meningitis. CT is the modality of choice to rule out contraindications to lumbar puncture (cerebral hemorrhage or increased ventricular pressure).

Encephalitis, a viral inflammation of the brain and meninges (meningoencephalitis), produces symptoms ranging from mild headache and fever to severe cerebral dysfunction, seizures, and coma. Approximately 30% of cases occur in children. Encephalitis caused by herpes simplex is an often fatal, fulminant (sudden severe infection, fever, or hemorrhage) process. Imaging appearance. The earliest and predominant findings in herpetic encephalitis are poorly marginated areas (with a patchy parenchymal pattern) in the temporal lobes and inferior frontal gray matter, which have high signal intensity on T2-weighted MR images and demonstrate low density on CT scans. These changes probably represent a combination of tissue necrosis and focal brain edema. A mass effect is common and may be seen as a midline shift or as a focal mass compressing the ventricles or the sylvian cisterns. Compromise of the blood–brain barrier in areas of rapid, more progressive hemorrhagic necrosis results in a nonhomogeneous pattern of contrast enhancement. CT reveals abnormalities 3 to 5 days after the onset of symptoms, when the patient may be comatose. In toxoplasmosis, nodular lesions demonstrate ring enhancement on contrast CT. MRI is the preferred modality, even though in acute cases a contrastenhanced image may appear normal. Follow-up CT scans typically demonstrate widespread low-­density encephalomalacia (sponginess) involving the temporal and frontal lobes. Treatment. In addition to confirming the clinical diagnosis of herpes simplex encephalitis and excluding the presence of an abscess or a tumor, MRI and CT are important because they can indicate the best site for biopsy. A definitive diagnosis of herpes infection is essential before the start of treatment with adenine arabinoside, a chemotherapeutic agent that may be neurotoxic, mutagenic, and carcinogenic. Acyclovir, an antiviral drug used in treating herpes infection, interferes with the deoxyribonucleic acid (DNA) synthesis and inhibits viral replication.

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A

B

FIGURE 8-5  Brain abscess. (A) T1-weighted MR image shows a central hypointense necrotic mass with an isointense capsule surrounded by low-signal intensity edema. (B) On the T2-weighted image, the hypointense capsule is highlighted by increased signal centrally and peripherally.

Brain Abscess Brain abscesses are usually a result of chronic infections of the middle ear, paranasal sinuses, or mastoid air cells or of systemic infections (pneumonia, bacterial endocarditis, and osteomyelitis). The organisms that most commonly cause brain abscesses are streptococci. In patients with AIDS, unusual infections such as toxoplasmosis and cryptococcosis often cause brain abscesses. The microorganisms lodge preferentially in the gray matter and spread to the adjacent white matter. Imaging appearance. The earliest sign of brain abscess on MRI or CT is an area of abnormal density with poorly defined borders and a mass effect reflecting vascular congestion and edema. Further progression of the inflammatory process leads to cerebral softening, which may undergo necrosis and liquefaction, resulting in a true abscess. MRI is considered superior for demonstrating a brain abscess, although CT can be employed when MRI is unavailable. On T1-weighted MR images, an abscess appears as a hypointense mass with an isointense capsule surrounded by low–signal intensity edema (Figure 8-5A). Both the mass and the edema are hyperintense on proton density and T2-weighted images (Figure 8-5B). After the intravenous administration of contrast material, an oval or circular peripheral ring of contrast enhancement outlines the abscess capsule. Although the wall is usually thin and of uniform thickness, an irregularly thick wall, resulting from the formation of granulation tissue, may mimic a malignant glioma. Diffusion MRI can distinguish necrotic tumors from abscesses by demonstrating a reduced diffusion coefficient. Multiple abscesses indicate the possibility of septic emboli from a systemic infection (Figure 8-6). Plain skull radiographs may show evidence of underlying sinusitis, mastoiditis, or osteomyelitis, although these

FIGURE 8-6  Pyogenic brain abscesses. CT scan shows one frontal and two occipital lesions (arrows) with relatively thin, uniform rings of enhancement.

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conditions are better evaluated by CT scanning with bone-window settings. Infection by gas-forming organisms occasionally produces an air–fluid level within the abscess cavity. Treatment. A broad-spectrum antibiotic is given to fight the infection. A craniotomy to totally excise the abscess is most successful in cases of a multiloculated abscess. Image-directed stereotactic aspiration to provide a specimen for microbial evaluation is better because it is less invasive. In some cases, the patient may require medication to reduce increased intracranial pressure. MRI and CT can be used to assess the results of therapy for a brain abscess and to document complications. These modalities can demonstrate the often fatal intraventricular rupture of an abscess and the development of increased intracranial pressure, which may lead to brain herniation.

Subdural Empyema Subdural empyema is a suppurative process in the space between the inner surface of the dura and the outer surface of the arachnoid. Approximately 25% of intracranial infections are subdural empyemas. The most common cause of subdural empyema is the spread of infection from the frontal or ethmoid sinuses. Less frequently, subdural empyema may result from mastoiditis, middle ear infection, purulent meningitis, penetrating wounds to the skull, craniectomy, or osteomyelitis of the skull. Subdural empyema is often bilateral and associated with a high mortality even if properly treated. The most common location of a subdural empyema is over the cerebral convexity; the base of the skull is usually spared. Imaging appearance. MRI is the procedure of choice in evaluating the patient with suspected subdural empyema. Unlike CT, MRI is free from bony artifacts adjacent to the inner table of the skull. In addition, signal characteristics may permit differentiation between benign effusions and infected empyemas. Noncontrast scans demonstrate a crescentic or lentiform (lenslike), extra-axial fluid collection (representing pus) adjacent to the inner border of the skull or the falx (Figure 8-7). There is compression and displacement of the ipsilateral ventricular structures. After the intravenous administration of contrast material, a narrow zone of enhancement of relatively uniform thickness separates the extracerebral collection from the brain surface. MRI can also demonstrate involvement of the adjacent parenchyma by means of retrograde thrombophlebitis with resultant infarction or abscess formation, both of which are signs associated with a poor prognosis.

FIGURE 8-7  Subdural empyema. T2-weighted MR image demonstrates high signal intensity of the fluid collections along the falx.

Epidural Empyema

FIGURE 8-8  Epidural empyema. Black rim of the dura ­delineates the epidural fluid collection in the right frontal region.

Epidural empyema (Figure 8-8) is almost invariably associated with osteomyelitis in a cranial bone originating from an infection in the ear or paranasal sinuses. The infectious process is localized outside the dural membrane and beneath the inner table of the skull. The frontal region is most frequently affected because of its close relationship to the frontal sinuses and the ease with which the dura can be stripped from the bone. Imaging appearance. Noncontrast CT scans demonstrate the epidural infection as a poorly defined area of low density adjacent to the inner table of the skull. An adjacent area

of bone destruction or evidence of paranasal sinus or mastoid infection (fluid and soft tissue thickening) can often be demonstrated on CT or plain skull radiographs. After the intravenous administration of contrast material, the inflamed dural membrane appears as a thickened zone of enhancement on the convex inner side of the lesion. If the collection lies in the midline, the attachment of the falx is displaced inward and separated from the adjacent skull, thus identifying its extradural location.

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Treatment of Subdural and Epidural Empyemas Subdural and epidural empyemas should be treated as medical emergencies. Immediate surgical drainage of an empyema and the underlying sinus infection aids in preventing recurrence. Craniotomy provides the most complete evacuation. The broad-spectrum antibiotic regimen used for a brain abscess is used here also.

Osteomyelitis of the Skull Osteomyelitis of the skull is most commonly caused by direct extension of a suppurative process from the paranasal sinuses, mastoid air cells, or scalp. As with osteomyelitis elsewhere in

the skeleton, the radiographic changes often develop 1 or 2 weeks after the onset of clinical symptoms and signs. Imaging appearance. Acute osteomyelitis first appears radiographically as multiple small, poorly defined areas of lucency (Figure 8-9). During the next several weeks, the lucencies enlarge and coalesce centrally with an expanding perimeter of small satellite foci. As the infection becomes more chronic (especially with syphilis, tuberculosis, or fungal infections), attempts at bone regeneration produce multiple areas of poorly defined reactive sclerosis. Treatment. Refer to the discussion on bacterial osteomyelitis in Chapter 4.

Summary of Findings for Infections of the Central Nervous System Disorder

Location

Imaging Appearance

Treatment

Meningitis

Acute inflammation of meninges

Immediate broad-spectrum antibiotics followed by specific antibiotics determined by culture results

Encephalitis

Viral inflammation of brain and meninges

Brain abscess

Microorganism infection of gray and white matter

Subdural empyema

Infection located between the dura and the arachnoid

CT/MRI—arterial or venous vasculitis or thrombosis, hydrocephalus, subdural effusion, and brain abscess MRI—enhancement of the two innermost layers of the meninges and subarachnoid distention with interhemispheric widening Radiographs—osteomyelitis, sinusitis, or fracture MRI—hyperintensity on T2-weighted images with mass effect CT—low-attenuation regions without focal enhancement; mass effect MRI—T1-weighted images show hypointense mass with isointense capsule; proton-density and T2-weighted images show hyperintensity of both the mass and surrounding edema; diffusion MRI distinguishes necrotic tumors from abscesses CT—contrast-enhanced scan identifies a high-attenuation capsule surrounding a hypodense necrotic center MRI—characteristic crescentic or lentiform extra-axial fluid collection that is mildly hyperintense to cerebrospinal fluid on T2-weighted images CT (noncontrast)—shows low-density area adjacent to the inner table of the skull, with possible bone destruction CT (contrast enhanced)—dural membrane appears as a thickened zone of enhancement on the convex inner side of the lesion Radiograph—multiple, small, poorly defined areas of lucency, 1–2 weeks after onset of symptoms

Epidural empyema

Infectious process above the dura and beneath the inner skull table

Osteomyelitis of the skull

Cranial bones

For herpes infection: adenine arabinoside

Broad-spectrum antibiotics Craniotomy to totally excise the multiloculated abscess Image-directed stereotactic aspiration provides a specimen for microbial evaluation Medication to reduce increased intracranial pressure if symptoms occur

Craniotomy for immediate surgical drainage of empyema and underlying sinus empyema; aids in preventing recurrence Same broad-spectrum antibiotic regimen as for brain abscess

See Chapter 4

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FIGURE 8-9  Osteomyelitis of the skull. Diffuse areas of osteolytic destruction affect most of the calvaria resulting from blastomycosis.

TUMORS OF THE CENTRAL NERVOUS SYSTEM Intracranial neoplasms manifest clinically as seizure disorders or gradual neurologic deficits (difficulty thinking, slow comprehension, weakness, and headache). Approximately 50% of CNS tumors are primary lesions, and the others represent metastases. Imaging appearance. The clinical presentation and radiographic appearance depend on the location of the tumor and the site of the subsequent mass effect. MRI is generally considered the most sensitive technique for detecting most suspected brain tumors. In general, both the tumor and its surrounding edema demonstrate high signal intensity on T2-weighted images. After the intravenous injection of contrast material, the enhancing tumor can usually be distinguished from nonenhancing edema on T1-weighted images (Figure 8-10). In addition to its exquisite sensitivity in detecting pathologic alteration of normal tissue constituents, MRI provides excellent delineation of tumor extent and can show associated abnormalities, such as hydrocephalus. This modality is of special value in imaging neoplasms of the brainstem and posterior fossa, which may be poorly demonstrated on CT due to bone artifact. CT with contrast enhancement is an excellent examination for evaluating a patient with suspected brain tumor. It is of special value for detecting punctate or larger calcification that cannot be shown by MRI. Although skull radiographs were used in the past to demonstrate tumoral calcification, bone erosion, and displacement of the calcified pineal gland, plain images are no longer indicated because this information can be more effectively obtained on CT scans.

Before the advent of CT, cerebral arteriography was used to demonstrate evidence of brain tumors, such as mass effect, contralateral displacement of midline arteries and veins, abnormal vessels with tumor staining, and early venous filling. Currently, the major use of arteriography is for precise delineation of the arterial and venous anatomy. This delineation provides a surgical map before operative therapy and for evaluation of those cases in which a vascular anomaly is a strong consideration in the differential diagnosis of a tumor. Radionuclide brain scans have a relatively high rate of detection of cerebral tumors but are far less specific than CT or MRI. Positron emission tomography (PET) scans demonstrate metabolic activity and specific location of a lesion for presurgical planning (Figure 8-11). Treatment. Therapy of a CNS tumor depends on its location and histology. If possible, the tumor is surgically resected, followed by radiation therapy if the tumor is not completely removed. Radiation therapy and chemotherapy are used when the tumor is inoperable.

Glioma Gliomas, the most common primary malignant brain tumors, consist of glial cells (supporting connective tissues in the CNS) that still have the ability to multiply. They spread by direct extension and can cross from one cerebral hemisphere to the other through connecting white matter tracts, such as the corpus callosum. Gliomas have a peak incidence in middle adult life and are infrequent in persons younger than 30 years of age. Glioblastomas are highly malignant lesions that are predominantly cerebral, although similar tumors may occur in the brainstem, cerebellum, or spinal cord. Astrocytomas (70% of all gliomas) are slow-growing tumors that have an

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FIGURE 8-10  Glioblastoma multiforme. The T1-weighted axial (A) and coronal (B) MR images after intravenous injection of contrast material demonstrate an irregular ring of contrast enhancement, representing solid vascularized tumor, surrounding a central low-density area of necrosis. (C) The tumor and its surrounding edema demonstrate high signal intensity on a T2-weighted axial image. (D) On a FLAIR axial image, the tumor demonstrates low signal intensity and the edema appears as high signal intensity, demonstrating the extent of involvement and a ventricular shift to the right.

infiltrative character and can form large cavities or pseudocysts. Favored sites are the cerebrum, cerebellum, thalamus, optic chiasm, and pons. Less frequent types of gliomas are ependymoma, medulloblastoma, and oligodendrocytoma. Ependymomas most commonly arise from the walls of the fourth ventricle, especially in children, and usually from the lateral ventricles in adults. Medulloblastomas are rapidly growing tumors, disseminating throughout the spinal fluid, which develop in the posterior portion of the vermis in children and rarely in the cerebellar hemisphere in adults. The tumor tends to spread

through the subarachnoid space, with metastatic deposits occurring anywhere within the brain or spinal column. Oligodendrocytomas are slow-growing lesions that usually arise in the cerebrum and have a tendency to calcify. Imaging appearance. On MR images (Figure 8-12), gliomas typically appear as masses of high signal intensity on T2-weighted images. They may be of low intensity or isointense on T1-weighted sequences. MR spectroscopy has a typical spectral pattern with a strongly increased choline peak, which indicates myelin or the breakdown of myelin (the chemical structure that goes into making white matter).

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FIGURE 8-11  Low-grade brain tumor studied by three-dimensional reconstruction of a PET cerebral study using 11C-methionine. (A) Mass effect near the thalamus is evident when the increased uptake (open arrow) is compared with a cystic component showing lack of uptake (solid arrow). (B) The greatest activity is noted in the right temporal lobe, corresponding to receptive and expressive language areas.

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FIGURE 8-12  Brainstem glioma. Sagittal MR images show enlargement of brainstem involving the pons and midbrain. Note that various imaging techniques alter the appearance of the tumor (T). (A) On a T1-weighted image, the tumor is gray (low-intensity signal). (B) On a T2-weighted image, the tumor appears white (high-intensity signal).

In MR spectroscopy, a highly elevated choline level, a drastically lower level of N-acetylaspartate (a neuronal marker), and a drastically lower creatine/phosphocreatine ratio confirm an infiltrating glioma (Figure 8-13). Ependymomas, often partially calcified and cystic, have a heterogeneous signal intensity and show enhancement.

On noncontrast CT scans, gliomas are most commonly seen as single, nonhomogeneous masses. Low-grade astrocytomas tend to be low-density lesions showing little or no enhancement (Figure 8-14); glioblastomas most frequently contain areas of both increased and decreased density, although a broad spectrum of CT appearances can occur.

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FIGURE 8-13  Infiltrating glioma. (A) T2-weighted MR image demonstrates a 3-cm hypointense lesion in the deep right parietal lobe with a hyperintense peripheral rim. A poorly defined hyperintense lesion is seen within the deep white matter of the left temporal and parietal lobes. (B) On the T1-weighted coronal image, the hyperintense periphery is seen surrounding a low-­ signal intensity and a high-signal intensity lesion. (C) On MR spectroscopy, the left frontal lobe demonstrates an elevated choline (first) peak, a slightly lower creatine/phosphocreatine (second) peak, and a mildly depressed N-acetylaspartate (third) peak. These findings help confirm a lowgrade, diffuse infiltrating glioma.

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FIGURE 8-14  Cystic astrocytoma. CT scan shows a hypodense mass with a thin rim of contrast enhancement.

Edema is often seen in the adjacent subcortical white matter. After the intravenous injection of contrast material, virtually all gliomas show enhancement, with the most malignant lesions tending to be enhanced to the greatest degree (see Figure 8-10). In MR spectroscopy, an elevated choline/creatine ratio suggests a malignant neoplasm. The most common pattern is an irregular ring of contrast enhancement, representing solid vascularized tumor, surrounding a central low-density area of necrosis. Contrast enhancement also can appear as patches of increased density distributed irregularly throughout a low-density lesion or as rounded nodules of increased density within the mass. Treatment. Therapy depends on the location and histology of the tumor. Astrocytomas have a good 5-year survival rate after surgery and radiation therapy. For ependymomas of the filum terminale, surgical removal provides a favorable prognosis.

Meningioma Meningiomas are benign tumors that arise from arachnoid lining cells and are attached to the dura. The most common sites of meningioma are the convexity of the calvaria, the olfactory groove, the tuberculum sellae, the parasagittal region, the sylvian fissure, the cerebellopontine angle, and the spinal canal. Of all spinal tumors, 25% are meningiomas. Seizures and neurologic defects are most often caused by mass effect. Imaging appearance. Because meningiomas tend to be isointense with brain on both T1- and T2-weighted images, anatomic distortion is the key to the MRI diagnosis (Figure 8-15).

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A thin rim of low intensity, consisting of a CSF cleft, the vascular rim, or dura, may separate the tumor from the adjacent brain. Calcification within a meningioma may produce nonuniform signal or focal signal void. Surrounding edema may make the lesion easier to identify. Just as the detection of meningiomas by CT is facilitated by the use of iodinated contrast material, paramagnetic contrast agents can enhance the detection of meningiomas on MRI. MR spectroscopy has a typical spectral pattern with a strongly increased choline peak; creatine is a marker of energy metabolism. Alanine is another specific amino acid marker producing a unique peak in meningiomas. CT typically shows a meningioma as a rounded, sharply delineated, isodense (25%) or hyperdense (75%) tumor abutting a dural surface. Calcification often is seen within the mass on noncontrast scans. After the intravenous injection of contrast material, there is intense homogeneous enhancement, which reflects the highly vascular nature of the tumor (Figure 8-16). Pronounced dilation of meningeal and diploic vessels, which provide part of the blood supply to the tumor, may produce prominent grooves in the calvaria on plain images of the skull. Calvarial hyperostosis (increased density) may develop because of invasion of the bone by tumor cells that stimulate osteoblastic activity. Dense calcification or granular psammomatous deposits may be seen within the tumor (Figure 8-17). Arteriography can demonstrate the feeding arteries, which most commonly arise from both the internal and the external carotid artery circulation. Preoperative embolization of the external carotid artery supply can decrease the amount of blood loss at surgery. Spinal meningiomas are best demonstrated on T1- or T2-weighted MR images using gadolinium enhancement as a homogeneous intense lesion. CT myelography demonstrates the location of the mass, which is usually intradural extramedullary (Figure 8-18). Treatment. Surgical resection is very successful because of the superficial position of the tumor and the lack of tumor infiltration. Incomplete resection results in a lobulated and mushroom pattern of tumor growth.

Acoustic Neuroma Acoustic neuromas are slowly growing benign tumors that may occur as solitary lesions or as part of the syndrome of neurofibromatosis. Such a tumor arises from Schwann cells in the vestibular portion of the auditory (eighth cranial) nerve. It usually originates in the internal auditory canal and extends into the cerebellopontine angle cistern. Imaging appearance. MR images (T1-weighted), the preferred modality, exquisitely show an acoustic neuroma as a focal or generalized enlargement of the eighth cranial nerve (Figure 8-19). This technique can even demonstrate small intracanalicular tumors confined to the internal auditory canal, which may be impossible to show on CT unless contrast material (nonionic water-soluble material or air) is administered into the ventricular system. CT scans demonstrate enlargement and erosion of the internal auditory

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FIGURE 8-15  Meningioma on MRI after intravenous injection of contrast material. A large mass (arrowheads) appears hyperintense on T1-weighted axial (A) and coronal (B) MR images. (C) The mass appears hypointense on a T2-weighted image. Note the dramatic shift of the ventricle (v) caused by the mass effect of the tumor. White arrow points to areas of hemorrhage within the neoplasm.

canal and a uniformly enhancing mass in the cerebellopontine angle (Figure 8-20). Very large tumors may compress the fourth ventricle and lead to the development of hydrocephalus. Treatment. Surgical excision of the lesion or gamma knife radiosurgery improves symptoms.

Pituitary Adenoma Pituitary adenomas, almost all of which arise in the anterior lobe, constitute more than 10% of all intracranial tumors. Most are nonsecreting chromophobe adenomas. As chromophobe tumors enlarge, the adjoining secreting cells within the sella turcica are compressed, leading to diminished

secretion and decreased levels of growth hormone, gonadotropins, thyrotropic hormone, and adrenocorticotropic hormone (ACTH). Large chromophobe adenomas can extend upward to distort the region of the optic chiasm, whereas lateral expansion of tumor can compress the cranial nerves passing within the cavernous sinus. A hormone-secreting pituitary tumor can cause clinical symptoms even if it is too small to have a mechanical mass effect. Hypersecretion of growth hormone results in gigantism in adolescents (before the epiphyses have closed) and acromegaly in adults (after the epiphyses have closed). Excess secretion of adrenocorticotropic hormone by a pituitary tumor results in the hypersecretion of steroid hormones

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FIGURE 8-16  Meningioma. (A) CT scan after intravenous injection of contrast material shows uniformly enhancing mass (arrow) with surrounding low-density edema attached to the falx. (B) Venous phase of carotid arteriogram shows the characteristic prominent vascular blush (arrow) of meningioma. Note that the superior sagittal sinus (arrowheads) is patent.

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FIGURE 8-17  Parietal meningioma. (A) Plain skull image shows dense calcification in the tumor. (B) CT scan of another patient demonstrating a midline calcified meningioma.

from the adrenal cortex and symptoms of Cushing’s disease. Hypersecretion of thyroid-stimulating hormone (TSH) leads to hyperthyroidism; excess secretion of prolactin by a pituitary tumor in women causes the galactorrhea–amenorrhea syndrome. Imaging appearance. Thin-section CT and MRI are the examinations of choice for evaluating a patient with a suspected pituitary tumor. After the intravenous administration of contrast material, large pituitary tumors are typically homogeneous and hyperdense with respect to surrounding brain tissue. Most pituitary microadenomas are of lower density

than the normal pituitary gland. CT can also demonstrate adjacent bone erosion, tumor extension beyond the confines of the sella, and impression on nearby structures, such as the third ventricle, optic nerves, or optic chiasm (­ Figure 8-21). The preferred modality for detecting and defining the extent of a pituitary tumor is MRI because of its superior sensitivity and multiplanar capability. Thin-section coronal and sagittal T1-weighted MR images show a microadenoma as a low–signal intensity focal lesion associated with contralateral deviation of the pituitary stalk and an upwardly convex contour of the gland (Figure 8-22). The intravenous injection

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FIGURE 8-18  Spinal meningioma. On anteroposterior (A) and lateral (B) myelogram images, the spine appears normal. Axial (C) and coronal (D) CT scans obtained after the subarachnoid injection of contrast material demonstrate a meningioma as a filling defect at the level of C1–C2.

of paramagnetic contrast material significantly improves diagnostic sensitivity in patients with tiny secreting pituitary tumors. Immediately after injection, small microadenomas appear hypointense relative to the normally enhancing pituitary gland. On delayed scans, the neoplasm may become hyperintense relative to the normal gland.

Although plain skull radiographs can show enlargement of the sella turcica, erosion of the dorsum sellae, and a double floor resulting from the unequal downward growth of the mass, this imaging modality is now of value only in the incidental detection of sellar enlargement on images taken for other purposes.

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FIGURE 8-19  Acoustic neuroma. MR T1-weighted axial (A) and coronal (B) and T2-weighted axial (C) images show considerable contrast enhancement of the right-sided lesion (arrows). Note the normal neural structures on the left.

Treatment. The size of the pituitary adenoma determines the extent of the treatment. For pituitary tumors not extending beyond the gland, surgical transsphenoidal resection has a good prognosis. Adenomas extending beyond the pituitary require surgical resection followed by radiation therapy for best results. The new stereotactic radiosurgery (Gamma Knife®) is another therapeutic alternative which requires no incision. Multiple gamma radiation beams are directed at the target.

Craniopharyngioma Craniopharyngiomas are benign tumors that contain both cystic and solid components and usually occur in patients younger than 20 years. They generally originate above the sella turcica, from embryonic remnants, depressing the optic chiasm and extending up into the third ventricle. Less

commonly, a craniopharyngioma lies within the sella, where it compresses the pituitary gland and may erode adjacent bony walls. Imaging appearance. Most craniopharyngiomas have calcification that can be detected on plain skull images or CT scans (Figure 8-23). In cystic lesions, the shell-like calcification lies along the periphery of the tumor; in mixed or solid lesions, the calcification is nodular, amorphous, or cloudlike. CT clearly demonstrates the cystic and solid components (isoattenuating) of the multilobulated mass. After the i­ntravenous administration of contrast material, there is variable enhancement, depending on the type of calcification within the tumor and the size of its cystic component (Figure 8-24). CT can also demonstrate hydrocephalus if the tumor has expanded to obstruct one or both of the foramina of Monro.

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FIGURE 8-20  Acoustic neuroma. CT scan shows widening and erosion of the right internal auditory canal (open arrows) associated with a large extra-axial mass (white arrows) in the right cerebellopontine angle. Small black arrows point to the normal internal auditory canal on the left.

FIGURE 8-21  Pituitary adenoma. Coronal CT scan shows enhancing mass filling and extending out from pituitary fossa. Note the erosion of the base of the sella. S

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FIGURE 8-22  Pituitary adenoma. Sagittal (A) and coronal (B) T1-weighted contrast-enhanced MR images demonstrate a large mass (M) that arises from sella turcica and extends upward to fill the suprasellar cistern.

The MRI appearance of craniopharyngioma depends on the tissue components of the tumor. Cystic areas have low signal intensity on T1-weighted images and high signal intensity on T2-weighted images; fat-containing regions have high signal intensity on T1-weighted images and show moderate signal intensity on T2-weighted images (Figure 8-25). Large areas of calcification appear dark on all imaging sequences. Newer MR sequences—gradient-echo, fluid-attenuated

inversion recovery, spectroscopy, and diffusion imaging— assist in differentiating tumor consistency. Treatment. One current treatment is MR-guided stereotactic resection via microsurgery. Some tumors are completely resectable; for others, surgical debulking and radiation therapy are performed. Surgery and radiation therapy, either alone or in combination, may provide long-term control in many patients.

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FIGURE 8-23  Craniopharyngioma. Plain skull radiograph shows a large suprasellar calcified mass in a child.

FIGURE 8-25  Craniopharyngioma. Sagittal MR image demonstrates a large multiloculated suprasellar mass with cystic (C) and lipid (L) components. c, Cerebellum; p, pons.

FIGURE 8-24  Craniopharyngioma. CT scan shows rim-­ enhancing tumor that contains dense calcification (straight arrows) and has a large cystic component (curved arrows) that extends into the posterior fossa. Note the associated hydrocephalus.

Pineal Tumors The most common tumors of the pineal gland are germinomas and teratomas, rapidly growing germ cell tumors, both of which occur predominantly in males younger than 25 years and may be associated with precocious puberty. Imaging appearance. Sagittal MR images are ideal for showing pineal tumors, which typically compress the midbrain from above and lift up the splenium of the corpus callosum (Figure 8-26). Although most germinomas are isointense to brain on both T1- and T2-weighted images, teratomas may

FIGURE 8-26  Pineal germinoma. Sagittal T1-weighted MR image shows a large isointense mass (white arrowheads) that compresses the midbrain (black arrowhead) and elevates the splenium of the corpus callosum.

have mixed signal intensity because they have cystic components and contain fat. On CT, germinomas appear as hyperdense or isodense masses that tend to deform or displace the posterior aspect of the third ventricle and often obliterate the quadrigeminal cistern. Punctate calcification can often be detected within the mass. Intense enhancement of the tumor occurs after the injection of contrast material. Teratomas in the pineal

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region typically appear as hypodense masses with internal ­calcification (Figure 8-27). Occasionally, other formed elements (e.g., teeth) are seen. Contrast enhancement is usually much less pronounced than with germinomas. Large pineal tumors may cause obstructive hydrocephalus with ventricular dilation. A small number of tumors with the histologic appearance of pinealomas appear elsewhere in the brain at some distance from the normal pineal gland. These “ectopic pinealomas” generally occur in the anterior aspect of the third ventricle or within the suprasellar cistern. They may produce the clinical triad of bitemporal hemianopsia, hypopituitarism, and diabetes insipidus that simulates a craniopharyngioma. Treatment. Surgery is the initial therapy of choice for pineal tumors. Radiation therapy following surgery may be helpful. Chemotherapy is used with radiation therapy if surgery is not a viable option.

Imaging appearance. On plain radiographs, a chordoma tends to be a bulky mass, causing ill-defined bone destruction or cortical expansion. Flocculent (fluffy or cloudlike) calcification may develop within a large soft tissue mass (Figure 8-28A). On CT scans, chordomas at the base of the skull tend to appear as lesions that are slightly denser than brain tissue and often demonstrate moderate contrast enhancement (Figure 8-28B). Sagittal MR images best demonstrate the clival origin of the mass and its effect on surrounding structures (Figure 8-29). Three-dimensional gradient-echo T1-weighted sequences are best for demonstrating the clival region. With gadolinium enhancement, chordomas have heterogeneous intensity and ring enhancement.

Chordoma Chordomas are tumors that arise from remnants of the notochord (the embryonic neural tube). Although any part of the vertebral column and base of the skull can be involved, the most common sites are the clivus and the lower lumbosacral region. The tumors are locally invasive but do not metastasize. Chordomas arising at the base of the skull produce the striking clinical picture of multiple cranial nerve palsies on one or both sides combined with a retropharyngeal mass and erosion of the clivus.

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FIGURE 8-27  Pineal teratoma. Nonenhanced CT scan shows an inhomogeneous mass containing a large amount of calcification.

FIGURE 8-28  Chordoma. (A) Plain skull radiograph shows dense calcification (arrows) within a large soft tissue mass that has eroded the dorsum sellae and the upper portion of the clivus. (B) In another patient, a CT scan shows an enlarging mass with destruction of the entire clivus (short arrows) and only small bone fragments remaining. The left petrous pyramid is also destroyed (long arrow).

CHAPTER 8  Nervous System Treatment. Chordomas of the clivus region are difficult to completely remove surgically, and thus the patient usually is also treated with radiation. For chordomas of the lumbar region, complete surgical resection is usually possible.

intensity that are most commonly situated at the junction between gray matter and white matter (Figure 8-30). Additional lesions can often be demonstrated after the injection of a paramagnetic contrast agent. On CT, brain metastases typically appear as multiple enhancing lesions of various sizes surrounded by different amounts of low-density edema (Figures 8-31 and 8-32). On noncontrast scans, metastatic deposits may be hypodense, hyperdense, or similar in density

Metastatic Carcinoma Carcinomas usually reach the brain by hematogenous spread. Infrequently, epithelial malignancies of the nasopharynx can spread into the cranial cavity through neural foramina or by direct invasion through bone. The most common neoplasms that metastasize to the brain arise in the lung and breast. Melanomas, colon carcinomas, and testicular and kidney tumors also cause brain metastases. Imaging appearance. On T2-weighted MR images, metastases appear as single or multiple masses of high signal

FIGURE 8-29  Clival chordoma. Sagittal MR image shows a low-intensity multilobulated mass deforming and displacing the brainstem, destroying the clivus, and extending into the sella turcica (upper arrowhead) and nasopharynx (two lower arrowheads).

FIGURE 8-31  Brain metastases. CT scan shows multiple enhancing masses of various shapes and sizes representing hematogenous metastases from carcinoma of the breast.

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FIGURE 8-30  Brain metastases. Axial T2-weighted (A) and FLAIR (B) MR images demonstrate two large masses (arrows) surrounded by extensive high–signal intensity edema.

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CHAPTER 8  Nervous System to normal brain tissue, depending on such factors as cellular density, tumor neovascularity, and degree of necrosis. In general, metastases from lung, breast, kidney, and colon tend to be hypodense or isodense; hyperdense metastases often reflect hemorrhage or calcification within or adjacent to the tumor. Single metastatic deposits in the brain may be indistinguishable from primary tumors. However, because primary brain neoplasms are unusual in older patients, single lesions in this population should suggest metastatic disease.

FIGURE 8-32  Brain metastases. CT scan shows enhancing metastases from squamous cell carcinoma of lung that are both ring enhancing (open arrow) and solid (solid arrow).

Treatment The number of lesions determines the choice of therapy. Single metastatic lesions or second-year postprimary (residual or regrowth) lesions require surgical intervention, which may provide relief from symptoms. Multiple metastases require irradiation or chemotherapy. Radiation therapy can be applied to the whole brain or by the gamma knife. Systemic chemotherapy is used if metastasis occurs after radiation treatment. Surgery combined with whole-brain radiation therapy is the most successful treatment.

Summary of Findings for Tumors of the Central Nervous System Disorder

Location

Imaging Appearance

Treatment

Glioma

Glial cells in CNS

MRI—masses of high signal intensity on T2-weighted images, and of low signal intensity or isointensity on T1-weighted images CT (noncontrast)—a single heterogeneous mass (isodense to hypodense) CT (contrast enhanced)—a homogeneous lesion with an irregular ring of enhancement

Meningioma

Arises from arachnoid lining and is attached to the dura Spinal

Acoustic neuroma

Schwann’s cells of cranial nerve VIII Most commonly from anterior lobe of the pituitary gland

MRI—isointense lesion on T1- and T2-weighted images; hyperintense on contrast-enhanced T1- and T2-weighted images CT—rounded, sharply delineated, hyperdense (75%) tumor MRI—T1- and T2-weighted images that have been contrast enhanced appear as homogenous intense lesions CT myelography—location of mass as a filling defect MRI—T1-weighted images show focal or generalized enlargement of cranial nerve VIII CT—best demonstrates bone involvement CT—large tumor typically homogeneous and hyperdense in comparison with normal brain tissue, bone erosion, and tumor extension MRI—T1-weighted images show hypointense mass associated with contralateral deviation MRI (contrast enhanced)—the microadenoma becomes hypointense initially; delayed scans demonstrate hyperintensity of the tumor

Depends on location and histology Astrocytomas: good 5-year survival rate with surgery and radiation therapy Ependymomas of the filum terminale: surgical removal provides the most favorable prognosis Surgical resection is very successful because of the superficial position of the tumor and the lack of tumor infiltration

Pituitary adenoma

Surgical excision of the lesion, or gamma knife radiosurgery, to improve symptoms Surgical resection by transsphenoidal approach Radiation therapy if tumor extends beyond pituitary gland Gamma Knife radiosurgery an alternative

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Summary of Findings for Tumors of the Central Nervous System—cont’d Disorder

Location

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Treatment

Craniopharyngioma

Usually superior to sella turcica

MR-guided stereotactic microsurgery for resection For unresectable tumors, surgical debulking followed by radiation therapy

Pineal tumor

Germ cell tumors of the pineal gland

Chordoma

Arises from the embryonic neural tube

Metastatic carcinoma

Carcinoma reaching the brain by hematogenous spread

CT—possible calcification in mass with cystic and solid components MRI—cystic regions produce low signal intensity on T1-weighted images, high signal intensity on T2-weighted images; fatty regions produce hyperintense signals on T1-weighted images MRI—sagittal images demonstrate compression of midbrain; germinomas are isointense on T1- and T2-weighted images; teratomas produce a mixed signal intensity because of their cystic components and fat CT—germinomas hyperdense or isodense, displacing third ventricle, and show intense contrast enhancement; teratomas are hypodense masses with internal calcifications Radiograph—ill-defined bone destruction or cortical expansion CT—base-of-skull mass is slightly denser than brain tissue and only moderately enhanced MRI—three-dimensional gradient-echo T1-weighted sequences in the sagittal plane best demonstrate the clival area and surrounding structures; gadolinium enhancement produces heterogeneous intensities with border-ring enhancement MRI—single or multiple masses of high signal intensity; additional lesions often seen with paramagnetic contrast agent CT—multiple enhancing lesions of various sizes with areas of low density surrounding edema

TRAUMATIC PROCESSES OF THE BRAIN AND SKULL In the patient with head trauma, the purpose of radiographic imaging is to detect a surgically correctable hematoma. Emergency CT has virtually replaced all other radiographic investigations in patients with suspected neurologic dysfunction resulting from head injury. Because the presence or absence of a skull fracture does not correlate with intracranial abnormalities, plain radiographs of the skull are no longer indicated in the patient with head trauma. Because of medicolegal reasons and the fear of missing a skull fracture, CT scans (and plain skull radiographs) are often overused. The following indications have been established for the use of radiographic procedures in the patient with head trauma: 1. Unexplained focal neurologic signs 2. Unconsciousness (including the unarousable alcoholic) 3. Documented decreasing level of consciousness or progressive mental deterioration

Surgery (first choice) followed by radiation therapy Chemotherapy with radiation therapy when surgery is not an option

Clival region—surgical resection followed by radiation therapy Lumbar area—complete surgical resection

Single lesion: surgical resection Multiple lesions: whole-brain radiation; chemotherapy if metastasis occurs after radiation therapy

4. History of previous craniotomy with shunt tube in place 5. Skull depression or subcutaneous foreign body palpable or identified by a probe through a laceration or puncture wound 6. Hemotympanum or fluid discharge from the ear 7. Discharge of CSF from the nose 8. Ecchymosis over the mastoid process (Battle’s sign) 9. Bilateral orbital ecchymoses (raccoon eyes)

Skull Fracture

Imaging appearance. A linear skull fracture appears on a plain radiograph as a sharp lucent line that is often irregular or jagged and occasionally branches (Figure 8-33). The fracture must be distinguished from suture lines, which generally have serrated edges and tend to be bilateral and symmetrical, and vascular grooves, which usually have a smooth curving course and are not as sharp or distinct as a fracture line. The location of a linear skull fracture can indicate possible complications. A fracture that crosses a dural vascular groove may cause vessel laceration, leading to an epidural hematoma.

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A

B

FIGURE 8-33  Skull fracture. (A) Lateral projection of the skull shows a widely separated fracture (arrow) extending to a star-shaped array of linear fractures. (B) In another patient, lateral projection shows a severely depressed skull fracture (arrows).

A

B

FIGURE 8-34  Skull fracture. (A) CT bone-window image demonstrates depressed temporal fracture (long arrow). Note the lateral orbital wall fracture (short arrow), the medial orbital wall fracture (large arrowhead), and the ethmoid opacification caused by hemorrhage. Also, air can be seen in the orbital soft tissues (small arrowhead), resulting from medial fracture into the ethmoids. (B) Trauma resulted in a nondisplaced fracture in the supraorbital plate (black arrowheads) in this 24-year-old woman.

A fracture involving the sinuses or mastoid air cells may result in post-traumatic pneumocephalus, with air seen in the ventricles on plain radiographs. A diastatic fracture is a linear fracture that intersects a suture and courses along it, causing sutural separation. More severe trauma, especially if localized to a small area of the skull, may force a fragment of bone to be separated and depressed into the cranial cavity (Figure 8-34). The underlying dura is frequently torn, and there is a relatively high incidence of cerebral parenchymal injury. Depressed fractures are often stellate (star shaped), with multiple fracture lines

radiating outward from a central point. When the fracture is viewed en face, the overlap of fragments makes the fracture line appear denser than the normal bone. Tangential views are required to determine the amount of depression. Fractures limited to the base of the skull are often hidden by the complex basal anatomy and may be very difficult to visualize on plain radiographs. A finding suggestive of a basilar skull fracture is an air–fluid level in the sphenoid sinus seen on an erect or cross-table lateral projection of the skull obtained with a horizontal x-ray beam. CT can demonstrate the presence of blood or fluid in the basilar cisterns and show

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FIGURE 8-35  Acute epidural hematoma in a trauma patient. CT scan illustrates the characteristic lens-shaped epidural hematoma. The mass effect associated with the hematoma causes midline shift.

some basilar skull fractures (using bone windows) that are not visible on routine skull radiographs. Potential complications of basal skull fractures include leakage of CSF, meningitis, and damage to the facial nerve or auditory apparatus within the petrous bone. It must be emphasized that the presence or absence of a skull fracture does not correlate with intracranial abnormalities. Indeed, serious treatable intracranial hematomas can be present without skull fractures. Treatment. The severity and location of the fracture and the complications resulting from the trauma determine the treatment.

Epidural Hematoma Epidural hematomas are caused by acute arterial bleeding and most commonly form over the parietotemporal convexity. Acute arterial bleeding is usually caused by laceration of the medial meningeal artery. Because of a high arterial pressure, epidural hematomas rapidly cause significant mass effect and acute neurologic symptoms. Imaging appearance. Because the dura is very adherent to the inner table of the skull, an epidural hematoma typically appears as a biconvex (lens-shaped), peripheral, high-density lesion (Figure 8-35). There is usually a shift of the midline structures toward the opposite side unless a contralateral balancing hematoma is present. If not promptly recognized, an epidural hematoma can lead to rapid progressive loss of consciousness, dilation of the ipsilateral pupil, compression of the upper midbrain, and eventually compression of the entire brainstem and death.

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FIGURE 8-36  Acute subdural hematoma. A high-density, crescent-shaped lesion (arrow) is adjacent to the inner table of the skull. Hematoma extends into interhemispheric fissure (arrowhead).

Treatment. To prevent death, emergency surgical decompression is required to relieve intracranial pressure.

Subdural Hematoma Subdural hematomas reflect venous bleeding, most commonly from ruptured veins between the dura and meninges. Symptoms may occur within the first few minutes; however, because of the low pressure of venous bleeding, patients with subdural hematomas tend to have a chronic course with symptoms of headache, agitation, confusion, drowsiness, and gradual neurologic deficits. Imaging appearance. An acute subdural hematoma typically appears on CT scans as a peripheral zone of increased density that follows the surface of the brain in a crescentic shape adjacent to the inner table of the skull (Figure 8-36). On CT, the finding of isodense to hypodense areas within a hyperdense hematoma indicates rapid bleeding with an accumulation of unclotted blood. There is usually an associated mass effect with displacement of midline structures and obliteration of sulci over the affected hemisphere. The absence of displacement away from the side of a lesion may indicate the not infrequent presence of bilateral subdural hematomas. On MR images, a subdural hematoma is detectable within a few days as an extra-axial mass of high signal intensity representing the accumulation of methemoglobin (Figure 8-37). Serial CT scans demonstrate a gradual decrease in the attenuation value of a subdural hematoma over a period of weeks.

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FIGURE 8-37  Bilateral subdural hematoma. Coronal MR image shows the high signal intensity of bilateral subdural collections (H).

With absorption and lysis of the blood clot, the hematoma becomes isodense with normal brain tissue, and the lesion may be identified only because of its mass effect. At this stage, scanning after the administration of contrast material may be of value because of enhancement of the membrane around the subdural hematoma and identification of the cortical veins. MR imaging of a lesion that is isodense on CT may show medial displacement of the superficial cerebral veins, an indication of an extracerebral mass and the entire extent of the hematoma over the cerebral convexity. A chronic subdural hematoma has a density similar to that of spinal fluid (Figure 8-38). Occasionally, the small bridging veins associated with a chronic subdural hematoma may bleed and produce the difficult problem of an acute subdural hematoma superimposed on a chronic one. Treatment. In small subdural hematomas without any inclination to rebleed, the hemorrhage resorbs naturally, and no treatment is necessary. Severe subdural hematomas require surgical ligation and evacuation of the hematoma to prevent transtentorial herniation. Less invasive methods of decreasing intracranial pressure include drug therapy and placement of an intraventricular catheter to remove CSF, which may prevent herniation.

FIGURE 8-38  CT scan of chronic left subdural hematoma. Crescent-shaped high- and low-density regions in the left parietal area. The anterior is isodense (chronic hygroma); posteriorly, a hyperdense crescent shape resulting from acute bleeding can be seen. Midline shift and dilated right lateral ventricle are evident.

Cerebral Contusion Cerebral contusion is an injury to brain tissue caused by movement of the brain within the calvaria after blunt trauma to the skull. Contusions occur when the brain contacts rough skull surfaces, such as the superior orbital roof and petrous ridges. The patient loses consciousness and cannot remember the traumatic event. Imaging appearance. Cerebral contusions typically appear on CT scans as low-density areas of edema and tissue necrosis, with or without nonhomogeneous density zones, reflecting multiple small areas of hemorrhage (Figure 8-39). The frontal and anterior temporal regions are the most common sites of injury. After the administration of intravenous contrast material, contusions generally enhance for several weeks

FIGURE 8-39  Cerebral contusion. CT scan shows small punctate hemorrhages (high density) within extensive areas of edema (low density).

after the injury because of a breakdown of the blood–brain barrier (BBB). On MR images, the cerebral edema causes high signal intensity on T2-weighted images; associated areas of hemorrhage may produce high–signal intensity regions on T1-weighted scans.

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Subarachnoid Hemorrhage Injury to surface veins, cerebral parenchyma, or cortical arteries can produce bleeding into the ventricular system, known as subarachnoid hemorrhage. Imaging appearance. On a CT scan, a subarachnoid hemorrhage appears as increased density within the basilar cisterns, cerebral fissures, and sulci. Identification of the falx cerebri, straight sinus, or superior sagittal sinus on noncontrast CT scans is often considered an indication of subarachnoid blood in the interhemispheric fissure. However, with high-resolution scanners this appearance may be seen in patients with a normal or calcified falx. MRI does not demonstrate the acute subarachnoid hemorrhage well unless a fluid-attenuated inversion recovery (FLAIR) sequence is used to demonstrate the increased signal intensity. However, T1-weighted scans can show subacute hemorrhage as a high signal intensity because of the conversion of fresh blood to methemoglobin. Treatment. Subarachnoid hemorrhage may require surgical evacuation and vessel repair if bleeding continues. Less invasive methods of decreasing intracranial pressure include drug therapy and the placement of an intraventricular catheter to remove CSF. FIGURE 8-40  Intracerebral hematoma. Note the large, homogeneous, high-density area (H) with acute bleeding into lateral ventricles (v).

Treatment. The patient with a cerebral contusion is hospitalized to allow observation of any changes in neurologic function. If the contusion causes swelling, medications to decrease intracranial pressure are prescribed. Surgery is usually not necessary.

Intracerebral Hematoma Traumatic hemorrhage into the brain parenchyma can result from shearing forces to intraparenchymal arteries, which tend to occur at the junction of the gray and white matter. Injury to the intima of intracranial vessels can cause the d ­ evelopment of traumatic aneurysms, which can rupture. Imaging appearance. On CT scans, an intracerebral hematoma appears as a well-circumscribed, homogeneous, high-density region that is usually surrounded by areas of low-density edema (Figure 8-40). As the blood components within the hematoma disintegrate, the lesion eventually becomes isodense with normal brain (usually 2 to 4 weeks after injury). On MR images, the hematoma shows high signal intensity. A chronic hematoma filled with hemosiderin appears black on T2-weighted images. Treatment. Although most intracerebral hematomas develop immediately after head injury, delayed hemorrhage is common. This is especially frequent after the evacuation of acute subdural hematomas that are compressing (tamponading) potential bleeding sites. Therefore, repeat CT or MRI is often performed within 48 hours in patients who have undergone decompressive surgery.

Carotid Artery Injury The extracerebral carotid arteries can be injured by penetrating trauma to the neck, such as from gunshot wounds or stabbing. Trauma to the internal carotid artery is associated in 50% of traumatic fistulas. Imaging appearance. Angiography can demonstrate laceration of the artery or intimal damage, which may result in either dissection or thrombotic occlusion (Figure 8-41). Hyperextension injuries from motor vehicle collisions can cause intimal damage to the carotid or vertebral arteries, which may result in pseudoaneurysm formation. Traumatic arteriovenous fistulas usually arise between the internal carotid artery and the cavernous sinus. In this condition, carotid arteriography demonstrates opacification of the cavernous sinus during the arterial phase. Reverse flow from the cavernous sinus may rapidly opacify a greatly dilated ophthalmic vein. The cavernous sinus and superior ophthalmic vein appear enlarged on a CT scan. MRI normally demonstrates strong enhancement of normal venous spaces (cavernous sinus). A fistula produces a signal void as a result of high flow. Treatment. The placement of a detachable balloon catheter within the fistula using angiographic guidance may eliminate the need for surgical intervention.

Facial Fractures Although it is padded by overlying skin, fat, and the muscles of expression, the face consists of thin and poorly supported bone, which can easily break in response to a traumatic force. The purpose of radiographic imaging in the patient with a facial injury is to demonstrate major disruptions of the facial skeleton and displacement of fracture fragments that will affect the surgical reduction and stabilization of the fracture.

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S

PP

A

FIGURE 8-41  Post-traumatic carotid–cavernous fistula. A lateral projection of an external carotid artery angiogram shows a pseudoaneurysm (A) and rapid filling of the cavernous sinus (S) and pterygoid plexus (PP). There is total interruption of the external carotid artery trunk beyond the takeoff of the facial artery.

Imaging appearance. Plain radiographs of the face are usually performed as an initial screening procedure, especially in a severely traumatized patient with substantial injuries to multiple organ systems. Whenever possible, images should be obtained with the patient in the erect position to demonstrate any air–fluid levels within the sinuses that could indicate recent hemorrhage and raise the suspicion of an underlying fracture. When erect images cannot be obtained, a cross-table lateral projection using a horizontal x-ray beam will demonstrate air–fluid levels. Complex-motion (pluridirectional) tomography can blur unrelated overlying structures and thus display details of injury that are obscure or only suspected on plain radiographs. CT can demonstrate soft tissue abnormalities, such as intraorbital or retrobulbar hematomas, that are impossible to detect by conventional means. In addition, bone detail and displacement can be exquisitely demonstrated when CT window and level settings are adjusted to optimize bony structures. Nasal bone fractures are the most common facial fractures. Isolated nasal fractures vary from simple, nondisplaced linear fractures to comminuted lesions with depression of the septum and lateral splaying of the fracture fragments (Figure 8-42). These fractures are best demonstrated on right and left (underexposed) soft tissue lateral projections, which also can define interruption of the anterior nasal spine—the anterior projection of the maxilla at the base of the cartilaginous nasal septum. Most fractures are transverse and tend to depress the distal portion of the nasal bones. A blowout fracture is caused by a direct blow to the front of the orbit that causes a rapid increase in intraorbital

FIGURE 8-42  Nasal bones. Depressed nasal fracture (arrow).

FIGURE 8-43  Blowout fracture. Conventional tomogram shows a comminuted fracture of the floor of the left orbit with inferior displacement of fracture fragments (solid arrows). Note the characteristic soft tissue shadow (open arrow) protruding through the floor into the superior portion of the maxillary sinus.

pressure. The fracture occurs in the thinnest, weakest portion of the orbit, which is the orbital floor just above the maxillary sinus. Plain radiographs (modified Waters’ method), the preferred screening study, and thin-section tomography can demonstrate most blowout fractures (Figure 8-43), although CT may be necessary for better visualization and for detecting entrapment of the extraocular muscles in the upper portion of the adjacent maxillary sinus (Figure 8-44). The fracture segment can be comminuted, with a sagging, hammock-like appearance, or can be of the trapdoor variety, with a displaced segment hanging into the antrum by a periosteal

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FIGURE 8-44  CT of orbital floor fracture. Coronal CT scan using bone window shows the fractured orbital floor as a double-hinged trap door with a separation in the center (open arrow). There is opacification of the right maxillary sinus. Note the displacement of the inferior rectus muscle (solid arrow) in this patient, who had limited upward gaze.

FIGURE 8-45  Zygomatic arch fracture. Submentovertex projection demonstrates two fractures on the right with depression of the zygomatic arch.

hinge. Herniation of orbital fat and extraocular muscles into the fractured orbital floor produces a characteristic soft tissue shadow protruding through the floor into the superior portion of the maxillary sinus. Opacification of the sinus caused by hemorrhage and mucosal edema is an indirect sign of orbital floor fracture. The presence of air within the orbit (orbital emphysema) indicates that there is a communication with a paranasal sinus, usually the ethmoid, as a result of an associated fracture of the medial wall of the orbit through the lamina papyracea. The zygomatic arch is vulnerable to a blow from the side of the face, which can produce a fracture with inward displacement of the central fragments and outward displacement of

315

FIGURE 8-46  Tripod fracture. Interruption of the orbital rim (white arrow), lateral maxillary fracture (black arrow), and nondisplaced zygomatic arch fracture (arrowheads) are demonstrated.

the fragments at the zygomatic and temporal ends of the arch (Figure 8-45). Zygomatic arch fractures are best demonstrated on underexposed images taken in the basal (submentovertex) projection (“jug-handle” view). A tripod fracture consists of fractures of the zygomatic arch and the orbital floor or rim combined with separation of the zygomaticofrontal suture (Figure 8-46). It is so named because it reflects separation of the zygoma from its three principal attachments. The resulting free-floating zygoma may cause facial disfigurement if the fracture is not diagnosed and properly treated. The mandible is a prominent, exposed segment of the facial skeleton and is thus a common site for both intentional and accidental trauma. Plain radiographs with oblique views, combined with panoramic tomography, can demonstrate most mandibular fractures (Figure 8-47). The angle of the mandible is the most common site of fracture, although fractures can involve any portion of the body and the condylar and coronoid processes. Because the mandible functions essentially as a bony ring, bilateral fractures are common. Le Fort fractures are severe injuries in which separation at the fracture site results in the formation of a large, complex, detached fragment that is unstable and may have its position altered relative to its site of origin. Le Fort fractures involve bilateral and horizontal fractures of the maxillae and are classified as type I, II, or III, depending on the extent of injury (Figure 8-48). Treatment. Treatment for nasal bone fractures varies depending on the amount of bony displacement. Reduction is required for fractures causing deviation of the nasal septum. More severe facial fractures require surgical reconstruction, possibly using internal or external fixation devices to prevent disfigurement.

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Summary of Findings for Traumatic Processes of the Brain and Skull Disorder

Location

Imaging Appearance

Treatment

Skull fracture

Any cranial bone

Treat associated complications

Epidural hematoma

Most commonly over parietotemporal convexity Most commonly from ruptured veins between dura and meninges

Linear fracture is an irregular or jagged, sharp lucent line Depressed fracture has stellate (star-shaped) fracture lines radiating outward CT—demonstrates fracture and associated intracranial complications CT—biconvex peripheral high-­density lesion, showing midline shift

Subdural hematoma

Cranial contusion

Injury to brain tissue Frontal and anterior temporal most common

Intracerebral hematoma

Hemorrhage into brain parenchyma

Subarachnoid hemorrhage

Injury to surface veins or cortical arteries bleeding into the ventricles

Carotid artery injury

Extracerebral carotid arteries

Facial fracture

Nasal bone (most common) Blowout (orbit) Tripod (zygoma separation from other facial and cranial bones) Mandible Le Fort (bilateral and horizontal fracture of maxillae)

FLAIR, Fluid-attenuated inversion recovery.

CT—acute: crescent-shaped peripheral high-density lesion; chronic: isodense lesion MRI—chronic: extracerebral mass with high signal intensity CT—low-density areas that usually enhance for several weeks MRI—increased signal intensity on both T2-weighted (cerebral edema) and T1-weighted images (if hemorrhage) CT—well-circumscribed, homogeneous, high-density region surrounded by low-density regions of edema MRI—high–signal intensity region; chronic hematoma is black on T2-weighted image CT—increased density within the basilar cisterns, cerebral fissures, and sulci MRI—acute hemorrhage on FLAIR imaging shows as an increased signal intensity; subacute hemorrhage shows high intensity on T1-weighted images Angiography—demonstrates laceration of artery or intimal damage CT—large cavernous sinus and superior ophthalmic vein MRI—signal void caused by large cavernous vein resulting from high flow Plain images—cranial and facial bones (upright or horizontal beam image shows fluid levels in the sinuses) CT—soft tissue abnormality and bone detail; three-dimensional imaging used for surgical planning

Emergency surgery to relieve increased intracranial pressure and to stop bleeding Resorption in small hematomas Surgical ligation and evacuation of hematoma Control intracranial pressure with drugs or intraventricular drainage catheter Observation for neurologic change Surgery not usually required

Surgical evacuation of hematoma

Surgical evacuation of the hemorrhage and vessel repair Drug therapy or an intraventricular catheter to decrease intracranial pressure

Placement of detachable balloon within fistula Surgical intervention to eliminate fistula

Reduction of fracture Some require surgery to place internal or external fixation device

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FIGURE 8-47  Mandibular fracture. Panoramic examination in edentulous (without teeth) patient shows fractures of the left angle and the right body of the mandible.

hemorrhage, arteritis, aneurysms, and arteriovenous malformations (AVMs). Imaging appearance. The radiographic evaluation of cerebrovascular disease depends on the symptoms and the most likely diagnosis. For ease of classification, cerebrovascular disease can be divided into three categories: completed stroke, transient ischemic attacks (TIAs), and intracranial hemorrhage. Imaging modalities used today include duplex color-flow Doppler ultrasound (ultrasonography), MR angiography (MRA), CT angiography (CTA), conventional angiography, and digital subtraction angiography (DSA).

Stroke Syndrome

FIGURE 8-48  Le Fort II fracture. Waters’ projection shows a large separated fragment produced by multiple fractures (arrows).

VASCULAR DISEASE OF THE CENTRAL NERVOUS SYSTEM Cerebrovascular Disease The term cerebrovascular disease refers to any process that is caused by an abnormality of the blood vessels or blood supply to the brain. Pathologic processes causing cerebrovascular disease include abnormalities of the vessel wall, occlusion by thrombus or emboli, rupture of blood vessels with subsequent hemorrhage, and decreased cerebral blood flow caused by lowered blood pressure or narrowed lumen caliber. Cerebrovascular diseases include arteriosclerosis, hypertensive

Stroke denotes the sudden and dramatic development of a focal neurologic deficit, which may vary from dense hemiplegia (paralysis on one side of the body) and coma to only a trivial neurologic disorder. The specific neurologic defect depends on the arteries involved. A stroke, also known as an acute brain infarction, most commonly involves the circulation of the internal carotid arteries and is seen with symptoms that include acute hemiparesis (weakness of one side of the body) and dysarthria (difficulty speaking). The purpose of radiographic evaluation in the patient with acute stroke is not to confirm the diagnosis of a stroke but to exclude other processes that can simulate the clinical findings (e.g., parenchymal hemorrhage and subdural hematoma). Although the abrupt onset of a stroke may permit differentiation from other conditions that have a more gradual onset of symptoms, patients with focal neurologic deficits of various causes may initially be found comatose so that the history of gradual onset is not elicited. Clearly, it is essential to exclude an intracranial hemorrhage before considering the possibility of using anticoagulant therapy in a patient with stroke. Imaging appearance. Noncontrast CT (or MRI, if available) is the examination of choice for the evaluation of the patient with stroke. Intravenous contrast material is contraindicated because it is a toxic substance that can cross the disrupted blood–brain barrier in the region of a cerebral infarct

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FIGURE 8-50  Chronic right middle cerebral artery infarct. Low-attenuation region (arrows) shows sharply defined borders and some midline shift. FIGURE 8-49  Acute left middle cerebral artery infarct. CT scan obtained 20 hours after onset of acute hemiparesis and aphasia shows obliteration of normal sulci (arrows) in the involved hemisphere. The gray matter and white matter in the distribution of the left middle cerebral artery demonstrate low density.

and lead to increased edema and a slower recovery for the patient. CT and MRI findings are normal in patients with small infarctions and in the early hours of large infarctions. The initial appearance (within 8 to 24 hours) of a cerebral infarction is a triangular or wedge-shaped area of hypodensity on CT (Figure 8-49) and high signal intensity on T2-weighted MRI sequences involving both the cortex and the underlying white matter down to the ventricular surface. The abnormality is confined to the vascular territory of the involved artery. Although little or no mass effect is evident during the first day, progressive edema produces a mass effect that is maximal 7 to 10 days after the acute event (Figure 8-50). As an infarct ages, brain tissue atrophies, and the adjacent sulci and ventricular system enlarge (Figure 8-51). A combination of nonenhanced MRI and MRA is more sensitive than CT in detecting an infarct or ischemic edema, especially involving the brainstem. Occlusion or stenosis of an artery or vein can be demonstrated along with the associated hemorrhage as a result of ischemic infarction. A diffusion-weighted MR image usually demonstrates a positive hyperintense signal within 2 hours of the incident and plays a critical role in diagnosing and determining the age of the stroke (Figure 8-52). There is only a small window of 2 or 3 hours after the onset of a stroke during which fibrinolytic agents are effective in decreasing the risk of permanent neurologic deficits. A T2-weighted image

FIGURE 8-51  Chronic right middle cerebral artery infarct. Low-attenuation region shows sharply defined borders (arrows) and some dilation of the adjacent ventricle.

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319

A

R

L

FIGURE 8-52  Right middle cerebral artery infarct. Diffusion-weighted MR image shows a high signal intensity involving both the cortex and the underlying white matter down to the ventricular surface.

detects edema sooner than CT and thus is considered more sensitive. In patients with classic stroke symptoms, follow-up CT or MRI is not indicated. Treatment. All patients with stroke are started on bed rest with reduced external stimuli to lower cerebral oxygen demands. Medications may be used to decrease intracranial pressure and intracranial edema. Patients with thrombotic strokes receive anticoagulants and possibly thrombolytic agents.

Transient Ischemic Attacks TIAs manifest as focal neurologic deficits that completely resolve within 24 hours. They may result from emboli originating from the surface of an arteriosclerotic, ulcerated plaque (embolic stroke), which causes temporary occlusion of cerebral vessels, or from stenosis of an extracerebral artery, which leads to a reduction in critical blood perfusion. Because almost two-thirds of arteriosclerotic strokes are preceded by TIAs and the 5-year cumulative risk of stroke in patients with TIAs may be as high as 50%, accurate diagnosis and appropriate treatment are essential. Imaging appearance. The most common location of surgically treatable arteriosclerotic disease causing TIAs is the region of the carotid bifurcation in the neck. In patients with an asymptomatic bruit (a rumbling noise heard by a stethoscope) or an unclear history of a TIA, carotid duplex colorflow Doppler scanning is often the initial screening study (­Figure 8-53). This technique combines high-resolution ultrasound imaging and Doppler ultrasound with spectral analysis into a “duplex” unit that avoids many of the problems associated with each of these modalities used alone. In most cases, carotid duplex scanning, when combined with MRA, can reliably determine whether the extent of the disease is sufficient to warrant more invasive procedures (angiography). Patients with a normal or near-normal carotid duplex scan do not need to undergo more invasive diagnostic procedures for assessment of the carotid bifurcation. Limitations of

FIGURE 8-53  Ultrasound scan of carotid arteriosclerotic occlusive disease. There is severe narrowing (arrow) of the origin of the internal carotid artery (I) by densely echogenic arteriosclerotic plaque (asterisks). C, Common carotid artery; J, jugular vein.

the usefulness of carotid duplex scanning include its extreme operator dependence and the fact that 10% of patients cannot be successfully imaged with carotid duplex scanning because of anatomic factors (extremely high carotid bifurcations and short, thick necks). High-resolution, real-time ultrasound techniques provide hemodynamic information about blood flow velocity. With use of ultrasound techniques, it may be impossible to differentiate a total occlusion of the internal carotid artery from a tiny residual lumen. This is an important clinical distinction because the patient with even a small remaining lumen can undergo a successful carotid endarterectomy (surgical removal of atherosclerotic plaque). Noninvasive MRA provides accurate imaging of the carotid bifurcation and demonstrates narrowing of the vertebral arteries (Figure 8-54). The reconstitution sign (flow gap) confirms a stenosis greater than 60%, indicating advanced disease requiring surgical intervention. Contrast-enhanced MRA also facilitates visualization of the aortic arch and the origins of the carotid and vertebral arteries. Patients with a clear-cut episode of a TIA or a neurologic deficit usually are subjected to an angiographic study for evaluating the carotid arteries. Either intravenous or intra-arterial digital subtraction angiography or selective intra-arterial carotid arteriography can be used to demonstrate TIA-producing stenotic or ulcerative lesions that may be amenable to surgical therapy (Figures 8-55 to 8-57). Angiographic evaluation of the aortic arch and vertebral arteries is infrequently indicated in the evaluation of patients with TIAs because surgery on the origins of the great vessels and posterior circulation is both difficult and not commonly performed and also because of the higher morbidity from arch and vertebral angiograms reported in some studies.

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5

/

FIGURE 8-54  Normal MRA of the carotid artery. The anteroposterior perspective of the neck demonstrates vessels from the subclavian arteries to the origin of the basilar artery, and the bifurcation of the common carotid arteries.

FIGURE 8-55  Normal carotid artery bifurcation. Common carotid arteriogram shows the bulbous origin of the internal carotid artery (solid arrow) and multiple branches of the external carotid artery (open arrows).

Treatment. Accurate diagnosis and appropriate treatment (antiplatelet therapy, anticoagulation therapy, or carotid endarterectomy) are essential to prevent permanent deficits. Thrombolytic agents may also be used.

Intraparenchymal Hemorrhage Aside from head trauma, the principal cause of intraparenchymal hemorrhage (hemorrhagic stroke) is hypertensive vascular disease. Less common causes are rupture of a congenital

FIGURE 8-56  Ulceration of the internal carotid artery. Common carotid arteriogram shows an ulcerated lesion (arrowhead) at the origin of the internal carotid artery, with severe stenosis of the internal carotid (open arrow) and external carotid (black arrow) arteries.

FIGURE 8-57  Occluded internal carotid artery. Intravenous DSA shows occlusion of the left internal carotid artery at its origin (arrowhead).

berry aneurysm and AVM. Hypertensive hemorrhages result in oval or circular collections that displace the surrounding brain and can have significant mass effect. Although they can occur at any location within the brain, hypertensive hemorrhages are most frequent in the basal ganglia, white matter, thalamus, cerebellar hemispheres, and pons. A common complication is rupture of the hemorrhage into the ventricular system or subarachnoid space. Intraparenchymal hemorrhages resulting from congenital berry (saccular) aneurysms are usually associated with subarachnoid hemorrhage and

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FIGURE 8-58  Intracerebral hematoma. Noncontrast CT scan shows a homogeneous, high-density area in the left thalamus. The low-density area (arrowheads) adjacent to the hematoma represents associated ischemia and edema. Hematoma has entered the ventricular system, and a prominent cerebrospinal fluid–blood level can be seen in the dependent lateral ventricle (arrow). Such extension of blood into the ventricular system is an extremely poor prognostic sign. Mass effect due to the hematoma has compressed the third ventricle and the foramen of Monro and has resulted in obstructive enlargement of the lateral ventricles.

tend to develop in regions where these congenital vascular anomalies most commonly occur. They include the sylvian fissure (middle cerebral artery) and the midline subfrontal area (anterior communicating artery). AVMs occur throughout the brain and tend to bleed into the white matter. Imaging appearance. Patients with a suspected intraparenchymal hemorrhage should be evaluated with MRI or noncontrast CT. A fresh hematoma appears on CT as a homogeneously dense, well-defined lesion with a round to oval configuration (Figure 8-58). Hematomas produce ventricular compression and, when large, considerable midline shift and brain herniation. A hematoma that is not homogeneously dense is suggestive of hemorrhage occurring within a tumor, an inflammatory process, or an infarction. As the hematoma ages, its density changes. On CT, after passing through an isodense stage, the hematoma becomes hypodense; by 6 months, it appears as a well-defined, low-density region that is often considerably smaller than the original lesion. Contrast enhancement usually develops around the periphery of a hematoma after 7 to 10 days. On MRI, the preferred study, the high signal intensity within a hematoma (caused by the conversion of normal hemoglobin to methemoglobin) arises

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after a few days and continues for several months (Figure 8-59). Once the methemoglobin is completely converted to paramagnetic hemosiderin, the hematoma demonstrates very low signal intensity on T2-weighted sequences. Arteriography is not indicated in patients with classic hypertensive hematomas. However, arteriography remains the gold standard for those patients in whom an aneurysm or AVM is suspected as the underlying cause of the hematoma. In patients with a suspected aneurysm, it is important to determine the number of aneurysms, which aneurysm has ruptured, the location of the neck of the aneurysm, and the patency of the circle of Willis. Statistically, the largest of multiple aneurysms is the one that has ruptured; it is rare for an aneurysm less than 5 mm in diameter to rupture. Because an aneurysm generally ruptures at its apex, an irregular, multiloculated dome is suggestive of a prior rupture. Spasm in adjacent vessels and adjacent hematomas also assist in identifying which of several aneurysms has bled. Noncontrast CT demonstrates an aneurysm as a slightly hyperdense region. The intravenous injection of contrast material produces a strong uniform enhancement. On MRI, an aneurysm produces a flow void on both T1- and T2-weighted images. Imaging has improved the ability to detect an aneurysm. CTA and MRA can visualize large and medium aneurysms, along with feeding and draining vessels associated with an AVM. However, angiography remains the gold standard for demonstrating abnormalities involving small vessels. In patients younger than 20 years of age, AVM is the most common cause of nontraumatic intraparenchymal hemorrhage. On MRI, a cerebrovascular malformation appears as a mass of vascular structures of varying intensity, depending on whether there is rapid flow (black) or slow flow (white) (Figure 8-60). On CT, the malformation consists of an irregular tangle of vessels (best seen after the intravenous injection of contrast material) and greatly dilated veins draining from the central tangle (Figure 8-61A). Arteriography demonstrates an irregular, racemose tangle of abnormal vessels that are fed by dilated cerebral or cerebellar arteries (Figure 8-61B). There is rapid shunting of blood into dilated, tortuous draining veins. Because of the often multiple sources of blood flow to an AVM, the arteriographic evaluation should include selective injections of contrast material into both internal and external carotid arteries. Treatment. Steroid therapy, especially in nontraumatic hematomas, usually controls the edema that produces much of the mass effect. In cases of hemorrhagic strokes, the first line of treatment consists of stopping the bleeding (i.e., correct any coagulopathy), and the second is to try to prevent a recurrence of bleeding (control blood pressure), and finally surgery is performed to correct pathology (aneurysm or AVM). For aneurysms, surgical placement of a clip at the neck of the lesion is required to close the pouch. AVMs require surgery or neurointerventional procedures.

Subarachnoid Hemorrhage A major cause of subarachnoid hemorrhage (hemorrhagic stroke) is rupture of a berry aneurysm (Figure 8-62). Patients

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CHAPTER 8  Nervous System A

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R

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FIGURE 8-59  Intracerebral brainstem hematoma. High signal intensity demonstrated within the hematoma on image B.

with this condition usually have a generalized excruciating headache followed by unconsciousness. The most common locations for berry aneurysms are the origins of the posterior cerebral and anterior communicating arteries and the trifurcation of the middle cerebral artery. Because of the 20% incidence of multiple aneurysms, the angiographic procedure should include evaluation of the internal carotid and vertebral arteries bilaterally. Imaging appearance. The radiographic procedure of choice is a noncontrast CT scan, which can demonstrate high-density blood in the subarachnoid spaces of the basal cisterns in more than 95% of cases (Figure 8-63). Bleeding may extend into the brain parenchyma adjacent to the aneurysm. Contrast-enhanced CT scans are not indicated in subarachnoid hemorrhage because the surgeon will not operate for a suspected aneurysm without an angiogram, and the patient would thus be exposed to the risk of an excessive load of

contrast material. MRI is relatively insensitive for identifying acute subarachnoid bleeds, but it does demonstrate chronic blood staining of the meninges by a marked hypointensity on T2-weighted images. High-resolution CTA can demonstrate aneurysms larger than 3 mm and is becoming more accepted for presurgical planning. The timing of angiography in subarachnoid hemorrhage depends on the philosophy of the surgeon. Blood in the subarachnoid space is an irritant that causes vasospasm of the vessels of the circle of Willis and the middle cerebral artery. This vasospasm, which can lead to cerebral ischemia and frank infarction, is greatest 3 to 14 days after the acute episode. Treatment. If emergency surgery within the first 72 hours after the hemorrhage is planned, emergency selective angiography is indicated. If surgical intervention is to be delayed, angiography should be postponed until just before surgery.

Summary of Findings for Vascular Disease of the Central Nervous System Disorder

Location

Imaging Appearance

Treatment

Stroke syndrome

Neurologic deficit due to lack of circulation; internal carotid artery most common site

Transient ischemic attack

Embolic stroke originating from arteriosclerotic ulcerated plaque

Bed rest and reduced external stimuli for all stroke victims Medications to treat increased intracranial pressure if symptoms arise Anticoagulants and/or thrombolytic agents to treat cause Surgical endarterectomy

Intraparenchymal hemorrhage

Hemorrhage into brain tissue

Subarachnoid hemorrhage

Bleed beneath arachnoid layer of meninges

CT (initial exam)—a triangular or wedge-shaped hypodensity on noncontrast scan MRI—T2-weighted image produces high signal intensity of vascular territory involved Diffusion-weighted MRI—hyperintense signals within 2 hours of onset CT/MRI—mass effect seen 7–10 days after onset Duplex color-flow Doppler US—provides hemodynamic information including flow velocity (total occlusion vs. tiny residual flow) MRA—size and shape of diseased carotid and vertebral arteries; contrast-enhanced scan shows aortic arch and origins of vessels DSA—invasive study provides the highest resolution of intraluminal vascular pathology CT—new hematoma appears as homogeneously dense, well-defined, round or oval lesion, becoming isodense over time; 6-month-old hematoma appears as a well-defined, low-density lesion MRI—high signal intensity after a few days on T1- and T2-weighted images; with time, a low signal intensity is seen on T2-weighted images CTA/MRA—shows arteriovenous malformations in large and medium vessels and can detect an aneurysm Arteriography—used for small vessels CT—noncontrast scan initially shows high attenuation of blood in the subarachnoid space MRI—best demonstrates chronic hemorrhages as hypointense areas on T2-weighted image CTA—high resolution demonstrates aneurysms greater than 3 mm MRA—shows large and medium vessels for detecting an aneurysm Arteriography—to localize and characterize small-­ vessel anatomy

Steroid therapy Surgical clipping of aneurysm Surgery or neurointerventional procedures to correct arteriovenous malformation

Stop bleeding Prevent recurrence Surgical intervention to correct pathology

CTA, CT angiography; DSA, digital subtraction angiography; MRA, MR angiography; US, ultrasound.

FIGURE 8-60  Arteriovenous malformation. Axial MR image shows large left parietal mass (large arrowheads) consisting of vascular structures of varying intensity, depending on whether there is rapid flow (black) or slow flow (white). Note the greatly dilated vessel (small arrowhead) that feeds the malformation.

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A

FIGURE 8-62  Ruptured berry aneurysm. Left carotid arteriogram demonstrates a left supraclinoid aneurysm of the internal carotid artery. The posterior bulge of the aneurysm (arrow) represents the site of rupture.

B

FIGURE 8-61  Arteriovenous malformation with hemorrhage. (A) CT scan shows an irregular tangle of vessels in the parietal lobe, seen without a contrast injection. (B) In another patient, a carotid arteriogram shows dilated blood vessels constituting an arteriovenous malformation.

MULTIPLE SCLEROSIS Multiple sclerosis is the most common demyelinating disorder; it manifests as recurrent attacks of focal neurologic deficits that primarily involve the spinal cord, optic nerves, and central white matter of the brain. The disease has a peak incidence between 20 and 40 years of age, a strong preponderance in women, and a clinical course characterized by multiple relapses and remissions. Impairment of nerve conduction caused by the degeneration of myelin sheaths leads to such symptoms as double vision, nystagmus (involuntary, rapid movement of the eyeball in all directions), loss of balance and poor coordination,

FIGURE 8-63  Berry aneurysm with subarachnoid hemorrhage. CT scan demonstrates subarachnoid bleed into the cisterns and ventricles (hyperdense) from a ruptured left middle cerebral aneurysm (arrow).

shaking tremor and muscular weakness, difficulty in speaking clearly, and bladder dysfunction. Imaging appearance. MRI is the modality of choice for demonstrating the scattered plaques of demyelination that are characteristic of multiple sclerosis. The plaques appear as multiple areas of increased signal intensity on

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FIGURE 8-64  Multiple sclerosis. (A) Axial T2-weighted MR image in a 35-year-old woman shows characteristic areas of increased signal intensity (arrowheads) in deep white matter. (B) Sagittal image demonstrates periventricular plaques (arrows). (C) Coronal image shows increased intensity of cervical cord plaque (arrow).

T2-weighted images; these areas involve primarily the periventricular white matter, cerebellum, brainstem, and spinal cord (Figure 8-64). Lesions involving the optic nerve or chiasm require contrast enhancement and fat-­ suppression imaging (which increases the contrast difference between fat and water) to improve their detectability. On T1-weighted images, the plaques appear as isointense or hypointense lesions that may have a beveled edge. The use of MRI sequences using fluid-attenuated inversion recovery and fast-spin echo as well as MR spectroscopy aid in determining the extent of the disease. CT shows old inactive disease as well-defined areas of decreased attenuation in the deep white matter and periventricular

regions. In the acute phase, CT performed after intravenous administration of contrast material demonstrates a mixture of nonenhancing focal areas of decreased density (representing old areas of demyelination) and enhancing regions that represent active foci. Treatment. As the disease progresses and the symptoms increase in severity, immunosuppressive agents may help limit the autoimmune attack. Antiviral drugs may slow the progress of the disease. To reduce the number and severity of attacks, some patients receive subcutaneous injections of disease-modifying immunomodulatory agents (interferon-β). The treatments can only aid in slowing the progress of multiple sclerosis; however, there is no cure.

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Summary of Findings for Multiple Sclerosis Disorder

Location

Imaging Appearance

Treatment

Multiple sclerosis

Most common demyelinating disorder of the CNS

MRI—plaques appear as a hyperintense signal on T2-weighted images and isointense to hypointense, possibly with beveled edges, on T1-weighted images MRI with contrast enhancement and fat suppression best demonstrates plaques involving the optic nerve and chiasm MRI—FLAIR imaging, fast-spin echo imaging, and MR spectroscopy—aid in determining extent of disease

Immunosuppressive agents Antiviral drugs Subcutaneous injections of interferon-β

CNS, Central nervous system; FLAIR, fluid-attenuated inversion recovery.

EPILEPSY AND CONVULSIVE DISORDERS Epilepsy is a condition in which brain impulses are temporarily disturbed, resulting in a spectrum of symptoms ranging from loss of consciousness for a few seconds to violent seizures (shaking and thrashing movements of all extremities). Although most cases of epilepsy are idiopathic, the disorder can be a result of injury (penetrating or nonpenetrating trauma and depressed skull fracture), birth trauma, or infection. The mildest type of epilepsy, which occurs primarily in children, is called petit mal. This results in brief episodes of loss of consciousness, which may be associated with mild muscular twitching. Petit mal epilepsy usually disappears in young adulthood. Grand mal epilepsy refers to generalized convulsions in which the patient falls to the floor, hypersalivates (foams at the mouth), and loses control of urine and sometimes feces. In many cases, an approaching seizure is heralded by an aura, such as a ringing in the ears, a tingling sensation in the fingers, or spots before the

eyes. After a seizure, the patient tends to be groggy and unaware of what has happened (i.e., in a postictal state). Imaging appearance. Whenever possible, the radiographic evaluation of a patient with a seizure disorder should be performed when the patient is clinically stable. The appropriate procedure is MRI to search for an unsuspected brain tumor, AVM, or hippocampal sclerosis (Figure 8-65). Hippocampal sclerosis (mesial temporal sclerosis) refers to neuronal loss and gliosis that occur in the temporal region. High-resolution, thin-section, coronal T2-weighted images are the most specific for diagnosis of this disorder. It is the most common cause of seizures that do not respond to medical therapy. Because most seizure disorders are attributable to small areas of cortical brain injury resulting from trauma or infarction, CT or MRI findings are usually normal. If the MRI findings are normal, PET using 18F-fluorodeoxyglucose (18F-FDG-PET) may localize the seizure focus in a patient with hippocampal sclerosis. PET has a 70% to 80% sensitivity and a very low rate of false-positive results (Figure 8-66).

Summary of Findings for Epilepsy and Convulsive Disorders Disorder

Location

Epilepsy and convulsive disorders

Brain impulses temporarily disrupted

Imaging Appearance MRI—high-resolution, thin-­section T2-weighted image is most specific PET—localizes seizure foci

Treatment Stabilize patient for safety Reverse chemical causes Medications to decrease number of seizures Surgical resection

PET, Positron emission tomography.

A

B

FIGURE 8-65  Seizure disorder caused by hippocampal sclerosis. (A) Coronal T2-weighted MR image shows high-intensity signal in the left hippocampal region (arrow). (B) Image in a normal patient for comparison.

CHAPTER 8  Nervous System Treatment. For the patient who has an acute seizure, initial efforts are directed toward stabilizing the patient (securing adequate ventilation and perfusion) and stopping the seizure. Subsequently, a careful history, physical examination, and appropriate laboratory studies should be performed to exclude reversible chemical causes of seizures, such as hypoglycemia, hyponatremia (decreased concentration of sodium in the blood) or hypernatremia, and hypocalcemia or hypercalcemia. If the patient shows no response to routine anticonvulsive treatment, CT may be indicated to search for causes of an acute seizure disorder (e.g., subdural hematoma and intracerebral hematoma), which may be amenable to surgical intervention. These conditions can be adequately assessed with a noncontrast CT scan; plain skull radiographs are not required. Medications may help decrease the number of seizures a patient experiences. Surgical resection of the lesion is associated with a very good outcome.

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in the periventricular regions on CT scans and high signal intensity on T2-weighted MR images (Figure 8-68).

Alzheimer’s Disease Alzheimer’s disease (presenile dementia) is a diffuse form of progressive cerebral atrophy that develops at an earlier age than the senile period.

DEGENERATIVE DISEASES Normal Aging During normal aging, a gradual loss of neurons results in enlargement of the ventricular system and sulci (Figure 8-67). Imaging appearance. Demyelination, which is also a part of normal aging, leads to the development of low density

FIGURE 8-67  Normal aging. CT scan of 70-year-old man shows generalized ventricular dilation with prominence of sulci over the surfaces of the cerebral hemisphere. A

B

FIGURE 8-66  Epilepsy. (A) In a patient with a history of epileptic seizures (ictal phase), FDG–PET brain images demonstrate an area of increased activity: the highlighted region in the posterior portion of the cerebrum (arrow). (B) The interictal phase (postseizure activity phase in the same patient) illustrates decreased activity in the temporal lobe (arrow) resulting from reduced blood flow during the seizure.

FIGURE 8-68  Degenerative changes of aging. Axial MR image demonstrates multiple areas of increased signal intensity around the ventricles and in the deep white matter, consistent with cerebral ischemia or infarction.

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Imaging appearance. CT and MRI demonstrate nonspecific findings of cerebral atrophy, including symmetrically enlarged ventricles with prominence of the cortical sulci (Figure 8-69). T2-weighted MR images show periventricular hyperintensities. FDG–PET metabolic brain imaging used in conjunction

with automated brain mapping can help distinguish changes associated with progressive neurodegenerative processes, such as Alzheimer’s dementia. When this map is superimposed on an Alzheimer’s database, areas of significantly reduced glucose metabolism correspond with Alzheimer’s regions (Figure 8-70). Treatment. Diet, education, memory aids, and safety issues may slow the progression of dementia, but there is no cure at this time. Medications available today help to slow the progression of the disease and may reverse early symptoms to some degree.

Huntington’s Disease

FIGURE 8-69  Alzheimer’s disease. Noncontrast CT scan of a 56-year-old woman with progressive dementia shows generalized enlargement of the ventricular system and sulci.

A

Huntington’s disease is an inherited (autosomal dominant) condition that predominantly involves men and appears in the early to middle adult years as dementia and typical choreiform movements (involuntary movements that are rapid, jerky, and continuous). Imaging appearance. The pathologic hallmark of Huntington’s disease is atrophy of the caudate nucleus and putamen, which produces the typical CT appearance of focal dilation of the frontal horns and a loss of their normal concave shape (Figure 8-71) as a result of caudate nucleus atrophy. Generalized enlargement of the ventricles and dilation of the cortical sulci can also occur. Single-photon emission computed tomography (SPECT) images demonstrate a decrease in glucose metabolism, specifically in the caudate, in comparison with the putamen. On PET scans, a decrease in the dopamine receptor sites provides an opportunity to track the condition before its clinical onset. Treatment. Currently, there is no cure for Huntington’s disease. Treatment with acetylcholinesterase inhibitors increases

B

FIGURE 8-70  Alzheimer’s dementia. (A) FDG–PET metabolic brain images demonstrate significantly reduced glucose metabolism in the left cerebrum on transverse images (arrows). (B) When the brain map was superimposed, the area of reduced uptake (represented by the medium gray area) superimposed the Alzheimer’s control data (represented by the dark gray area [black arrows]). Significantly reduced glucose metabolism can be seen on the patient’s left, a finding consistent with a diagnosis of Alzheimer’s dementia.

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B

FIGURE 8-71  Huntington’s disease. (A) CT scan in a normal patient shows the heads of the caudate nucleus (black arrowheads) producing a normal concavity of the frontal horns (white arrowheads). (B) In a patient with Huntington’s disease, atrophy of the caudate nucleus causes a characteristic loss of the normal concavity (white arrowheads) of the frontal horns.

cognition but does not halt progression of the disease. Counseling is essential because of the hereditary genetic relationship.

Parkinson’s Disease Parkinson’s disease (shaking palsy) is a progressive degenerative disease characterized by stooped posture, stiffness and slowness of movement, fixed facial expression, and involuntary rhythmic tremor of the limbs that disappears with voluntary movement. A disorder of middle or later life, Parkinson’s disease is very gradually progressive and has a prolonged course. The major degenerative changes in nerve cells in Parkinson’s disease occur in the basal ganglia, especially the globus pallidus, the substantia nigra, and the fibers of the corpus striatum. The essence of the condition seems to be an enzyme defect that results in an inadequate production of the neuronal transmitter substance dopamine. The newest method of treatment is the administration of l-dopa, a substance that is converted to dopamine in the brain. Although this drug therapy does not stop the neuronal degeneration, it dramatically improves both the appearance and the behavior of the patient. Imaging appearance. CT scans in patients with Parkinson’s disease often demonstrate cortical atrophy. However, because this condition is usually seen in older individuals, the ventricular enlargement and prominent cortical sulci found on CT scans may be indistinguishable from those caused by the normal aging process. SPECT and PET are the most useful imaging modalities to demonstrate degenerative changes. The basal ganglia have decreased uptake and retention of 18F-DOPA (l-dihydroxyphenylalanine) in cases of Parkinson’s disease.

FIGURE 8-72  Cerebellar atrophy. Sagittal MR image shows dramatic loss of substance of the vermis of the cerebellum (arrows) in a patient with severe alcoholism.

Treatment. Drug treatment is the first choice for controlling symptoms because no cure currently exists. Stereotactic pallidotomy is a surgical option for some cases and may aid in long-term reduction of symptoms by creating lesions that destroy the globus pallidus.

Cerebellar Atrophy Isolated atrophy of the cerebellum may represent an inherited disorder, a degenerative disease, or the toxic effect of prolonged use of such drugs as alcohol and phenytoin (Dilantin) (Figure 8-72).

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Summary of Findings for Degenerative Diseases of the Central Nervous System Disorder

Location

Imaging Appearance

Treatment

Normal aging

Cerebral atrophy, enlarged ventricular system, demyelination Cerebral atrophy before senile period

CT—low-density periventricular regions MRI—high signal intensity of periventricular regions on T2-weighted images

None in normal aging process

CT—cerebral atrophy with enlarged ventricles and prominent cortical sulci MRI—similar to CT; periventricular high-intensity on T2-weighted images PET—reduced glucose metabolism consistent with Alzheimer’s regions CT—focal ventricular dilation; loss of normal shape of frontal horns SPECT—demonstrates a decrease in glucose metabolism, specifically in the caudate, compared with the putamen PET—dopamine receptor sites decrease, providing early onset tracking prior to clinical onset CT—appearance similar to that of normal aging process SPECT/PET—demonstrates degenerative changes in the basal ganglia as decreased uptake and retention of 18F-DOPA MRI—size changes in cerebellum

No cure Diet, education, and safety factors to slow progression Medications to slow progression

Alzheimer’s disease

Huntington’s disease

Atrophy of caudate nucleus and putamen

Parkinson’s disease

Degeneration of basal ganglia

Cerebellar atrophy Amyotrophic lateral sclerosis

Degeneration of cerebellum Upper and lower motor neurons

18F-DOPA, l-Dihydroxyphenylalanine;

CT/MRI/myelography—inconclusive for diagnostic purposes; can demonstrate other causes of similar symptoms

No treatment at present Acetylcholinesterase inhibitors increase cognition but do not halt the disease progression Genetic counseling of families

Drug treatment No cure known Stereotactic pallidotomy

Discontinue prolonged use of drugs (alcohol and phenytoin) Incurable Psychological support Education

PET, positron emission tomography; SPECT, single-photon emission CT.

Amyotrophic Lateral Sclerosis (Lou Gehrig’s Disease) In amyotrophic lateral sclerosis, a relentlessly progressive condition of unknown cause, there is widespread selective atrophy and loss of motor nerve cells leading to extensive paralysis and death from respiratory weakness or aspiration pneumonia. Imaging appearance. Although this disease cannot be diagnosed radiographically, CT, MRI, or myelography is often performed to exclude a spinal malignancy, which could produce a similar clinical appearance. Treatment. Amyotrophic lateral sclerosis is uniformly fatal because there currently is no cure. Psychological support and education can be provided.

HYDROCEPHALUS Hydrocephalus refers to dilation of the ventricular system that is usually associated with increased intracranial pressure. In noncommunicating (obstructive) hydrocephalus, there is an obstruction to the flow of CSF somewhere along the ventricular pathways from the lateral ventricles to the outlets of the fourth ventricle. Enlargement of the lateral ventricles with normal-sized third and fourth ventricles indicates an obstruction at the level of the foramen of Monro. This is most commonly attributable to a colloid cyst (Figure 8-73) or a suprasellar tumor, especially craniopharyngioma. Enlargement of the

FIGURE 8-73  Hydrocephalus with obstruction at the level of the foramen of Monro. T1-weighted MR image shows a hyperintense colloid cyst causing bilateral enlargement of the frontal horns.

CHAPTER 8  Nervous System

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lateral and third ventricles with a normal-sized fourth ventricle indicates an obstruction at the level of the aqueduct of Sylvius (Figures 8-74 and 8-75). The most common causes of this appearance are congenital aqueduct stenosis or occlusion and neoplasm (pinealoma and teratoma). Enlargement of the entire ventricular system (with the fourth ventricle often dilated out of proportion [Dandy–Walker cyst]) indicates an obstruction at the level of the outlet of the fourth ventricle (Figure 8-76), a condition that may reflect congenital atresia, infection, neoplasm, or downward herniation of the cerebellar tonsils through the foramen magnum. In the much more common communicating hydrocephalus, the ventricular fluid passes freely into the extraventricular subarachnoid space. There is generalized ventricular enlargement, and the sulci are normal or absent. Obstruction of the normal CSF pathway distal to the fourth ventricle usually involves the subarachnoid space at the basal cisterns, cerebral convexity, or foramen magnum. Causes include infection (meningitis and empyema), subarachnoid or subdural hemorrhage, congenital anomalies, neoplasm, and dural venous thrombosis. A similar radiographic pattern is seen in normal-pressure hydrocephalus, a syndrome of gait ataxia, urinary incontinence, and dementia associated with ventricular dilation and relatively normal CSF pressure. Imaging appearance. CT clearly shows ventricular di­lation. MRI is more specific than CT in demonstrating the

underlying cause of obstruction or in excluding obstruction (communicating hydrocephalus). Contrast-enhanced MRI may assist in distinguishing a congenital posterior fossa cyst from an enhancing cystic neoplasm. Ultrasound can demonstrate the ventricular dilation either in utero or after birth as long as the sound waves can traverse the open fontanels.

FIGURE 8-74  Hydrocephalus caused by obstruction at the level of the cerebral aqueduct. Dilation of the lateral (L) and third (T) ventricles can be seen in this patient with c­ ongenital hydrocephalus. Symptoms of headache and papilledema resolved after ventricular shunting.

FIGURE 8-76  Hydrocephalus caused by obstruction at the level of the outlet of the fourth ventricle. A huge low-density cyst (a Dandy–Walker cyst) occupies most of the enlarged posterior fossa and represents an extension of the dilated fourth ventricle.

FIGURE 8-75  Aqueductal stenosis. T1-weighted sagittal MR image shows pronounced narrowing of the inferior portion of the aqueduct (arrow). There is flaring of the upper portion of the aqueduct and considerable enlargement of the third and lateral ventricles. Note that the fourth ventricle is of normal size.

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Generalized enlargement of the ventricular system can also be attributed to the overproduction of CSF by a papilloma (Figure 8-77) or by carcinoma arising in the choroid plexus (CSF-secreting vascular tissue in the ventricles). These rare tumors usually occur in the fourth ventricle in adults and the lateral ventricles in children. Treatment. Hydrocephalus can often be treated by the placement of a shunt between the dilated ventricles and the heart or the peritoneal cavity. Successful shunting causes a decrease in the intracranial pressure and ventricular size; the latter can be monitored by CT or MRI. If radiation exposure is of concern (because of patient age or pregnancy), MRI is the modality of choice.

Imaging appearance. Radiographically, acute or chronic sinusitis causes mucosal thickening, which appears as a soft tissue density lining the walls of the involved sinuses (Figure 8-78). The maxillary antra are most commonly affected and are best visualized on the Waters’ projection. An air–fluid level in a sinus is usually considered a manifestation of acute inflammatory disease (Figure 8-79). To demonstrate this finding, it is essential that all sinus images be obtained with the patient erect and with the use of a horizontal beam. The destruction of the bony wall of a sinus is an ominous sign indicating secondary osteomyelitis (Figure 8-80). CT, the procedure of choice, demonstrates bony sinonasal anatomy; coronal images can show air–fluid levels (Figure 8-81). Coronal MRI provides

SINUSITIS The paranasal sinuses (maxillary, ethmoid, frontal, and sphenoid) are paired, air-filled cavities that are lined with a mucous membrane that is directly continuous with the nasal mucosa. The size and shape of the sinuses vary in different age periods, in different individuals, and on the two sides of the same individual. At birth, the maxillary sinus is only a slitlike space that later expands to fill the maxilla and is thus responsible for the growth of the face. The ethmoid sinuses can be seen radiographically by 6 years of age, whereas the frontal sinuses usually are not well demonstrated until approximately 10 years of age. The sphenoid sinuses begin to develop at approximately 2 or 3 years of age and are fully developed by late adolescence. Viral infection of the upper respiratory tract may lead to obstruction of drainage of the paranasal sinuses and the development of localized pain, tenderness, and fever. FIGURE 8-78  Chronic sinusitis. Mucosal thickening appears as soft tissue density (arrows) lining the walls of the maxillary antra.

FIGURE 8-77  Choroid plexus papilloma. T1-weighted MR image shows a lobulated isointense mass (arrows) in a greatly dilated right lateral ventricle.

FIGURE 8-79  Acute sinusitis. Mucosal thickening involves most of the paranasal sinuses, and air–fluid levels (arrows) are present in both maxillary antra.

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FIGURE 8-80  Mucormycosis causing pansinusitis with osteomyelitis. Destruction of the roof of the right orbit and outer margins of the right frontal sinus can be seen.

B

A

C

FIGURE 8-81  Pansinusitis in a 29-year-old woman with headache. Coronal CT scans show fluid in the frontal sinus (A), in the maxillary and ethmoid sinuses (B), and in the sphenoid sinus (C).

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Summary of Findings for Other Diseases of the Central Nervous System Disorder

Location

Imaging Appearance

Treatment

Hydrocephalus

Cerebral ventricular system Paranasal sinuses; maxillary most common

CT—demonstrates ventricular dilation MRI—may also show underlying cause Sinus radiograph—mucosal thickening and fluid levels CT—demonstrates sinonasal anatomy and fluid levels on coronal imaging MRI—suspected complications

Shunt placement

Sinusitis

the best method to detect suspected complications, such as mucocele, osteomyelitis, and underlying intracranial disease. Treatment. Sinusitis caused by bacteria is treated with antibiotics to eradicate the infection. Decongestants may be used

Antibiotics for bacterial infection Decongestants Surgery

to relieve symptoms and aid in sinus drainage. Steroid nasal sprays help reduce mucosal inflammation. Chronic sinusitis may require surgery to clean and drain the sinus and to repair a deviated septum or nasal obstruction that may be the cause of recurrent inflammation.

  REVIEW QUESTIONS 1. The imaging modality of choice to evaluate patients with suspected neurologic dysfunction caused by head trauma is _________________. a. ultrasound b. MRI c. CT d. skull radiographs 2. Arterial bleeding sometimes associated with head trauma can cause _________________ hematomas. a. intracranial b. subdural c. epidural d. acute 3. Venous bleeding sometimes associated with head trauma can cause _________________ hematomas. a. intracranial b. subdural c. epidural d. acute 4. Movement of the brain within the calvaria following blunt trauma to the skull sometimes results in a cerebral _________________. a. subdural hematoma b. epidural hematoma c. acute hematoma d. contusion 5. Bleeding into the ventricular system caused by injury to surface veins, cerebral parenchyma, or cortical arteries can cause _________________ hemorrhage. a. epidural b. subdural c. epiarachnoid d. subarachnoid 6. Plain radiographs of the facial bones should always be made with the patient in the _________________ position if possible. a. supine b. erect c. lateral decubitus d. anterior

7. The most common primary brain tumor is a ________ _________. a. glioma b. glioblastoma c. meningioma d. neurinoma 8. A benign tumor that arises from arachnoid lining cells and is attached to the dura is called a _________________. a. glioma b. glioblastoma c. meningioma d. neurinoma 9. The most common neoplasms that metastasize to the brain arise in the _________________ and ________ _________. a. lung, stomach b. lung, breast c. stomach, breast d. breast, prostate 10. A viral inflammation of the brain and meninges is called _________________. a. meningitis b. hydrocephalus c. encephalitis d. encephalomalacia 11. The best imaging modality to evaluate brain abscesses is _________________. 12. The two imaging procedures of choice to evaluate the extent of a stroke in the brain are _________________ and _________________. 13. The acronym TIA stands for _________________. 14. The imaging modality of choice to demonstrate the plaques of demyelination that are characteristic of multiple sclerosis is _________________. 15. A condition in which brain impulses are temporarily disturbed, the results of which range from loss of consciousness to violent seizures, is termed _________________.

CHAPTER 8  Nervous System 16. A diffuse form of progressive cerebral atrophy that develops at an earlier age than the senile period is called _________________. 17. A progressive degenerative disease characterized by involuntary tremors of the extremities that disappear with voluntary movement is named _________________. 18. Sinus radiographs should be taken using a(n) _______ __________ beam and with the patient in the ______ ___________ position.

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19. The pathologic condition that refers to dilation of the ventricular system and is usually associated with increased intracranial pressure is _________________. 20. If a patient needing facial or sinus radiographs is unable to stand or sit erect, a(n) _________________ using a(n) _________________ beam may be performed to demonstrate any air–fluid levels that may be present.

9 Hematopoietic System OUTLINE Physiology of the Blood Diseases of Red Blood Cells Anemia Polycythemia Treatment of Polycythemias

Diseases of White Blood Cells Leukemia Lymphoma Infectious Mononucleosis

Diseases of Platelets (Bleeding ­Disorders) Hemophilia Purpura (Thrombocytopenia)

leukocytes lymphatic leukemia monocytes myelocytic leukemia neutrophils (polymorphonuclear leukocytes)

pernicious anemia platelets sickle cell anemia spherocytosis thalassemia

KEY TERMS anemia basophil coagulation factors eosinophils erythrocytes hemoglobin

OBJECTIVES After reading this chapter, the reader will be able to: • Define and describe all boldface key terms in this chapter • Describe the physiology of the hematopoietic system

• Identify the basic blood structures on diagrams • Differentiate the various pathologic conditions affecting the hematopoietic system as well as their radiographic manifestations

RADIOGRAPHER NOTES

PHYSIOLOGY OF THE BLOOD

Although the hematopoietic system cannot be directly imaged, many blood disorders result in abnormalities that can be demonstrated radiographically. It may be necessary to increase or decrease exposure factors when imaging patients who manifest advanced stages of these diseases (see Box 1-1). The radiographer must be aware of the severe pain experienced by patients undergoing a sickle cell crisis. Patients with advanced leukemia or lymphoma who have an altered immune status may require protective isolation. Because many hematopoietic system diseases cause significant demineralization of bone, the radiographer must be alert to the possibility of pathologic fracture and thus must exercise caution when moving and positioning patients with these diseases. Radiographers need to be aware of the importance of using proper radiation safety shielding, pelvic shielding for patients, and aprons for technologists to prevent possible lack of blood cell formation in the pelvis, which could ultimately result in anemia.

Blood and the cells within it are vital to life. An adequate blood supply to all body tissues is necessary to bring oxygen, nutrients, salts, and hormones to the cells and to carry away the waste products of cellular metabolism. The components of blood are also a major defense against infection, toxic substances, and foreign antigens. Red bone marrow (found in vertebrae, proximal femurs, and flat bones such as the sternum, ribs, skull, and pelvis) and lymph nodes are the blood-forming tissues of the body. Red blood cells (erythrocytes) and platelets (thrombocytes) (Figure 9-1) are made in red bone marrow, whereas white blood cells (leukocytes) (Figure 9-2) are produced in both red marrow and lymphoid tissue. If a bone marrow puncture is necessary for diagnostic testing, the iliac rim and sternum are good sites. Erythrocytes are biconcave disks without a nucleus that contain hemoglobin, an iron-based protein that carries oxygen from the respiratory tract to the body’s tissues. In a normal

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CHAPTER 9  Hematopoietic System person, there are 4.5 million to 6 million red blood cells in each cubic millimeter of blood. The amount of hemoglobin per deciliter is approximately 14 g in women and 15 g in men. Leukocytes, or white blood cells, normally number from 5000 to 10,000/mm3 of blood (see Figure 9-2). Unlike erythrocytes, there are several types of white blood cells. Neutrophils (polymorphonuclear leukocytes), which make up 55% to 75% of white blood cells, defend the body against bacteria by ingesting these foreign organisms and destroying them (phagocytosis). The number of polymorphonuclear leukocytes in the blood increases enormously in acute infections because the bone marrow rapidly releases into the bloodstream the large numbers of these cells kept in reserve. Eosinophils (1% to 4%) are red-staining cells whose number greatly increases in allergic and parasitic conditions. The third type of leukocyte is the basophil (0% to 1%), which contains granules that stain blue. These three types of cells are formed in the sinusoids of bone marrow, and they, like red blood cells, go through immature stages before reaching the adult form. Lymphocytes represent approximately 25% to 40% of white blood cells. They play a major role in the immune system and aid in the synthesis of antibodies and the production of immunoglobulins. The final type of white blood cell is the monocyte, which is actively phagocytic and plays an important role in the inflammatory process. Monocytes are formed in the bone marrow and represent approximately 2% to 8% of white blood cells. PLATELETS (THROMBOCYTES)

RED BLOOD CELLS (ERYTHROCYTES)

FIGURE 9-1  Red blood cells (erythrocytes) and platelets (thrombocytes).

Platelets, the smallest blood cells, are essential for blood clotting (see Figure 9-1). Normally, there are approximately 150,000 to 400,000 platelets in every cubic millimeter of blood.

DISEASES OF RED BLOOD CELLS Anemia Anemia refers to a decrease in the amount of oxygen-carrying hemoglobin in the peripheral blood. This reduction can be attributable to improper formation of new red blood cells, an increased rate of red blood cell destruction, or a loss of red blood cells as a result of prolonged bleeding. Regardless of the cause, a hemoglobin deficiency causes the anemic person to appear pale. This is best appreciated in the mucous membranes of the mouth and conjunctiva, and in the nail beds. A decrease in the oxygen-carrying hemoglobin impairs the delivery of an adequate oxygen supply to the cells and tissues, leading to fatigue and muscular weakness and often to shortness of breath on exertion (dyspnea). To meet the body’s need for more oxygen, the respiratory rate increases and the heart beats more rapidly.

Iron Deficiency Anemia Iron deficiency is the most common cause of anemia. It most frequently results from chronic blood loss, such as from an ulcer, a malignant tumor, or excessive bleeding during ­menstruation (menorrhagia). Other causes of iron deficiency ­anemia are inadequate dietary intake of iron and increased iron loss caused by intestinal parasites. Iron deficiency anemia also may develop during pregnancy because the mother’s iron supply is depleted by red blood cell development in the fetus. Treatment. If chronic blood loss causes the iron deficiency, the cause must be determined and treated. The first choice of treatment is for the patient to change dietary habits to include more foods rich in iron. The second option is an oral iron supplement: ferrous sulfate. When a patient is taking an iron supplement, it is important to remember that other products influence iron absorption. For example, increasing vitamin C intake enhances iron absorption. Iron deficiency can be treated successfully in most cases.

WHITE BLOOD CELLS (LEUKOCYTES) Granular leukocytes

Basophil

Neutrophil

Eosinophil

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Nongranular leukocytes

Lymphocyte

FIGURE 9-2  White blood cells (leukocytes).

Monocyte

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Hemolytic Anemia The underlying abnormality in hemolytic anemia is a shortened life span of the red blood cells with resulting hemolysis and the release of hemoglobin into the plasma. Most hemolytic anemias are caused by a hereditary defect that may produce abnormal red blood cells or abnormal hemoglobin. Less commonly, hemolytic anemia is acquired and related to circulating antibodies from autoimmune or allergic reactions (e.g., drugs such as sulfonamide) or the malarial parasite. Spherocytosis, sickle cell anemia, and thalassemia are the major hereditary hemolytic anemias. In spherocytosis, the erythrocytes have a circular rather than a biconcave shape, making them fragile and susceptible to rupture. In sickle cell anemia, which is generally confined to African Americans, the hemoglobin molecule is abnormal and the red blood cells are crescentic or sickle shaped and tend to rupture. A defect in hemoglobin formation is also responsible for thalassemia, which occurs predominantly in persons living near the Mediterranean Sea, especially those of Italian, Greek, or Sicilian descent. The breakdown of hemoglobin produces bilirubin, a pigmented substance that is normally detoxified by the liver and converted into bile. The accumulation of large amounts of this orange pigment in plasma causes the tissues to have a yellow appearance (jaundice). Hemolytic anemia of the newborn (erythroblastosis fetalis) can result when the mother is Rh negative and the fetus has Rh-positive blood inherited from the father. Although the fetal and maternal circulations are separate, fetal blood can enter the mother’s blood through ruptures in the placenta that occur at delivery. The mother thus becomes sensitized to the Rh factor of the fetus and makes antibodies against it. Any antibodies reaching the fetal blood through the placenta in future pregnancies cause hemolysis of the fetal red blood cells. The severity of the disease ranges from mild anemia with jaundice to fetal death. Imaging appearance. The hemolytic anemias produce a variety of radiographic abnormalities. Although the radiographic findings are similar in the various types of hemolytic anemia, they tend to be most severe in thalassemia and least prominent in spherocytosis. Extensive marrow hyperplasia, the result of ineffective erythropoiesis and rapid destruction of newly formed red blood cells, causes generalized osteoporosis with pronounced widening of the medullary spaces and thinning of the cortices in long and tubular bones (Figure 9-3). As the fine secondary trabeculae are resorbed, new bone is laid down on the surviving trabeculae, thickening them and producing a coarsened pattern. Normal modeling of long bones does not occur because the expanding marrow flattens or even bulges the normally concave surfaces of the shafts. In the skull, there is widening of the diploic space and thinning or complete obliteration of the outer table. When the hyperplastic marrow perforates or destroys the outer table, it proliferates under the invisible periosteum, and new bone spicules are laid down perpendicular to the inner table. This produces the characteristic hair-on-end appearance of vertical striations in a radial pattern (Figure 9-4).

FIGURE 9-3  Thalassemia. Pronounced widening of medullary spaces with thinning of cortical margins. Note the absence of normal modeling caused by the pressure of expanding marrow space. Localized radiolucencies simulating multiple osteolytic lesions represent tumorous collections of hypoplastic marrow.

FIGURE 9-4  Thalassemia. Lateral projection of the skull demonstrates hair-on-end appearance. Note the normal appearance of the calvaria inferior to the internal occipital protuberance, an area in which there is no red marrow, and poor pneumatization of the visualized paranasal sinuses.

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FIGURE 9-5  Extramedullary hematopoiesis in thalassemia. A lateral projection of the chest demonstrates lobulated posterior mediastinal masses of hematopoietic tissue (arrows) in the lower thoracic region.

Extramedullary hematopoiesis is a compensatory mechanism of the reticuloendothelial system (liver, spleen, and lymph nodes) in patients with prolonged erythrocyte deficiency resulting from the destruction of red blood cells or the inability of normal blood-forming organs to produce them. Paravertebral collections of hematopoietic tissue may appear on chest radiographs as single or multiple, smooth or lobulated, posterior mediastinal masses that are usually located at the lower thoracic levels (Figure 9-5). In sickle cell anemia, expansile pressure of the adjacent intervertebral disks produces characteristic biconcave indentations on both the superior and the inferior margins of the softened vertebral bodies, giving the appearance of fish vertebrae (Figure 9-6A). Another typical appearance is the result

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of the development of localized steplike central depressions of multiple vertebral end plates (Figure 9-6B). This is most often caused by circulatory stasis and ischemia, which retard growth in the central portion of the vertebral cartilaginous growth plate. The periphery of the growth plate, which has a different blood supply, continues to grow at a more normal rate. Bulging of the abnormally shaped red blood cells in sickle cell anemia typically causes focal ischemia and infarction in multiple tissues. Bone infarcts commonly occur in infants and children. They most frequently involve the small bones of the hands and feet, producing an irregular area of bone destruction with overlying periosteal calcification, which may be indistinguishable from osteomyelitis. In older children and adults, bone infarction may initially appear as an ill-­defined lucent area that becomes irregularly calcified. Acute osteomyelitis, often caused by Salmonella infection, is a common complication in sickle cell disease. The resulting lytic destruction and periosteal reaction may be extensive, often involving the entire shaft and multiple bones (Figure 9-7). Radiographically, it may be impossible to distinguish between osteomyelitis and bone infarction without infection (Figure 9-8). Throughout their lives, patients with sickle cell anemia are plagued by recurrent painful crises. These episodes are attributable to recurrent vaso-occlusive phenomena and may appear with explosive suddenness and attack various parts of the body, especially the abdomen, chest, and joints. It is often difficult to distinguish between a painful sickle cell crisis and some other type of acute process, such as biliary colic, appendicitis, or a perforated viscus. In the extremities, a sickle cell crisis may mimic osteomyelitis or an acute arthritis, such as gout or rheumatoid arthritis. The most common extraskeletal abnormality in the hemolytic anemias is cardiomegaly caused by severe anemia and increased cardiac output. The heart has a globular configuration, reflecting enlargement of all chambers. Increased pulmonary blood flow produces engorgement of the pulmonary vessels, giving a hypervascular appearance to the lungs. Pulmonary infarction, pulmonary edema with congestive failure, and pneumonia are frequent complications. Renal abnormalities can be demonstrated by excretory urography in approximately two-thirds of patients with sickle cell disease. A serious complication is renal papillary necrosis (see Figure 6-21), which is probably related to vessel obstruction within the papillae and may produce sinuses or cavity formation within one or more papillae. Treatment. The cause and type of hemolytic anemia must be determined to successfully begin treatment. For spherocytosis, a splenectomy is curative. For sickle cell anemia, no cure currently exists. Therefore, treatment consists of management and control of symptoms. The most invasive treatment, bone marrow transplantation, offers a possible cure. During a crisis, bed rest, maintenance of oxygen levels to prevent sickling, folic acid to aid in red blood cell production, maintenance of fluids to keep electrolyte balance stable, and possible blood transfusion (of packed

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A

B

FIGURE 9-6  Sickle cell anemia. (A) Biconcave indentations on both the superior and the ­inferior margins of the soft vertebral bodies produce a characteristic fish vertebrae appearance. (B) ­Localized steplike central depressions of multiple vertebral end plates.

FIGURE 9-7  Acute osteomyelitis in sickle cell anemia. Diffuse lytic destruction of the proximal humerus can be seen along with extensive periosteal reaction (arrows).

FIGURE 9-8  Aseptic necrosis of the femoral head in sickle cell anemia. Mottled areas of increased and decreased density reflect osteonecrosis without collapse. Trabeculae in the neck and intertrochanteric region are thickened by the apposition of new bone. A solid layer of new bone along the inner aspect of the cortex of the femoral shaft causes narrowing of the medullary canal.

CHAPTER 9  Hematopoietic System red blood cells) are appropriate. In some cases, prophylactic antibiotics are given. Gene therapy requires removing a defective cell, fixing the gene, and replanting the new cell into the bone marrow. This procedure may help manage and control symptoms and, in some cases, may even provide a cure. If an Rh-negative mother delivers or aborts an Rh-positive infant, she is given a vaccine of Rh immunoglobulin within 24 hours to prevent the production of antibodies against the Rh factor. Blood testing to determine whether Rh incompatibility exists is now an essential part of prenatal care. An Rh-positive infant born to an Rh-negative mother receives a blood transfusion within 24 hours after birth.

Megaloblastic Anemia A deficiency of vitamin B12 or of folic acid leads to defective deoxyribonucleic acid (DNA) synthesis and an anemia in which there is a decreased number of red blood cells, although each cell contains the normal amount of hemoglobin. The most common cause of vitamin B12 deficiency is pernicious anemia, in which there is inadequate intrinsic factor secretion related to atrophy of the gastric mucosa. Intrinsic factor acts as a carrier in the small bowel absorption of vitamin B12, which is essential for erythrocyte development. A deficiency of folic acid (and vitamin B12) may also be related to intestinal malabsorption. This in turn may be related to intestinal parasites or bacterial overproduction, especially in patients with stasis of bowel contents, such as in blind loop syndrome and multiple jejunal diverticula. Other causes of megaloblastic anemia include a poor diet, such as strict vegetarianism, in which there are no sources of vitamin B12, and long-term alcoholism, in which no folic acid is available. Imaging appearance. Gastric atrophy is seen radiographically as a tubular stomach with a bald appearance that reflects

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a decrease or absence of the usually prominent rugal folds (Figure 9-9). It must be emphasized, however, that the radiographic findings of atrophic gastritis are often seen in older persons with no evidence of pernicious anemia. Treatment. The treatment of megaloblastic anemia consists of correcting the deficiency of vitamin B12 or folic acid. Vitamin B12 deficiency requires an injection because taking vitamin B12 orally does not reverse the process. Folic acid deficiency can be treated with an oral supplement. If needed, a blood transfusion is given.

Aplastic Anemia A generalized failure of the bone marrow to function (aplastic anemia) results in decreased levels of erythrocytes, leukocytes, and platelets. In addition to anemia, the patient cannot fight infection (a white blood cell function) and has a bleeding tendency (platelet depletion). Causes of aplastic anemia include exposure to chemical agents or drugs, infections, and invasion of the bone marrow by cancer. Treatment. Patient prognosis depends on the severity and duration of the bone marrow aplasia. Regular blood transfusions are generally necessary for survival and to reduce symptoms. Because the patient has a suppressed immune response, preventive antibiotics are sometimes prescribed. Situations exposing the patient to an infection or a viral illness should be avoided. Some clinicians recommend medications to stimulate the bone marrow to produce more blood cells. Bone marrow transplantation is a new technique for treating patients with aplastic anemia. Myelophthisic Anemia Infiltration of bone marrow with nonhematopoietic cells, such as tumor cells, or encroachment on marrow cavities

FIGURE 9-9  Megaloblastic anemia. A patient with chronic atrophic gastritis, which is signified by the tubular stomach with a striking decrease in the usually prominent rugal folds.

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caused by cortical thickening can result in severe myelophthisic anemia and pancytopenia (decreases in red and white blood cells and platelets). Tumors may arise from cells that are normally found in the bone marrow (leukemia, lymphoma, and myeloma), or the marrow may be invaded by extensive metastases to bone (from carcinomas of the breast, prostate, lung, and thyroid). Less common causes of marrow replacement include lipid storage disorders (Gaucher’s disease), osteopetrosis (marble bones), and myelofibrosis. Imaging appearance. Skeletal images may demonstrate lytic or blastic lesions, depending on the progression of metastases. A radionuclide bone scan detects bone marrow abnormalities and skeletal metastases. Magnetic resonance imaging (MRI) can demonstrate the extent of bone marrow infiltration. Treatment. Treatment is focused on the underlying cause of the myelophthisic anemia. A packed red blood cell transfusion is used to treat the anemia and help stabilize the patient.

Polycythemia

FIGURE 9-10  Primary polycythemia. Severe hypoventilation caused by profound obesity causes engorgement of pulmonary vessels. Although cardiomegaly is uncommon in polycythemia, in this case it reflects pronounced elevation of the diaphragm as a result of a huge abdominal girth and some underlying cardiac decompensation.

Primary Polycythemia (Polycythemia Vera) Polycythemia vera is a hematologic disorder characterized by hyperplasia of the bone marrow (neoplastic) that results in increased production of erythrocytes, granulocytes, and platelets. The disease is slowly progressive and produces symptoms associated with increased blood volume and viscosity. Cerebrovascular and peripheral vascular insufficiencies are common, and many patients give a history of some thrombotic or hemorrhagic event during the course of their disease. There is an increased incidence of peptic ulcer disease, and the excessive cellular proliferation often results in increased levels of uric acid with secondary gout and the formation of urate stones. The spleen is often massively enlarged and may be seen as a left upper quadrant mass. Imaging appearance. Increased blood volume in polycythemia vera can lead to prominence of the pulmonary vascular shadows, usually without the cardiomegaly associated with the increased pulmonary vascularity that occurs in patients with congenital heart disease (Figure 9-10). Intravascular thrombosis may cause pulmonary infarctions that appear as focal areas of consolidation or as bands of fibrosis.

findings in congenital hemolytic anemias. Computed tomography (CT) may be used to investigate the kidneys and their function if a suspicion of tumor exists.

Secondary Polycythemia Secondary polycythemia may be the result of long-term inadequate oxygen supply in patients with severe chronic pulmonary disease or congenital cyanotic heart disease, or it may develop in persons living at high altitudes. An elevated hemoglobin concentration may also be caused by certain neoplasms (renal cell carcinoma, hepatoma, and cerebellar hemangioblastoma) that result in an increased production of erythropoietin, which stimulates red blood cell formation. Imaging appearance. Because secondary polycythemia is a compensatory phenomenon, the pulmonary vasculature is normal in appearance and there is no evidence of the disease on chest radiographs. In children with severe secondary polycythemia due to cyanotic heart disease, the skull may show thickened tables and a hair-on-end appearance, similar to the

Leukemia is a neoplastic proliferation of white blood cells. The two major types of leukemia are named for the site of malignancy. Myelocytic leukemia is a cancer of the bone marrow (myelocytes are the primitive white blood cells in bone marrow). In this condition, a huge increase in the number of circulating granulocytes occurs, and the production of red blood cells and platelets is decreased. Lymphatic leukemia is a malignancy of the lymph nodes; in lymphocytic leukemia, the only white blood cells that dramatically increase are lymphocytes. Leukemia may be chronic or acute. Acute lymphocytic leukemia, which has an abrupt onset and progresses rapidly, is the most common form in children. Acute myelocytic leukemia is more common in adults. Chronic leukemias run a more prolonged course and may involve either cell type.

Treatment of Polycythemias Treatment for both primary and secondary polycythemias starts with bloodletting to remove excessive cellular elements. This maneuver improves circulation by lowering blood viscosity and is continued until the hemoglobin and hematocrit levels become normal. Chemotherapy helps lower the platelet count and suppresses production of blood elements by the marrow. For primary polycythemia, clinicians may consider a splenectomy to alleviate painful enlargement of the organ and for patients with repeated episodes of thrombosis causing splenic infarction. Patients who receive these treatments can expect to live approximately 15 to 20 years after their condition is diagnosed.

DISEASES OF WHITE BLOOD CELLS Leukemia

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Summary of Findings for Diseases of Red Blood Cells Disorder

Hemolytic anemias

Location

Imaging Appearance

Treatment

Shortened life span of red blood cells

Sickle cell anemia—­ hemoglobin molecule abnormal; red blood cells crescentic or sickle shaped

Long bones—osteoporosis, widened medullary spaces with thinning of cortices; in later stages: thickened, coarsened trabecular patterns Skull—thinning of outer table; vertical striation results from new bone formation Spine—characteristic biconcave indentations superiorly and inferiorly on vertebral body Chest—cardiomegaly IVU/US—renal papillary necrosis

Spherocytosis—splenectomy curative Rh-negative mother and Rh-positive fetus—blood transfusion for baby and Rh immunoglobulin vaccine for mother Sickle cell anemia—no cure exists Most invasive treatment— bone marrow transplantation offers possible cure Crisis—bed rest, maintenance of oxygen, folic acid, maintenance of fluids, possible blood transfusion

Lack of small bowel absorption of vitamin B12 or folic acid

GI series—tubular stomach with bald appearance (decreased or absence of rugal folds)

Vitamin B12 deficiency ­requires an injection Folic acid deficiency can be treated with an oral ­supplement Possible blood transfusion

Megaloblastic anemia

Polycythemia

Primary (neoplastic)— Chest image—prominent vascular increased production of markings without cardiomegaly erythrocytes, granulocytes, and platelets Secondary (non­neoplastic)— Chest image—normal elevated hemoglobin Skull (of child)—thickened tables, concentration hair-on-end appearance; similar to congenital hemolytic anemia

Bloodletting Chemotherapy Splenectomy

GI, Gastrointestinal; IVU, intravenous urography; US, ultrasound.

Because of the exuberant white blood cell production, there is generally a decrease in the number of circulating red blood cells and platelets. This decrease in red blood cells results in a typical clinical appearance of weakness, shortness of breath, and cardiac palpitations. A decrease in the number of platelets interferes with the blood-clotting mechanism and results in a bleeding tendency. Even though there are more circulating white blood cells than normal, most are immature, and thus the patient becomes highly susceptible to infection. Diffuse infiltration of white blood cells into the spleen and liver may cause massive enlargement of these organs (hepatosplenomegaly). Imaging appearance. In childhood leukemia, radiographically detectable skeletal involvement is extremely common as a result of the infiltration of leukemic cells into the marrow. The earliest radiographic sign of disease is usually transverse radiolucent bands at the metaphyseal ends of the long bones, most commonly about the knees, ankles, and wrists (Figure 9-11). In infancy, this appearance is nonspecific because it also occurs with malnutrition or systemic disease.

The presence of these transverse lucent metaphyseal bands after 2 years of age is strongly suggestive of acute leukemia. As the proliferation of neoplastic cells in the marrow becomes more extensive, actual destruction of bone may occur. This may cause patchy lytic lesions, a permeative moth-eaten appearance, or diffuse destruction with cortical erosion (Figure 9-12). A reactive response to proliferating leukemic cells can cause patchy or uniform osteosclerosis; subperiosteal proliferation incites the formation of periosteal new bone. Diffuse skeletal demineralization may result in vertebral compression fractures. Enlargement of mediastinal and hilar lymph nodes is the most common abnormality on chest radiographs. Diffuse bilateral reticular changes may simulate lymphangitic spread of carcinoma. The nonspecific pulmonary infiltrates seen in patients with acute leukemia are usually attributable to hemorrhage or secondary infection. The radiographic abnormalities in chronic leukemia are often similar to those in the acute disease, although their frequency and degree may vary. Skeletal changes are much

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FIGURE 9-11  Acute leukemia. In addition to radiolucent metaphyseal bands, there is frank bone destruction with cortical erosion involving many metatarsals and proximal phalanges.

less common and are usually limited to generalized demineralization in the flat bones, where active marrow persists in adulthood. The demonstration of focal areas of destruction or periosteal new bone formation indicates probable transformation into an acute phase of the disease. Hilar and mediastinal adenopathy are common, especially in chronic lymphocytic leukemia. Congestive heart failure commonly results from the associated severe anemia. Splenomegaly is an almost constant finding in patients with chronic leukemia (Figure 9-13). Leukemic infiltration of the gastrointestinal tract can produce single or multiple intraluminal filling defects, and the infiltrative process may be indistinguishable from carcinoma. Renal infiltration can cause bilateral enlargement of the kidneys. In chronic lymphocytic leukemia, enlargement of retroperitoneal or mesenteric lymph nodes can cause displacement or obstruction of structures in the genitourinary or gastrointestinal tracts. Treatment. Leukemia treatment may require multidrug chemotherapy, bone marrow transplantation, antibiotics to aid in preventing infections, or a transfusion to reverse the blood cell imbalance. Interferon therapy is a drug regimen to help the body produce antiviral proteins that decrease the production of leukemia cells, resulting in an increase in the effectiveness of the immune system. Stem cell transplantation, although controversial and very expensive, helps

FIGURE 9-12  Acute leukemia. Proliferation of neoplastic cells in the marrow has caused extensive destruction of bone in both femurs.

by increasing the production of normal cells to replace cells damaged or destroyed by radiotherapy and chemotherapy.

Lymphoma Lymphomas are neoplasms of the lymphoreticular system, which includes the lymph nodes, the spleen, and the lymphoid tissues of parenchymal organs, such as the gastrointestinal tract, lung, and skin. They are usually divided into two major types, Hodgkin’s and non-Hodgkin’s lymphomas. Ninety percent of cases of Hodgkin’s disease originate in the lymph nodes; 10% are of extranodal origin. In contrast, parenchymal organs are more often involved in non-Hodgkin’s lymphomas, approximately 40% of which are of extranodal origin. Imaging appearance. Mediastinal lymph node enlargement is the most common radiographic finding in lymphoma (Figure 9-14). It is seen on initial chest radiographs of approximately half the patients with Hodgkin’s disease and approximately one-third of those with non-Hodgkin’s lymphoma. Mediastinal lymph node enlargement is usually bilateral but asymmetric. Involvement of anterior mediastinal and retrosternal nodes is common, a major factor in differentiating lymphoma from sarcoidosis, which rarely produces radiographically visible enlargement of nodes in the anterior compartment. Calcification may develop in intrathoracic lymph nodes after mediastinal irradiation.

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A

A

B

B FIGURE 9-14  Lymphoma. (A) Initial chest image demonstrates considerable widening of upper half of the mediastinum caused by pronounced lymphadenopathy. (B) After chemotherapy, there is a dramatic decrease in the width of the upper mediastinum.

FIGURE 9-13  Chronic leukemia. (A) Massive splenomegaly causes downward displacement of splenic flexure of colon on an upper abdomen image. Arrows point to the inferior margin of the spleen. (B) Indium-111 whole-body scan. Indium-111 tagged to white blood cells illustrates a grossly enlarged spleen on images taken 27 hours after injection.

Involvement of the pulmonary parenchyma and pleura usually occurs by direct extension from mediastinal nodes along the lymphatic vessels of the bronchovascular sheaths. Radiographically, this may appear as a coarse interstitial pattern (Figure 9-15), as solitary or multiple ill-defined nodules, or as patchy areas of parenchymal infiltrate that may coalesce to form a large homogeneous mass. At times, it may be difficult to distinguish a superimposed infection after radiation therapy or chemotherapy from the continued spread of lymphomatous tissue. Pleural effusion occurs in up to one-third

FIGURE 9-15  Lymphoma. Diffuse reticular and reticulonodular changes causing prominence of interstitial lung markings. Note the enlargement of the left hilar region.

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FIGURE 9-16  Lymphoma manifesting as a large mass almost filled by a huge ulcer (arrows).

of patients with thoracic lymphoma. Extension of the tumor to the pericardium can cause pericardial effusion. Approximately 5% to 10% of patients with lymphoma have involvement of the gastrointestinal tract, primarily of the stomach and small bowel. Gastric lymphoma is often seen as a large, bulky polypoid mass, usually irregular and ulcerated, that may be indistinguishable from a carcinoma (Figure 9-16). A multiplicity of malignant ulcers or an aneurysmal appearance of a single huge ulcer (the diameter of which exceeds that of the adjacent gastric lumen) is characteristic of lymphoma. Additional findings suggestive of lymphoma include relative flexibility of the gastric wall, enlargement of the spleen, and associated prominence of retrogastric and other regional lymph nodes that cause extrinsic impressions on the barium-filled stomach. Other manifestations of gastric lymphoma are thickening, distortion, and nodularity of rugal folds (Figure 9-17) and generalized gastric narrowing caused by a severe fibrotic reaction. Lymphoma can produce virtually any pattern of abnormality in the small bowel. The disease may be localized to a single intestinal segment, it may be multifocal, or it may cause diffuse involvement. The major radiographic appearances include irregular thickening of mucosal folds, large ulcerating masses, and multiple intraluminal or intramural filling defects simulating metastatic disease. Skeletal involvement can be demonstrated in approximately 15% of patients with lymphoma (Figure 9-18). Direct extension from adjacent lymph nodes causes bone erosion, especially of the anterior surface of the upper lumbar and lower thoracic spine. Paravertebral soft tissue masses may occur. The hematogenous spread of lymphoma produces a mottled pattern of destruction and sclerosis, which may simulate metastatic disease. Dense vertebral sclerosis (ivory vertebra) may develop in Hodgkin’s disease (Figure 9-19). Diffuse lymphomatous infiltration may cause renal enlargement, with distortion, elongation, and compression of the calyces (Figure 9-20). Single or multiple renal nodules or perirenal masses may displace or distort the kidney. Diffuse

FIGURE 9-17  Lymphoma of the stomach. Note the diffuse thickening, distortion, and nodularity of the gastric folds.

retroperitoneal lymphoma can displace the kidneys or ureters and obliterate one or both psoas margins. Staging. Once the diagnosis of lymphoma is made, it is essential to determine the status of the abdominal and pelvic lymph nodes. This step is necessary both for the initial staging and treatment planning and for assessing the efficacy of treatment and detecting tumor recurrence. Although lymphography was the procedure of choice in the past, MRI and positron emission tomography (PET) are now the noninvasive techniques employed to demonstrate lymphomatous involvement of the abdominal and pelvic

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A

R

L

B

C

D

FIGURE 9-18  Skeletal lymphoma. Right shoulder radiograph and T1-weighted axial MR image demonstrate multiple lytic lesions with a moth-eaten appearance of the scapula (A) (black arrows) and humeral head (B) (white arrow ). The coronal (C) and sagittal (D) PET-CT fusion images appear with increased uptake demonstrating the extent of shoulder girdle involvement.

FIGURE 9-19  Lymphoma. Ivory vertebra.

FIGURE 9-20  Lymphoma. Right kidney is completely replaced by a lymphomatous mass (L). Note the extensive involvement of lymph nodes (M  ).

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nodes. In practice, CT of the chest, abdomen, and pelvis is generally the first imaging procedure used in staging lymphoma, especially non-Hodgkin’s lymphoma, which tends to produce bulky masses in the mesenteric and high retrocrural areas. Abnormal CT scans may eliminate the need for more invasive procedures (Figure 9-21); normal CT scans obtained at 2-cm intervals can exclude retroperitoneal adenopathy with a high degree of confidence. CT is usually used because of standardization and repeatability for patients. Malignant nodes appear round or oval, and their transverse-to-longitudinal ratio is greater than 2. Narrowing or absence of the hilus of the node also suggests malignancy. Ultrasound (ultrasonography) can detect enlarged retroperitoneal nodes, characterize them, and measure them accurately. For retroperitoneal adenopathy, ultrasound is 80% to 90% accurate, and it has the ability to detect extranodal

FIGURE 9-21  Lymphoma. CT scan demonstrates anterior displacement of abdominal aorta (A) away from the spine, caused by lymphomatous involvement of the retroaortic and para-aortic nodes.

disease, which typically produces discrete hyperechoic masses. MRI is considered the superior technique because it can detect subtle detail with the use of multiple sequences. Tumor involvement on T1-weighted MR images appears as a relatively homogeneous mass with a low signal intensity that is similar to that of muscle. Edema, inflammation, immature fibrosis, or granulomatous tissue produces high signal intensity equal to or slightly greater than that of fat on T2-weighted MR images. Gallium scanning may illustrate increased nodal uptake (indicating swelling or inflammation) and can assess the response to treatment and detect early recurrence of tumor tissue. PET using fluorodeoxyglucose (FDG) uptake (FDG– PET) is considered superior to gallium scanning and CT because it can detect microscopic tumor foci and alterations in function within normal-size nodes (see Figure 9-18). PET also has the ability to distinguish large nodes that contain tumor from those that have only benign reactive changes. PET can also be used to monitor the effectiveness of the therapy and to identify tumor recurrence (Figure 9-22). To ensure proper diagnosis and staging of both Hodgkin’s and non-Hodgkin’s lymphomas, biopsies are performed to extract cell and tissue samples. Free-hand fine-needle aspiration biopsy works best for superficial nodes, whereas CT-guided or ultrasound-guided biopsy is required for deep node evaluation. Patients unable to tolerate surgical procedures may undergo a large-needle core biopsy to determine the extent of the disease before treatment is begun. Treatment. The best treatment available for Hodgkin’s lymphoma consists of multidrug chemotherapy and highdose radiation therapy. For non-Hodgkin’s lymphoma, more aggressive chemotherapy is required if the disease process is diffuse (Figure 9-23), whereas conservative chemotherapy is used for low-level disease. Bone marrow transplantation may be necessary.

FIGURE 9-22  Lymphoma in a 16-year-old girl with a 3-week history of supraclavicular adenopathy. The PET body scan demonstrates FDG uptake in the supraclavicular fossae, the mediastinum, and the lungs; this finding indicates a metabolically active neoplasm, which is consistent with the clinically suspected lymphoma.

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Summary of Findings for Diseases of White Blood Cells Disorder

Location

Imaging Appearance

Treatment

Leukemia

Neoplastic proliferation of white blood cells

Multidrug chemotherapy Bone marrow transplantation Antibiotics Blood transfusion

Lymphoma

Neoplasm of lymphoreticular system

Infectious mononucleosis

Viral disease of lymphoreticular system

Skeletal radiograph in child—radiolucent bands at metaphyses on long bones after 2 years of age, bone destruction (moth-eaten appearance with resulting osteosclerosis), possible pathologic fractures Chest image—enlarged mediastinal and hilar lymph nodes, bilateral reticular changes; ­congestive heart failure KUB/US—splenomegaly With organ infiltration there is displacement or obstruction of GI or GU system Chest image—asymmetrical, bilaterally enlarged mediastinal lymph nodes GI series—irregular and ulcerated polypoid mass (multiple ulcers or a huge single ulcer); ­thickening of rugal folds Skeletal radiograph—bone erosion of ­thoracolumbar spine with mottled pattern and sclerosis (ivory vertebra) CT—detects increased node size PET—metabolically active neoplasm Generalized lymphadenopathy and ­splenomegaly

Hodgkin’s lymphoma—multidrug chemotherapy and radiation therapy Non-Hodgkin’s lymphoma— aggressive chemotherapy for ­diffuse disease; conservative ­chemotherapy for low-level disease Bone marrow transplantation

Self-limited—supportive treatment, bed rest, and hydration

GI, Gastrointestinal; GU, genitourinary; KUB, kidney–ureter–bladder radiograph; PET, positron emission tomography; US, ultrasound.

FIGURE 9-23  CT scan of patient with non-Hodgkin’s lymphoma. The patient was diagnosed 8 months earlier with a pancreatic tumor measuring 4 × 6 × 4 cm. After chemotherapy, this scan shows a smaller tumor (3 × 5 × 3 cm) and no mass in the tail.

Infectious Mononucleosis Mononucleosis is a self-limited viral disease of the lymphoreticular system characterized by vague symptoms of mild fever, fatigue, sore throat, and swollen lymph nodes caused by an intense increase of lymphoid cells. The Epstein–Barr

virus may cause this disease process. It primarily infects young adults and, although often termed the “kissing disease,” is not particularly contagious. Blood tests show an elevated white blood cell count with an abnormally high percentage of atypical lymphocytes, which resemble monocytes. The diagnosis is based on the presence of antibodies to the virus in the blood. Imaging appearance. Generalized lymphadenopathy and splenomegaly are characteristic clinical and radiographic findings in infectious mononucleosis. Hilar lymph node enlargement, which is usually bilateral, can be demonstrated in approximately 15% of cases (Figure 9-24). Pneumonia is a rare complication that can appear as a diffuse reticular pattern, indicating interstitial disease, or as a patchy, nonspecific air-space consolidation. Treatment. Because infectious mononucleosis is a self-­ limited disease, the usual treatment involves supportive ­therapy, adequate bed rest, and hydration.

DISEASES OF PLATELETS (BLEEDING DISORDERS) Blood coagulation (clotting) is a complicated mechanism requiring platelets, calcium, and 12 coenzymes and proteins called coagulation factors. A deficiency in quantity or activity of any of these elements may lead to an inability to control hemorrhage or even to spontaneous bleeding.

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CHAPTER 9  Hematopoietic System

A

B

FIGURE 9-24  Infectious mononucleosis. Frontal (A) and lateral (B) projections of the chest demonstrate pronounced enlargement of hilar lymph nodes bilaterally (arrows).

Hemophilia Hemophilia is an inherited (by a sex-linked recessive gene) anomaly of blood coagulation that appears clinically only in males. Patients with this disease have a decreased serum concentration or absence of antihemophilic globulin (factor VIII) and suffer a lifelong tendency to spontaneous hemorrhage or severe bleeding from even minor cuts or injuries. Imaging appearance. The major radiographic changes in hemophilia are complications of recurrent bleeding into the joints, most commonly involving the knees, elbows, and ankles. Initially, the hemorrhage produces a generalized nonspecific soft tissue prominence of the distended joint. Deposition of iron pigment may produce areas of cloudy, increased density in the periarticular soft tissues. Although complete resorption of intra-articular blood may leave no residual change, subsequent episodes of bleeding result in synovial hypertrophy. In chronic disease, the hyperplastic synovium causes cartilage destruction and joint space narrowing and often leads to the development of multiple subchondral cysts of varying sizes in the immediate juxta-articular bone (Figure 9-25A). Destruction of articular cartilage and continued use of the damaged joint lead to subchondral sclerosis and collapse, extensive and bizarre spur formation, and often pronounced soft tissue calcification. Hemorrhage extending into the adjacent bony structures may cause extensive destruction (pseudotumor of hemophilia), which can mimic a malignant tumor (Figure 9-25B). Repeated joint hemorrhages lead to increased blood flow in the region of the epiphysis and growth plate. These structures may ossify prematurely, become abnormally large, or fuse prematurely with the metaphysis. The increased blood flow and atrophy of bone and muscle that may follow an episode of joint bleeding result in severe osteoporosis. Common

signs suggestive of, although not pathognomonic for, hemophilia include widening and deepening of the intercondylar notch of the femur (Figure 9-26) and “squaring” of the inferior border of the patella. Asymmetric growth of the distal tibial epiphysis may result in “slanting” of the talotibial joint. Hemarthrosis can cause occlusion of epiphyseal vessels and result in avascular necrosis. This process most commonly involves the femoral and radial heads, both of which have a totally intracapsular epiphysis and are therefore especially vulnerable to deprivation of their vascular supply from compression by a tense joint effusion. As in the other bleeding disorders, submucosal bleeding into the wall of the gastrointestinal tract may develop in patients with hemophilia. It most commonly involves the small bowel and produces a short or long segment with regular thickening of folds. In the colon, bleeding may produce the thumbprint pattern of sharply defined, finger-like, marginal indentations along the contours of the colon wall. Treatment. Hemophilia is usually treated with transfusions and factor VIII replacement.

Purpura (Thrombocytopenia) Purpura refers to a deficiency in the number of platelets, and it results in spontaneous hemorrhages in the skin, mucous membranes of the mouth, and internal organs. The reduced number of platelets results from decreased production, increased destruction, or splenic sequestration of platelets. In the skin, purpura leads to the development of small, flat, red spots (petechiae) or larger hemorrhagic areas (ecchymoses). Acute idiopathic thrombocytopenic purpura typically involves the sudden onset of severe purpura 1 to 2 weeks after a sore throat or upper respiratory infection in an otherwise

CHAPTER 9  Hematopoietic System

A

351

B

FIGURE 9-25  Hemophilia. (A) Large subchondral cysts about the elbow. (B) Destructive, expansile lesion of the lower tibial shaft.

healthy child. In most patients, the disorder is self-limited and clears spontaneously within a few weeks. Unlike the acute form, chronic idiopathic thrombocytopenic purpura occurs primarily in young women and has an insidious onset with a relatively long history of easy bruising and menorrhagia. This condition is generally considered to be an autoimmune disorder because most patients have a circulating platelet autoantibody that develops without underlying disease or significant exposure to drugs. Purpura can also be a complication of conditions that suppress the bone marrow (aplastic anemia) or infiltrate the bone marrow with tumor cells (leukemia, lymphoma, myeloma, and metastases). Imaging appearance. The radiographic changes caused by either acute or chronic idiopathic thrombocytopenic

purpura primarily involve the gastrointestinal tract. Hemorrhage into the small bowel produces characteristic uniform, regular thickening of mucosal folds in the affected intestinal segment (Figure 9-27). Splenomegaly is commonly present; splenectomy is often required to remove this important site of platelet destruction and major source of platelet antibody synthesis. Treatment. Blood platelet transfusions are being used to increase low platelet counts. Anti–human immunodeficiency virus (anti-HIV) drugs are effective in slowing or stopping the production of autoantibodies that attack the platelets. Drug-induced thrombocytopenia responds well to ­ discontinuation of the offending drug. Virus-induced thrombocytopenia shows improvement following a cure of the infection.

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FIGURE 9-26  Hemophilia. The intercondylar notch is greatly widened, and coarse trabeculae, narrowing of joint space, and hypertrophic spurring can be seen.

FIGURE 9-27  Chronic idiopathic thrombocytopenic purpura. Hemorrhage into the wall of the small bowel causes regular thickening of the mucosal folds.

Summary of Findings for Bleeding Disorders Disorder

Location

Imaging Appearance

Treatment

Hemophilia

Anomaly of blood coagulation

Blood transfusion Factor VIII replacement

Purpura

Deficiency in number of platelets

Joint images—cloudy increased ­density in periarticular soft tissues Chronic—cartilage destruction with joint narrowing, multiple subchondral cysts; widening and deepening of intracondylar notch Small bowel—uniform regular ­thickening of mucosal folds Splenomegaly

Self-limited—spontaneous recovery Drug-induced—discontinuation of drug Virus-induced—improves with cure of infection Splenectomy

  REVIEW QUESTIONS 1. When diseases of the hematopoietic system result in demineralization of bone, the radiographer must be alert to the possibility of _________________. a. patient infection b. self-infection c. pathologic fracture d. syncope 2. Red blood cells are called _________________. a. erythrocytes b. leukocytes c. thrombocytes d. hemoglobin 3. Platelets are called _________________. a. erythrocytes b. leukocytes c. thrombocytes d. lymphocytes

4. White blood cells are called _________________. a. erythrocytes b. leukocytes c. thrombocytes d. pericytes 5. The smallest blood cells, platelets, are essential for what process? a. immunity b. clotting c. carrying oxygen d. fighting infection 6. Lymphocytes play a major role in the ______________ system. a. endocrine b. hematopoietic c. immune d. metabolic

CHAPTER 9  Hematopoietic System 7. Which term refers to a decrease in the amount of ­oxygen-carrying hemoglobin in the blood? a. spherocytosis b. thalassemia c. anemia d. hematopoiesis 8. What type of anemia can cause painful bone infarcts and is generally confined to African Americans? a. spherocytosis b. thalassemia c. sickle cell d. Salmonella 9. A hematologic disorder characterized by an increase in the production of erythrocytes, granulocytes, and platelets is _________________. a. polycythemia vera b. erythrocytosis c. sickle cell anemia d. hemolytic anemia 10. A cancerous disease of the hematopoietic system characterized by an increase in white blood cells is _________________. a. anemia b. thrombocytopenia c. leukemia d. hemophilia

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11. What is the name of an inherited anomaly of blood coagulation? a. sickle cell anemia b. hemophilia c. leukemia d. leukocytosis 12. What pathologic condition consists of a deficiency in the number of platelets resulting in spontaneous hemorrhages in the skin, internal organs, and mucous membranes of the mouth? a. hemophilia b. purpura c. leukemia d. sickle cell anemia

10 Endocrine System OUTLINE Physiology of the Endocrine System Adrenal Glands Physiology of the Adrenal Glands Diseases of the Adrenal Cortex Diseases of the Adrenal Medulla

Pituitary Gland Physiology of the Pituitary Gland Diseases of the Pituitary Gland Thyroid Gland Physiology of the Thyroid Gland Diseases of the Thyroid Gland

Parathyroid Glands Physiology of the Parathyroid Glands Diseases of the Parathyroid Glands Diabetes Mellitus

hyperglycemia hypoactive medullary carcinoma mineralocorticoids papillary carcinoma parathormone

primary hyperparathyroidism primary hypoparathyroidism secondary hyperparathyroidism tertiary hyperparathyroidism thyroxine triiodothyronine

KEY TERMS acromegaly androgens follicular carcinoma gigantism glucocorticoids hyperactive

OBJECTIVES After reading this chapter, the reader will be able to: • Define and describe all boldface terms in this chapter • Describe the physiology of the endocrine system • Identify anatomic structures on both diagrams and images of the endocrine system

• Differentiate the various pathologic conditions affecting the endocrine system and their radiographic manifestations

RADIOGRAPHER NOTES Imaging modalities are used to diagnose both the underlying endocrine disorder and the secondary changes that may occur in various areas of the body. Disorders of the endocrine glands themselves are usually evaluated by ultrasound, computed tomography (CT), magnetic resonance imaging (MRI), and radionuclide scanning, including positron emission tomography (PET). Secondary pathologic manifestations elsewhere in the body are generally evaluated on plain radiographs, for which the routine exposure techniques may have to be altered (see Box 1-1). For example, Cushing’s syndrome causes extensive osteoporosis, which requires a decrease in kilovolts-peak for adequate visualization of the demineralized bones. Also note that patients with this condition can easily sustain pathologic fractures and thus should always be handled with caution.

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PHYSIOLOGY OF THE ENDOCRINE SYSTEM The endocrine system is a biochemical communication network through which several small glands control a broad range of vital body activities. The endocrine glands secrete chemical messengers called hormones, which circulate in the blood and may affect a single target organ or the entire body. Hormones may be proteins (growth hormone), steroids (cortisone), peptides (antidiuretic hormone [ADH]), amino acids (thyroxine), or amines (epinephrine). They range from small to large molecules and have chemical structures of various complexities. The major endocrine glands are the pituitary, adrenal, thyroid, and parathyroid glands. Inadequate (hypoactive) or excess (hyperactive) production of hormones from these endocrine glands can give rise to a wide variety of clinical symptoms and radiographic abnormalities.

CHAPTER 10  Endocrine System

Adrenal gland

355

Capsule Cortex Medulla

Kidney

FIGURE 10-1  Structure of the adrenal gland.

Because hormones are powerful chemicals, it is essential that their circulating levels be carefully controlled. One type of control is called the negative feedback mechanism. In this system, an adequate level of a hormone in the blood automatically stops the release of additional hormone (somewhat like a thermostat). As the blood level of the hormone decreases, the gland is stimulated to secrete more of it. Another control mechanism is the production of two different hormones whose actions are opposite to each other. For example, insulin is secreted by the pancreas when the blood glucose level rises. When the blood glucose level falls below normal, a second hormone, glucagon, is secreted by the pancreas to raise the blood glucose level. Thus, these two hormones are balanced so that a proper blood glucose level is continually maintained.

ADRENAL GLANDS Physiology of the Adrenal Glands Each of the adrenal glands, which are situated at the top of each kidney, consists of an outer cortex and an inner medulla (Figure 10-1). The adrenal cortex secretes several different types of steroid hormones, which can be divided into three general groups. The mineralocorticoids (primarily aldosterone) regulate salt and water balance by controlling sodium retention and potassium excretion by the kidneys. The production of aldosterone is regulated primarily by the secretion of renin from specialized cells (the juxtaglomerular apparatus) in the kidney. Reduced blood volume (as in hemorrhage) causes low blood pressure, which is detected by the juxtaglomerular apparatus and eventually results in increased aldosterone secretion from the adrenal cortex. Glucocorticoids (especially cortisone) regulate carbohydrate metabolism and are under the regulation of adrenocorticotropic hormone (ACTH) from the anterior pituitary

gland. Cortisone also depresses the inflammatory response to almost all forms of injury, thus leading to its use in the treatment of trauma, rheumatoid arthritis, bursitis, and asthma and as an immunosuppressive agent to help limit rejection after organ transplantation. Androgens are sex hormones that tend to masculinize the body, to retain amino acids, and to enhance protein synthesis. These hormones are used both illegally and unwisely by athletes in an attempt to increase body strength. The adrenal medulla secretes epinephrine (adrenaline) and norepinephrine. These fight-or-flight hormones are secreted in stress situations when additional energy and strength are needed. Epinephrine stimulates heart activity, raises blood pressure, and increases the level of blood glucose. By constricting some blood vessels and dilating others, epinephrine shunts blood to active muscles where oxygen and nutrients are urgently needed.

Diseases of the Adrenal Cortex

Cushing’s Syndrome The excess production of glucocorticoid hormones in Cushing’s syndrome may be attributable to generalized bilateral hyperplasia of the adrenal cortex, or it may be a result of a functioning adrenal or even nonadrenal tumor. It can also be the result of the exogenous administration of cortisone. Excess secretion of glucocorticoid hormones mobilizes lipids and increases their level in the blood. This increase produces a characteristic obesity that is confined to the trunk of the body and is associated with a round, moon-shaped face and a pathognomonic fat pad that forms behind the shoulders (buffalo hump). Retention of salt and water results in hypertension. Imaging appearance. Generalized enlargement of the adrenal glands is best demonstrated by CT, which shows

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FIGURE 10-2  Cushing’s syndrome caused by large adrenal adenoma. Nephrotomogram demonstrates a huge suprarenal mass (arrows) causing indentation and downward displacement of left kidney.

thickening of the wings of the adrenal gland; the wings appear to have a stellate or Y-shaped configuration in cross section. Ultrasound can also show diffuse adrenal gland enlargement. Benign and malignant tumors of the adrenal cortex are less common causes of Cushing’s syndrome than is nontumorous adrenal hyperfunction. As a general rule, the larger the adrenocortical tumor and the more abrupt the onset of clinical symptoms and signs, the more likely the tumor is to be malignant (Figure 10-2). However, the differentiation between adenoma and carcinoma may be impossible at the time of histologic examination, and the nature of the tumor may have to be defined by the clinical course alone. Both CT and ultrasound can demonstrate an adrenal tumor (Figure 10-3), but CT is often more valuable because the abundance of retroperitoneal fat may prevent an optimal ultrasound examination. Adrenal venography has been widely used to demonstrate adrenal masses, and it also permits the aspiration of blood samples for assessment of the level of adrenal hormones. Cushing’s syndrome produces radiographic changes in multiple systems. Diffuse osteoporosis causes generalized skeletal demineralization, which may lead to the collapse of vertebral bodies, spontaneous fractures, and aseptic necrosis of the head of the femur or humerus. Widening of the mediastinum as a result of excessive fat deposition sometimes develops in Cushing’s syndrome and can be confirmed by CT. Hypercalciuria caused by elevated steroid values can lead to renal calculi and nephrocalcinosis. Imaging of the sella turcica by conventional tomography or CT is important in the routine assessment of a patient with Cushing’s syndrome. Most patients with nontumorous adrenal hyperfunction are found at surgery to have an intrasellar lesion. It is important to emphasize, however, that small pituitary microadenomas may be present in asymptomatic patients. The modality of choice to detect a functioning microadenoma causing adrenal hyperplasia is ­contrast-enhanced MRI. A pituitary adenoma develops in up

FIGURE 10-3  Cushing’s syndrome caused by functioning cortical adenoma. A 4-cm mass in the left adrenal gland (arrows) can be seen posterior to the tail of the pancreas and anterior to the kidney (K). Arrowhead points to the normal right adrenal gland.

to one-third of patients after adrenal surgery and produces progressive sellar enlargement. For this reason, yearly follow-up sellar tomograms may be indicated after adrenalectomy. Nonpituitary tumors producing ACTH may cause adrenal hyperfunction and Cushing’s syndrome. The most common sites of origin are the lung, thymus, and pancreas; approximately half of these tumors can be demonstrated on chest radiographs. Octreotide scintigraphy (a nuclear medicine examination) detects ectopic ACTH tumors on the basis of increased uptake of tumor cell surface receptors for somatostatin. Treatment. Treatment for Cushing’s syndrome depends on the cause of the excess production of glucocorticoid hormones. Surgical resection is the treatment of choice to eliminate the excess hormone production. Medical suppression of abnormal endocrine stimulation and radiation therapy directed to the hyperfunctioning tumor are alternatives if the tumor is inoperable.

Aldosteronism An overproduction of mineralocorticoid hormones produced by the most superficial layer of the adrenal cortex causes retention of sodium and water and abnormal loss of potassium in the urine. This condition results in hypertension, muscular weakness or paralysis, and excessive thirst (polydipsia). Aldosteronism may be attributable to an adrenocortical adenoma (Conn’s syndrome) or to bilateral hyperplasia of the superficial cortical layer. Aldosteronism may also be the result of renin-secreting tumors, renal artery stenosis, malignant hypertension, and bilateral chronic renal disease. The biochemical assay is the basis for diagnosing aldosteronism, and CT or MRI is used for adrenal identification. Imaging appearance. The role of diagnostic imaging is to demonstrate the location of adenomas that may otherwise be difficult to detect during exploratory surgery. Noncontrast CT, the most widely used imaging modality, demonstrates the small adrenocortical adenoma as a contour

CHAPTER 10  Endocrine System

FIGURE 10-4  Aldosteronoma. Note the small mass (arrow) anterior to the left kidney.

abnormality of the gland (Figure 10-4). With use of CT or MRI, the adrenal gland can be measured quite accurately; the normal adrenal measures 3 to 6 mm thick, 4 to 6 mm long, and 2 to 3 cm wide. However, the scan or image may not demonstrate any abnormal findings. With newer CT scanners, specificity has increased to 75%, and tumors larger than 1 cm can be consistently identified. Adenomas may be isointense or hypointense relative to the liver on T1-weighted MR images. On T2-weighted images, they have slight hyperintensity. Chemical-shift imaging can aid in identifying and characterizing an adrenal mass. In adenomas smaller than 1 cm, nuclear medicine studies using 131I attached with a cholesterol binder can differentiate a normal gland from hyperplasia on the basis of the time course of radionuclide uptake. Early uptake (less than 5 days) in both adrenal glands indicates hyperplasia, whereas unilateral early uptake implies an adrenal adenoma. Adrenal venography with biochemical assay of a sample of adrenal blood is another important technique for localizing aldosteronomas and determining whether the hyperaldosteronism is primary or secondary. Treatment. Hypertension and other clinical manifestations of aldosteronism can be cured by the resection of an adenoma but are little affected by the removal of both adrenal glands in the patient with bilateral hyperplasia. Medical antihypertensive agents, especially long-acting calcium channel blockers, are available if the adenoma is inoperable.

Adrenogenital Syndrome The adrenogenital syndrome (adrenal virilism) is caused by the excessive secretion of androgenically active substances by the adrenal gland. In the congenital form, a specific enzyme deficiency that prevents the formation of androgenic hormones causes continuous ACTH stimulation and bilateral hyperplasia. The elevated levels of androgens result in accelerated skeletal maturation along with premature epiphyseal fusion, which may lead to dwarfism. In women, the syndrome causes masculinization, with the development of hair on the face (hirsutism). The breasts diminish, the clitoris enlarges, and ovulation and menstruation cease.

357

FIGURE 10-5  Adrenogenital syndrome. Caused by a functioning adrenocortical tumor (arrow).

Imaging appearance. Most cases of acquired adrenogenital syndrome are caused by adrenocortical tumors, which can be detected by CT (Figure 10-5), ultrasound, or adrenal venography. CT is currently the imaging modality of choice. Treatment. Surgical resection of a hyperfunctioning tumor with replacement therapy allows normal development. Medical suppression of abnormal stimuli prevents the excessive release of ACTH, allowing female features to develop normally. If not treated, a masculinized woman may require reconstructive surgery.

Hypoadrenalism The clinical manifestations of adrenal insufficiency vary from those of a chronic insidious disorder (easy fatigability, anorexia, weakness, weight loss, and increased melanin pigmentation) to those of an acute collapse with hypotension, rapid pulse, vomiting, and diarrhea. The most common cause of adrenal insufficiency is the excessive administration of steroids. Primary adrenocortical insufficiency (Addison’s disease) results from progressive cortical destruction, which must involve more than 90% of the glands before clinical signs of adrenal insufficiency appear. In the past, Addison’s disease was usually attributed to tuberculosis; currently, most cases reflect idiopathic atrophy, probably on an autoimmune basis. In areas where the disease is endemic, histoplasmosis is an occasional cause of adrenal insufficiency. Imaging appearance. Acute inflammatory disease causes generalized enlargement of the adrenal glands, which can be demonstrated by a variety of imaging techniques (Figure 10-6). MRI can differentiate adrenal masses better than CT, but MRI cannot distinguish a tumor from an inflammatory process. Other radiographic findings occasionally seen in patients with adrenal insufficiency include a small heart and calcification of the cartilage of the ear. Treatment. Corticosteroids produce a fast recovery and must be administered regularly for the patient’s survival. Morbidity and mortality are high without treatment.

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CHAPTER 10  Endocrine System

Adrenal mass

A Kidney

FIGURE 10-6  Adrenocortical insufficiency. Caused by disseminated histoplasmosis. CT scan demonstrates bilateral adrenal enlargement (arrows).

Adrenal Carcinoma Approximately half of adrenal carcinomas are functioning tumors that cause Cushing’s syndrome, virilization, feminization, or aldosteronism. The tumors grow rapidly and are usually large necrotic masses at the time of clinical presentation. Imaging appearance. Ultrasound demonstrates the tumor as a complex mass that may be difficult to separate from an upper pole renal tumor (Figure 10-7). CT demonstrates an adrenal carcinoma as a large unilateral mass with an irregular edge that often contains low-density areas resulting from central necrosis or prior hemorrhage (Figure 10-8) and high-density calcifications. On contrast-enhanced CT, the tumor enhancement is irregular and greatest on the periphery. For adrenal examinations, spiral CT with 3- to 5-cm section reconstructions offers the best resolution and may identify tumors 1 cm or smaller. Because lymphatic and hepatic metastases are common at the time of clinical presentation, CT scans at multiple abdominal levels are necessary to define the extent of the primary tumor and to detect metastases before surgical resection is attempted. Extension of the tumor into the renal vein and inferior vena cava can also be detected by CT, especially after the injection of intravenous contrast material, or by MRI (Figure 10-9). On MR images, the higher signal intensity of the tumor in comparison with the liver on T2-weighted images (lower signal intensity on T1-weighted images) may distinguish adrenal carcinoma from nonfunctioning adenomas and pheochromocytomas. Treatment. The treatment of choice for adrenal carcinoma is surgical resection by open laparotomy or laparoscopy. Chemotherapy using mitotane, an adrenocortical cytotoxin and adrenal inhibitor, may improve symptoms if resection is not an option. Metastases to the Adrenal Gland The adrenal gland is one of the most common sites of metastatic disease. The primary tumors that most frequently metastasize to the adrenal gland are carcinomas of the lung, breast, kidney, ovary, and gastrointestinal tract, and ­melanomas.

B

FIGURE 10-7  Adrenal carcinoma. (A) Ultrasound image identifies a heterogeneous lobulated mass (12 × 7 × 11 cm) involving the upper pole of the left kidney. (B) CT scan 1 month later shows diffuse inhomogeneous enhancement with the appearance of some low-density areas suggesting necrosis.

FIGURE 10-8  Adrenal carcinoma. Large soft tissue tumor (T) invades the anteromedial aspect of the left kidney (K) and the left crus of the diaphragm (arrow).

Imaging appearance. Metastatic enlargement of an adrenal gland can cause downward displacement of the kidney with flattening of the upper pole. Ultrasound and CT ­demonstrate adrenal metastases as solid, soft tissue masses that vary considerably in size and are frequently bilateral (Figure 10-10). However,

CHAPTER 10  Endocrine System the ultrasound (hypoechoic lesions) and CT patterns are indistinguishable from those of primary malignancies of the gland. Therefore, when a known primary tumor exists elsewhere, it is usually assumed that an adrenal mass is metastatic. On MRI, metastases typically have higher signal intensity on T2-weighted images than do benign adenomas, and they also demonstrate increased contrast enhancement on T1-weighted, fat-suppressed images. In-phase and out-ofphase pulse sequences (also known as chemical-shift imaging) are highly accurate for distinguishing between adrenal

359

adenomas and metastases. Lipid-laden adenomas show low signal intensity on out-of-phase images and intermediate to high signal intensity on in-phase images. If necessary, a needle biopsy using ultrasound or CT guidance may be of value to determine whether the adrenal lesion is primary or metastatic. Treatment. The most common form of treatment for adrenal metastases is an adrenalectomy, followed by replacement therapy; however, because metastasis has occurred, the prognosis is unfavorable.

Summary of Findings for Diseases of the Adrenal Cortex Disorder

Location

Imaging Appearance

Treatment

Bilateral adrenal hyperplasia, cortical Adrenal tumor

CT (noncontrast)—thickening of adrenal wings, which appear stellate or in a Y shape US—diffuse adrenal gland enlargement CT—to evaluate sella turcica MRI—detects functioning pituitary microadenoma causing adrenal hyperplasia

Surgical resection for erosive hormone production Medical suppression of endocrine stimulation if tumor is inoperable Radiation therapy if tumor is inoperable

Aldosteronism

Overproduction of mineralocorticoid hormones

Resection of altered adrenal gland Therapeutic option: antihypertensive drugs

Adrenogenital syndrome

Hypoadrenalism

Excessive secretion of androgenically active substances Adrenal insufficiency

CT—locates small adrenocortical adenoma as a contour abnormality of the gland MRI—lesion is hypointense or isointense to liver on T1-weighted images, and hyperintense on T2-weighted images NM—unilateral early uptake of the affected gland Venography (adrenal)—to acquire material for biochemical assay CT/US—demonstrates underlying adrenal neoplasm or hyperplasia Venography (adrenal)—to acquire material for biochemical assay CT—enlarged or atrophic adrenal glands

Adrenal carcinoma

Tumor of adrenal cortex

Corticosteroids Morbidity and mortality high without treatment Surgical resection Chemotherapy

Adrenal metastases

Adrenal gland

Cushing’s syndrome

NM, Nuclear medicine study; US, ultrasound.

US—complex tabulated mass above upper pole of kidney; homogeneous when small; heterogeneous when large, with central necrosis or hemorrhage CT—irregular mass containing low-density areas often with calcifications; periphery enhances with contrast agent; metastasis also detected MRI—has higher signal intensity than liver on T2-weighted images US/CT—demonstrates type of mass and whether bilateral MRI—metastases have high signal intensity on T2-weighted images; greater contrast enhancement with metastases than with benign adenoma Chemical-shift imaging—lipid-laden adenoma produces low signal intensity on an out-of-phase image US/CT—guided biopsy

Surgical resection Medical suppression Reconstructive surgery if necessary

Adrenalectomy with replacement therapy

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A

B

FIGURE 10-9  Adrenal carcinoma. (A) Axial MR image demonstrates a large left adrenal tumor invading the left renal vein and inferior vena cava (arrow). (B) In another patient, a coronal MR image shows an adrenal mass (A) above the kidney with a tumor thrombus of slightly higher signal intensity filling the inferior vena cava (T).

FIGURE 10-10  Adrenal metastases. Note the huge irregular low-attenuation mass (M) representing adrenal metastasis from oat cell carcinoma of the lung. The left adrenal gland (arrow) is normal. G, Gallbladder; L, liver.

Diseases of the Adrenal Medulla

Pheochromocytoma A pheochromocytoma is a tumor that most commonly arises in the adrenal medulla and produces an excess of

vasopressor substances (epinephrine and norepinephrine), which can cause an uncommon but curable form of hypertension. Approximately 10% of pheochromocytomas are extra-adrenal in origin. Approximately 10% of patients with pheochromocytoma have bilateral tumors, and a similar percentage of pheochromocytomas are malignant. Because in almost all patients the diagnosis of a pheochromocytoma can be made with biochemical tests, radiographic imaging serves as a confirmatory study and as a means of localizing the tumor. Excretory urography, even with nephrotomography, may be of limited value because the kidney is often not displaced even when the adrenal pheochromocytoma is large. Imaging appearance. CT and ultrasound (Figure 10-11) are very useful in the localization of pheochromocytomas. The cross-sectional images not only detail the extent of the adrenal lesion but also define the status of adjacent structures and can demonstrate bilateral or multiple pheochromocytomas, extra-adrenal tumors, and metastases. Pheochromocytomas generally appear as round, oval, or pear-shaped masses, often greater than 3 cm, that are slightly less echogenic than liver and kidney parenchyma on ultrasound and have an attenuation value less than these organs on CT (Figure 10-12). Necrosis, hemorrhage, and fluid levels are common findings in larger lesions. Most extraadrenal pheochromocytomas arise in the abdomen (Figure 10-13); a few are found in the chest or neck. The tumor may be located anywhere along the sympathetic nervous system, in the organ of Zuckerkandl, and in chemoreceptor tissues such as the carotid body and the glomus jugulare, in the wall of the urinary bladder, or even in the kidney or ureter. Masses may displace the ureter or kidney or may appear as filling defects in the bladder. MRI can demonstrate the relationship of the tumor to surrounding structures in the coronal plane (Figure 10-14) and has a higher sensitivity than CT. On T2-weighted spin-echo images, the extreme hyperintensity of the tumor (because of its water content) makes it stand out from the surrounding structures. When CT and MRI findings are inconclusive, a radionuclide scan using meta-iodobenzylguanidine is highly sensitive for localizing ectopic pheochromocytomas, but this agent is not readily available. In patients with pheochromocytomas, the arterial injection of contrast material causes a sharp elevation in blood pressure, which must be controlled by α-adrenergic blocking agents. Therefore, arteriography is hazardous in these patients. Treatment. Surgical removal of the tumor results in stabilizing the blood pressure and curing the hypertension. Most tumors are benign and well encapsulated, enabling their successful removal.

Neuroblastoma Neuroblastoma, a tumor of adrenal medullary origin, is the second most common malignancy in children. Approximately 10% of these tumors arise outside the adrenal gland,

CHAPTER 10  Endocrine System

A

361

B

C

M

FIGURE 10-11  Pheochromocytoma. Longitudinal (A) and transverse (B) ultrasound images show a cystic and necrotic mass superior to the right kidney (note the measuring markers). (C) The mass (M) elevates the inferior vena cava (arrows). The patient’s history of increased heart rate (up to 200 beats per minute) and elevated blood pressure are consistent with a diagnosis of pheochromocytoma.

FIGURE 10-12  Pheochromocytoma. Large, pear-shaped mass (arrows) is shown anterior to left kidney.

primarily in sympathetic ganglia in the neck, chest, abdomen, or pelvis. The tumor is highly malignant and tends to attain great size before its detection. Imaging appearance. Calcification is common in neuroblastoma (occurring in approximately 50% of cases), in contrast to the relatively infrequent calcification in Wilms’ tumor, from which neuroblastoma must be differentiated. Calcification in a neuroblastoma has a fine granular or stippled appearance (Figure 10-15A). Occasionally, there may be a single mass of amorphous calcification. Calcification can also develop in metastases of neuroblastoma in the paravertebral lymph nodes and the liver. Intravenous urography usually demonstrates downward and lateral renal displacement by the tumor mass (Figure 10-16). Neuroblastoma tends to cause the entire kidney and its collecting system to be displaced as a unit, unlike Wilms’

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A

B

FIGURE 10-13  Ectopic pheochromocytoma. (A) Soft tissue mass (arrow) can be seen adjacent to the aorta and in front of the left renal vein. (B) CT scan taken at a higher level demonstrates that both right and left adrenal glands are normal (arrows). L, Liver; S, spleen. A

B

C

FIGURE 10-14  Pheochromocytoma. (A and B) Axial MR images at two levels demonstrate bilateral low-intensity lesions (arrows). (C) Coronal MR image (in a different patient) shows a left suprarenal mass.

A

B

FIGURE 10-15  Neuroblastoma metastatic to bone. (A) Plain image of the upper abdomen shows a diffuse granular calcification within a large primary tumor. (B) Lateral projection of the skull shows similar calcified deposits within a metastatic lesion in the calvaria. Note the sutural widening (arrowhead) consistent with increased intracranial pressure.

CHAPTER 10  Endocrine System

FIGURE 10-16  Neuroblastoma. Nephrotomogram demonstrates downward and lateral displacement of the upper pole of the left kidney.

FIGURE 10-17  Neuroblastoma. Bilateral widening of the paravertebral stripes (arrows) represents metastatic deposits.

tumor, which has an intrarenal origin and thus tends to distort and widen the pelvicalyceal system. Because of its nonionizing character, ultrasound is a superb modality for evaluating abdominal masses in children. A neuroblastoma appears as a solid or semisolid mass that is separate from the kidney. It appears as a poorly defined heterogenic mass, unlike the well-defined and relatively homogeneous Wilms’ tumor. A neuroblastoma is often diffusely hyperechogenic, probably because of necrosis, calcification, and hemorrhage. On contrast-enhanced CT, necrosis and hemorrhage cause the tumor to appear heterogeneous

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FIGURE 10-18  Neuroblastoma. Bone scan performed in a 1-year-old boy with left adrenal neuroblastoma to evaluate for osseous involvement. Temporal bones and orbital zygomatic region demonstrate increased uptake appearing as “raccoon eyes.”

and often lobulated. Because CT can demonstrate evidence of tumor spread to lymph nodes and the sympathetic chain, widening of the paravertebral stripe (also seen on plain images) (Figure 10-17), and metastases to the liver and chest, it has become the most commonly used imaging study to diagnose neuroblastomas. This modality is also used to assess the response to treatment. MRI, which like ultrasound does not use ionizing radiation, may offer a safer approach to demonstrating characteristics typical of tumor tissue. Neuroblastomas usually produce a hypointense signal on T1-weighted images and are hyperintense on T2-weighted images. On contrast-enhanced T1-weighted images, hemorrhage appears as a hyperintense signal. Metastases to bone, liver, and lungs are common in neuroblastoma. Metastases to the skull typically cause spreading of cranial sutures because of plaques of tumor tissue growing along the surface of the brain (Figure 10-18). Bone destruction leads to a granular pattern of osteoporosis that is often associated with thin, whisker-like calcifications coursing outward and inward from the tables of the skull (see Figure 10-15B). Metastases in long tubular bones are often multiple and relatively symmetric and present a permeative destructive pattern. On T2-weighted MR images, bone metastases appear as hyperintense (bright) and heterogeneous signals. Neuroblastomas arising in the chest appear as posterior mediastinal masses. Metastases to the chest most commonly cause asymmetric enlargement of mediastinal nodes; metastases to the pulmonary parenchyma are infrequent. Treatment. Combining surgery, multiple-agent chemotherapy, and radiation therapy for treatment of neuroblastoma has dramatically improved the prognosis to approximately a 90% cure rate. Infants tend to have a more favorable outcome when chemotherapy and surgery are the combined treatment.

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Summary of Findings for Diseases of the Adrenal Medulla Disorder

Location

Imaging Appearance

Treatment

Pheochromocytoma

Adrenal medulla—­ excessive epinephrine and norepinephrine

Surgical resection

Neuroblastoma

Adrenal medullary origin

CT—round, oval, or pear-shaped mass with lower attenuation than liver or kidney parenchyma; larger lesions may manifest as necrosis; hemorrhage and fluid levels may be apparent US—mass shows lower echogenicity than normal liver and kidney parenchyma MRI— has hyperintense signal on T2-weighted spinecho sequences NM meta-iodobenzylguanidine scan—supersensitive for localizing lesions ectopic Radiograph—calcification of tumor; destructive metastatic bone lesions IVU—inferior and lateral kidney displacement US—solid to semisolid mass separate from kidney; poorly defined, heterogeneous mass with irregular hyperechoic areas CT—heterogeneous and lobulated appearance MRI—lesion is hypointense on T1-weighted images; with contrast enhancement, the lesion’s T1 signal becomes hyperintense

Combination treatment: s­ urgical resection, chemotherapy, and radiation therapy

IVU, Intravenous urography; NM, nuclear medicine; US, ultrasound.

PITUITARY GLAND Physiology of the Pituitary Gland The pituitary gland is often called the master gland because the many hormones it secretes control the level of most glandular activity throughout the body. The hormone secretion of the pituitary gland itself is controlled by the hypothalamus. The pituitary is a tiny gland, about the size of a pea, that is suspended from the base of the brain by a slender stalk (infundibulum) and sits in the bony depression of the sella turcica. It is divided into anterior and posterior portions, each of which secretes different hormones (Figure 10-19). The anterior lobe of the pituitary gland secretes growth hormone, thyroid-stimulating hormone (TSH), ACTH, and a group of hormones that affect the sex organs, or gonads. These gonadotropins include follicle-stimulating hormone (FSH) and luteinizing hormone (LH), which regulate the menstrual cycle and secretion of male and female sex hormones, and prolactin, which stimulates the production of milk during pregnancy and after delivery. Growth hormone affects all parts of the body by promoting the growth and development of the tissues. Before puberty, it stimulates the growth of long bones (increasing the child’s height) and the size of such organs as the liver, heart, and kidneys. After adolescence, growth hormone is secreted in lesser amounts but continues to function in promoting tissue replacement and repair. TSH controls the secretion of thyroid hormone, which regulates the body’s metabolism (production and use of energy). ACTH controls the level of activity of the adrenal cortex. The posterior lobe of the pituitary gland (neurohypophysis) produces two hormones: vasopressin (ADH) and oxytocin. ADH increases the rate of reabsorption of water and

electrolytes by the renal tubules, thus decreasing the output of urine and protecting the individual from excessive water loss. Oxytocin causes contraction of smooth muscle, especially in the uterus, and thus strengthens contractions during labor and helps prevent hemorrhage after delivery.

Diseases of the Pituitary Gland

Hyperpituitarism Hyperpituitarism results from an excess of growth hormone produced by a tumor (see Figures 8-21 and 8-22) or generalized hyperplasia of the anterior lobe of the pituitary gland. The development of this condition before enchondral bone growth has ceased results in gigantism; hyperpituitarism beginning after bone growth has stopped produces acromegaly. Generalized overgrowth of all the body tissues is the underlying abnormality in acromegaly. Although the long bones can no longer grow because the epiphyses are closed, the bones of the hands, feet, and face enlarge, and there is excessive growth of soft tissues. Proliferation of cartilage may cause joint space widening, especially of the metacarpophalangeal and hip joints. The slight increase in length of each of the seven articular cartilages for each digit leads to perceptible lengthening of the fingers. Overgrowth of the tips of the distal phalanges produces thick bony tufts with pointed lateral margins. The associated hypertrophy of the soft tissues produces the characteristic square, spade-shaped hand of acromegaly. Degenerative changes develop early and are associated with prominent hypertrophic spurring. Unlike typical osteoarthritis, acromegaly results in joint spaces that remain normal or are even widened. Imaging appearance. Thickening of the heel pads (the soft tissue inferior to the plantar aspect of the calcaneus) to

CHAPTER 10  Endocrine System Hypothalamic neurosecretory cell

S A

P I

Bone

Posterior pituitary

Anterior pituitary Growth hormone (GH)

Antidiuretic hormone (ADH)

Adrenocorticotropic hormone (ACTH)

Adrenal cortex

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Thyroidstimulating hormone (TSH) Gonadotropic hormones (FSH and LH)

Thyroid gland

Oxytocin (OT) Prolactin (PRL)

Uterus smooth muscle

Testis Ovary

Kidney tubules

Mammary glands

Mammary glands

FIGURE 10-19  Pituitary gland and hormones.

FIGURE 10-20  Acromegaly. Prominent thickening of the heel pad measuring 32 mm, which is highly suggestive of acromegaly.

more than 23 mm is highly suggestive of acromegaly (Figure 10-20). However, a similar appearance may also be seen in a patient with obesity, myxedema, or generalized edema. The bones of the skull become thickened and have increased density, often with obliteration of the diploic space. This bone thickening is especially prominent in the frontal and occipital regions, leading to characteristic frontal

bossing and enlargement of the occipital protuberance (Figure 10-21). The paranasal sinuses (especially the frontal) become enlarged, and the mastoid processes are usually overpneumatized. Lengthening of the mandible and an increased mandibular angle produce prognathism, one of the typical clinical features of acromegaly. Thickening of the tongue may lead to slurred speech. Pituitary enlargement causes expansion and erosion of the sella turcica (Figure 10-22). In the spine, hypertrophy of cartilage causes an increased width of the intervertebral disk spaces. An increase in the size of the vertebral bodies is best seen on lateral projections. Hypertrophy of soft tissues may produce an increased concavity of the posterior aspect of the vertebral bodies (scalloping) that is most prominent in the lumbar spine (Figure 10-23). Extraskeletal manifestations of acromegaly include visceral enlargement, especially of the heart and kidney; enlargement of the tongue; and calcification of cartilage in the pinna of the ear. Gigantism is manifested as an excessively large skeleton. If hypersecretion of growth hormone continues after epiphyseal closure, the soft tissue and bony changes of acromegaly are superimposed. For diagnosis of the pituitary tumor causing the excessive growth, MRI provides the most exact definition of the sella turcica and the tissue contained within. Its superior sensitivity and multiplanar capabilities make MRI the modality of choice. Thin-section coronal and sagittal T1-weighted

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FIGURE 10-22  Pituitary adenoma causing acromegaly. Ballooning of the sella turcica with downward displacement of the floor is demonstrated.

FIGURE 10-21  Acromegaly. Lateral skull projection demonstrating a thickened frontal bone with characteristic frontal bossing.

spin-echo images permit clear distinction of the sphenoid sinus and carotid artery for surgical planning. After gadolinium injection, normal pituitary tissue enhances more than an adenoma, which appears as a hypoenhancing lesion. Treatment. Surgical resection of the tumor remains the treatment of choice. Even with treatment, any changes or damage in the skeleton will remain unchanged. Radiation therapy or medications to decrease growth hormone levels may provide some relief if resection is not a viable option for the patient.

Hypopituitarism Because the pituitary gland controls the level of secretion of gonadal and thyroid hormones and the production of growth hormone, decreased function of the pituitary gland causes profound generalized disturbances in bone growth and maturation. In children, hypopituitarism typically leads to a type of dwarfism in which the delayed appearance of epiphyseal centers causes the failure of bones to grow normally in length or width. This results in a person who is small in stature and sexually immature, although well proportioned and of normal mentality. In many patients, there is a delay in the eruption of the teeth, which tend to become impacted because their size is not affected. The arrest in the growth of the skeleton occurs during childhood, when the cranial vault is proportionally greater in relation to the facial bones than in the adult. Because this discrepancy remains into adulthood in hypopituitary dwarfism, the relatively large skull may be mistakenly believed to result from hydrocephaly. Hypopituitarism occurring after adolescence results in hypofunction of the thyroid gland, adrenal glands, and gonads but usually causes few radiologic findings. The heart

FIGURE 10-23  Acromegaly. Posterior scalloping (arrows) associated with enlargement of vertebral bodies (especially in anteroposterior dimension).

and kidneys are often small, and calcification or ossification may develop in the articular cartilages. Imaging appearance. MRI is the preferred imaging modality because it has superb sensitivity and can directly image the sellar and parasellar regions in multiple planes. The use of contrast enhancement may help define a microadenoma or detect sarcoidosis in an older patient with Addison’s disease. Treatment. For children, a subcutaneous injection of recombinant growth hormone several times per week during puberty and earlier is recommended to prevent the arrest in growth. Tumor location and type will determine whether surgery is needed. In adults, usually no treatment is required.

CHAPTER 10  Endocrine System Diabetes Insipidus The impaired ability of the kidneys to conserve water in diabetes insipidus results from low blood levels of ADH, reflecting deficient vasopressin release by the posterior lobe of the pituitary gland in response to normal physiologic stimuli. In response to excessive water loss in the urine (polyuria), the body compensates by developing an insatiable thirst (polydipsia). Another type of diabetes insipidus occurs when the kidneys fail to respond to circulating ADH; this is known as nephrogenic diabetes insipidus. It must be stressed that diabetes insipidus is completely unrelated to diabetes mellitus.

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Imaging appearance. On T1-weighted MR images, an absence of signal in the posterior pituitary indicates diabetes insipidus. Severe polyuria can lead to massive dilation of the renal pelves, calyces, and ureters. This dilation probably represents a compensatory alteration to accommodate the huge volume of excreted urine. Treatment. Treatment for diabetes insipidus consists of taking drugs that mimic ADH, delivered most commonly in a nasal spray. For the nephrogenic type, treatment with thiazide diuretics allows the kidney to resorb an increased amount of fluid.

Summary of Findings for Diseases of the Pituitary Gland Disorder

Location

Imaging Appearance

Treatment

Hyperpituitarism

Excessive growth hormone—anterior pituitary

Surgical resection of pituitary tumor

Hypopituitarism

Loss of secretion of any anterior pituitary hormone

Radiograph—widened joints, thickened heel pad, thickened skull tables with frontal bossing, paranasal sinus enlargement, mandibular changes, vertebral enlargement with scalloping, hypertrophy of cartilage MRI—superior sensitivity and multiplanar imaging to evaluate the pituitary gland; after contrast enhancement, adenoma appears as a hypoenhancing lesion on T1-weighted spin-echo images Radiograph—skeletal changes in size; dwarfism MRI—detects pituitary tumor by multiplanar imaging; loss of signal of posterior pituitary on T1-weighted images

Diabetes insipidus

Deficient release of hormones from the posterior lobe of the pituitary

MRI—detection of pituitary tumor by multiplanar imaging as an absence of signal in the posterior pituitary gland

THYROID GLAND Physiology of the Thyroid Gland The thyroid is a butterfly-shaped gland located in the neck at the level of the larynx. It consists of two lobes, one on each side of the trachea, and a connecting strip (the isthmus) that runs anterior to the trachea and connects the lower portions of the two lobes (Figure 10-24). The thyroid lies just below the Adam’s apple, the protrusion formed by the cricoid cartilage of the larynx. Microscopically, the thyroid gland consists of innumerable follicles surrounding a central core of colloid, the storage form of the active material known as thyroxine, which is the only natural iodine-containing substance in the body. The thyroid gland picks up iodine from the bloodstream and combines it with the amino acid tyrosine to synthesize thyroid hormones, which are stored in the gland until released into the bloodstream when stimulated by TSH from the anterior lobe of the pituitary gland. The active hormone, thyroxine, is a small molecule that may contain either three iodine molecules (triiodothyronine [T3]) or four iodine molecules (T4). These substances stimulate cellular metabolism in response to the body’s need for increased energy production. The higher cellular metabolism requires that additional oxygen be circulated to the cells and that more waste materials be removed, which in

Children—subcutaneous injection of growth hormone Adults—usually no treatment required Drugs to mimic antidiuretic hormone

turn requires increased blood flow and greater cardiac output. The increased demand for oxygen stimulates the respiratory center and results in a faster rate and greater depth of breathing. Increased cellular metabolism produces heat, which is dissipated by perspiration and by increased blood flow through dilated vessels in the skin, giving the person a flushed appearance. Thyroid hormone also increases the secretion of digestive juices and the movement of ingested material through the intestinal tract. The release of thyroid hormone is controlled by TSH, which is secreted by the anterior lobe of the pituitary gland. This process is a negative feedback mechanism, in which a high blood level of thyroxine inhibits the anterior pituitary and TSH release, whereas a low level of thyroxine forces the anterior pituitary to release TSH again.

Diseases of the Thyroid Gland

Radioactive Iodine Scanning Scanning after the administration of radioactive iodine is the superior imaging modality for demonstrating both functioning and nonfunctioning thyroid tissue. This technique is used to localize palpable nodules, to determine the function of nodules, to detect nonpalpable lesions (especially in patients with a history of neck irradiation), and to evaluate the extent of residual tissue after surgical or radioisotopic thyroid ablation. Radionuclide

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CHAPTER 10  Endocrine System Epiglottis Hyoid bone

Larynx Superior parathyroid gland

Thyroid gland

Inferior parathyroid glands

Trachea

FIGURE 10-24  Thyroid and parathyroid glands.

FIGURE 10-25  Normal radioactive iodine scan. There is uniform distribution of nuclide activity throughout the thyroid gland.

scanning may be combined with uptake, stimulation, or suppression techniques to better characterize the thyroid lesions. Imaging appearance. The distribution of radioactivity is uniform throughout the normal thyroid gland (Figure 10-25). Diffuse thyroid enlargement without hyperthyroidism most frequently represents a multinodular goiter of Hashimoto’s thyroiditis. In a patient with hyperthyroidism, diffuse thyroid enlargement is suggestive of Graves’ disease. Masses within the thyroid gland appear as hyperfunctioning (“hot”) or poorly functioning (“cold”) nodules. A hot nodule demonstrates greater radionuclide uptake than surrounding thyroid tissue (Figure 10-26). Hot nodules usually represent autonomously functioning thyroid tissue and are rarely malignant, although malignancy is sometimes reported

elsewhere in the same gland. Large hyperfunctioning nodules may completely suppress the remaining thyroid tissue so that only the nodule itself is visualized. An autonomous nodule may eventually develop central hemorrhage or cystic change and evolve into a nonfunctioning (cold) nodule. Cold thyroid nodules contain less radionuclide per unit tissue mass than adjacent normal thyroid tissue (Figure 10-27). Most cold nodules represent poorly functioning adenomas. Thyroid cysts, carcinoma, and thyroiditis can also produce this appearance. In a young patient, the absence of uptake in the region of a solitary cold thyroid nodule is associated with a 10% to 25% probability that the nodule is malignant. Ultrasound can establish the precise location of the palpable mass and determine whether it is within the thyroid or in adjacent tissue. In patients who are at risk because of irradiation of the neck during their youth or because of a family history, but who have no palpable lesion, ultrasound may detect an occult thyroid nodule. Although ultrasound can distinguish a thyroid cyst from the other causes of cold nodules, this modality is of little value in further characterizing noncystic thyroid masses.

Hyperthyroidism Hyperthyroidism results from the excessive production of thyroid hormone, either from the entire gland (Graves’ disease) or from one or more functioning adenomas. Graves’ disease is a relatively common disorder that most often develops in the third and fourth decades and has a strong female predominance. The major clinical symptoms include nervousness, emotional lability, an inability to sleep, tremors, rapid pulse rate (tachycardia), palpitations, excessive sweating, and heat intolerance. Weight loss is common, usually despite an

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FIGURE 10-26  Hyperfunctioning (hot) nodules. Radioactive iodine scans in two patients, with increased uptake representing nodules. Note the variable amount of suppression in the remainder of the thyroid gland. Thyroid cartilage marker

A

B

Suprasternal notch marker

FIGURE 10-27  Nonfunctioning (cold) nodules on radioactive iodine scans in two patients. (A) Uptake within the gland is normal. A cold nodule in the left lobe of the thyroid corresponds to the nodule that was seen on ultrasound. (B) Inhomogeneous right and left lobes demonstrate multiple cold nodules. There is a dominant cold nodule in the inferior left pole.

increased appetite. A characteristic physical finding is exophthalmos, outward protrusion of the eyeball caused by edema in the tissue behind the eyes. Imaging appearance. Radioactive iodine scans in patients with Graves’ disease typically demonstrate diffuse enlargement of the thyroid gland with increased radioiodine uptake (Figure 10-28), which rules out a single toxic adenoma. The extent of increased uptake on the scan helps to determine the dose of radioactive iodine for treatment. In severe cases, high-output cardiac failure may develop along with generalized cardiomegaly and pulmonary congestion. Unilateral or bilateral exophthalmos as a result of Graves’ disease can be demonstrated by CT as thickening of the extraocular muscles. Ultrasound imaging helps determine the size and location of the thyroid (Figure 10-29), and the image can be correlated with the radioactive scans. Treatment. Antithyroid drugs are used to decrease thyroid response. Destruction of thyroid cells by radioactive iodine (131I) or total thyroidectomy results in hypothyroidism.

Hypothyroidism Hypothyroidism can result from any structural or functional abnormality that leads to an insufficient synthesis of thyroid hormone. Hypothyroidism dating from birth (cretinism)

results in multiple developmental abnormalities. Children with cretinism typically have a short stature; coarse features with a protruding tongue, a broad, flattened nose, and widely set eyes; sparse hair; dry skin; and a protuberant abdomen with an umbilical hernia. Adult hypothyroidism has an insidious onset with nonspecific symptoms including lethargy, somnolence (sleeping up to 16 hours a day), constipation, cold intolerance, slowing of intellectual and motor activity, and weight gain despite a decreased appetite. Dry skin; stiff, aching muscles; and a deepening voice with hoarseness often occur. The facial features are thickened, and there is a doughy thickening of the skin (myxedema). Imaging appearance. The major radiographic abnormalities in children with hypothyroidism include a delay in the appearance and subsequent growth of ossification centers and retarded bone age. Skull changes are common and include an increase in the thickness of the cranial vault, underpneumatization of the sinuses and mastoid air cells, widened sutures with delayed closure, and a delay in the development and eruption of the teeth (Figure 10-30). Radiographically, the heart in adults is typically enlarged because of pericardial effusion. Soft tissue thickening is often seen on images of the extremities, and adynamic ileus is a common finding on abdominal radiographs.

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FIGURE 10-28  Hyperthyroidism. Radioactive iodine scans in two patients with Graves’ disease show symmetrically enlarged thyroid glands with homogeneously increased iodine uptake.

T

FIGURE 10-29  Thyroid goiter. Ultrasound image shows a thickened isthmus (arrows) and enlarged bilateral lobes. T, Trachea.

Treatment. If a tumor is the cause of hypothyroidism, a combination of surgery, chemotherapy, and radiation therapy is the treatment of choice. For functional hypothyroidism, the thyroid hormone is replaced with a synthetic product (thyroxine).

FIGURE 10-30  Cretinism. Lateral projection of the skull shows an increased density at the base, small underdeveloped sinuses, and hypoplasia of teeth with delayed eruption. Retardation of facial maturation makes face appear small relative to size of calvaria.

Goiter A goiter is an enlargement of the thyroid gland that does not result from an inflammatory or neoplastic process and is not initially associated with hyperthyroidism or myxedema. A simple (nontoxic) goiter results when one or more factors impair the capacity of the thyroid gland in the basal state to secrete the quantities of active hormones necessary to meet the needs of the body. Because the blood level of thyroid hormone is low, there is nothing to inhibit the anterior pituitary, which continues to secrete TSH, causing the thyroid gland to enlarge. In most cases, there is a sufficient increase in both the functioning thyroid mass and the cellular activity to overcome the mild or moderate impairment of hormone synthesis, permitting the patient to remain metabolically normal although goitrous.

Although goiters were once endemic in areas where there was insufficient iodine in the diet, this situation is now rare because iodine is added commercially to salt and bread. Imaging appearance. On a radioactive iodine scan, a nontoxic goiter usually appears as a symmetric or an asymmetric enlargement of the thyroid gland. Plain radiographs and esophagrams often show the enlarged thyroid gland impressing on or displacing the trachea and esophagus (Figure 10-31). A toxic multinodular goiter may be a consequence of a long-standing nontoxic goiter. In this condition, one or more areas of the gland become independent of TSH stimulation. Radioactive iodine scans most commonly show accumulation of iodine in diffuse but patchy foci throughout the gland (Figure 10-32). Another pattern consists of iodine accumulation in one or more discrete nodules within

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371

A

FIGURE 10-31  Goiter. Greatly enlarged thyroid gland appears as a soft tissue mass impressing the trachea (arrows) and displacing it to the left.

B

FIGURE 10-33  Multinodular goiter. (A) Ultrasound image demonstrates solid nodular lesions (8 × 15 mm) in both lobes of the thyroid (left lobe shown here). (B) The Doppler image demonstrates increased vascularity.

FIGURE 10-32  Multinodular goiter. Radioactive iodine scan shows patchy uptake of the nuclide caused by increased and decreased uptake by the thyroid.

the gland, with the remainder of the gland being essentially nonfunctional. Ultrasound is indicated to determine whether a nonfunctioning mass detected on a radioactive iodine scan is cystic or solid (Figure 10-33). Ultrasound may be used to monitor growth of thyroid nodules. CT or MRI is employed only when there is a substernal thyroid that cannot be seen with ultrasound. Treatment. The first-line treatment of small goiters is to control the nodule size with oral thyroxine. If the goiter continues to enlarge, the thyroid is surgically resected to relieve the compression of anatomic structures in the neck (trachea and esophagus).

Benign Thyroid Adenomas Benign thyroid adenomas are encapsulated tumors that vary greatly in size and usually compress adjacent tissue. They may be located within the neck, where they tend to cause deviation or compression of the trachea, or they may extend substernally and appear as masses in the superior portion of the anterior mediastinum.

Imaging appearance. Calcification may develop within the mass of a thyroid adenoma (Figure 10-34). These tumors can appear as hot or cold nodules on radionuclide imaging, depending on their functional capacity. Ultrasound usually demonstrates an adenoma as a solid mass with a consistent echogenicity. There is often a thick and smooth peripheral hypoechoic halo caused by the fibrous capsule and blood vessels. Cystic lesions as small as 2 mm and solid lesions of 3 mm can be visualized.

Thyroid Carcinomas The three major types of thyroid carcinomas are papillary, follicular, and medullary. Papillary carcinoma, the most common type, has peaks of incidence in adolescence and young adulthood and again in later life, during the third to fifth decades. The tumor is usually slow growing and cystic, and it typically spreads to regional lymph nodes, where it may remain silent for many years. Distant metastases to the lungs are rare and often cause only mild, nonspecific thickening of bronchovesicular markings, although the metastases may also appear as miliary and nodular densities that predominantly involve the lower lobes. Follicular carcinoma has a histologic appearance that closely mimics that of normal thyroid tissue. Typically

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FIGURE 10-34  Thyroid adenoma. Lateral projection of the neck shows a huge calcified thyroid mass.

FIGURE 10-35  Thyroid carcinoma. Radioactive iodine scan shows a solitary cold nodule that corresponds to the patient’s palpable mass.

(in approximately 75% of cases), this tumor occurs in women older than 40 years of age. The tumor usually undergoes early hematogenous spread, especially to the lung and bone. Skeletal metastases, which may be the initial manifestation, tend to produce entirely lytic, expansile destruction that extends into the soft tissues and is associated with little or no periosteal reaction. Medullary carcinoma is the least common type of thyroid malignancy. At least 10% of the cases are familial, most often appearing as a component of a syndrome in which there are multiple endocrine tumors. Dense, amorphous calcifications can often be seen within the tumor. Medu­llary carcinomas readily metastasize via the lymphatic channels. There is a substantially increased risk of thyroid cancer in persons with a history of therapeutic neck irradiation in childhood. In the past, such irradiation was used for benign disease, such as enlargement of the tonsils, adenoids, and thymus; middle ear disease; and a variety of skin disorders, including acne. Imaging appearance. On radioactive iodine scans, thyroid carcinoma usually appears as a solitary cold nodule that corresponds to a palpable mass (Figure 10-35). The finding of a nodule that is functioning (hot) essentially excludes a diagnosis of thyroid carcinoma. On ultrasound, 90% of papillary carcinomas appear as solid hypoechoic masses that may contain microcalcifications, which appear as tiny hyperechoic foci (Figure 10-36). Follicular carcinomas, which have similar tissue consistency, cannot be distinguished from adenomas unless they demonstrate irregular tumor margins and a thick irregular halo (Figure 10-37). Color Doppler imaging commonly shows a tortuous or disordered blood vessel arrangement. Medullary carcinomas appear similar to papillary carcinomas, with bright echogenic foci caused by calcifications.

A

B

FIGURE 10-36  Ultrasound images of a complex thyroid mass. (A) The mass has solid components and intercystic septations of various thicknesses. (B) Echogenic foci with shadowing are evident (arrows). Together with the radioactive iodine scan, which showed a cold nodule, these findings suggest a malignant lesion.

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CHAPTER 10  Endocrine System

A

B

FIGURE 10-37  Degenerative follicular adenoma. (A) Radioactive iodine scan shows a prominent cold nodule. (B) Ultrasound illustrates a lesion that is not smooth (note papillary projections, arrow) and that lacks back wall enhancement. These features most often indicate a degenerative follicular adenoma.

MRI and CT demonstrates a substernal thyroid that ultrasound cannot detect because of bone interference. MRI may aid in defining the extent of the neoplasm.

Treatment of Thyroid Tumors Thyroid adenoma treatment may be as simple as observation or as complex as a surgical lobectomy. Drug therapy options include TSH suppression and radioactive iodine. Appropriate treatment depends on the size and location of the thyroid adenoma.

Thyroidectomy is the first choice of treatment for thyroid carcinomas, especially for papillary carcinomas. Approximately 80% of patients survive longer than 10 years. If the patient cannot undergo surgery, alternative choices are suppressive drugs and chemotherapy with radioactive iodine, which may result in hypothyroidism. For patients with follicular carcinoma and widespread metastases, radioactive iodine treatment is the best treatment.

Summary of Findings for Diseases of the Thyroid Gland Disorder

Location

Imaging Appearance

Treatment

Hyperthyroidism

Excessive hormone production

NM—diffuse enlarged thyroid with increased uptake

Hypothyroidism

Insufficient synthesis of thyroid hormone

Goiter

Enlarged ­thyroid gland

Imaging not used for diagnosis Radiograph—retarded bone age; increased skull thickness with widened sutures and delayed suture closure Chest image (in adult)—enlarged heart with pericardial effusion NM—enlargement of thyroid gland Esophagram—thyroid gland impresses or displaces trachea and esophagus

Benign thyroid adenomas

Encapsulated tumor

Antithyroid drugs Radioactive iodine Partial or total resection of thyroid Replacement therapy If caused by tumor— surgery, radiation therapy, and chemotherapy Thyroxine to manage goiter size Resection of enlarged portion of thyroid Observation Lobectomy Drug therapy

Thyroid carcinomas

Papillary, follicular, or medullary

NM, Nuclear medicine study; US, ultrasound.

Radiography—calcification NM—hot or cold nodule US—solid homogeneous mass with peripheral hypoechoic halo NM—solitary cold nodule US—papillary carcinoma appears as a solid hypoechoic mass with hyperechoic foci; follicular carcinoma has irregular tumor margins and a thick irregular halo Color Doppler—tortuous or disordered blood vessel arrangement; medullary carcinomas appear similar to papillary carcinomas with bright echogenic foci MRI/CT—demonstrates substernal thyroid and may aid in defining the extent of the neoplasm

Thyroidectomy Suppressive drugs Chemotherapy with radioactive iodine Radiation therapy

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FIGURE 10-38  Hyperparathyroidism. Subperiosteal bone resorption can be seen that predominantly involves the radial margins of the middle phalanges of the second, third, and fourth digits (arrows). Note also resorption of the terminal tufts.

PARATHYROID GLANDS Physiology of the Parathyroid Glands The parathyroids are four tiny glands, two on each side, that lie behind the upper and lower poles of the thyroid gland (see Figure 10-24). They secrete parathormone (parathyroid hormone [PTH]), which is responsible for regulating the blood levels of calcium and phosphate. Parathormone raises a low serum calcium level by three mechanisms. First, it increases the amount of calcium absorbed from the intestinal tract by interaction with ingested vitamin D. Second, the hormone prevents a loss of calcium through the kidneys and releases calcium from bones by stimulating osteoclastic activity. Third, serum phosphate levels are reduced.

Diseases of the Parathyroid Glands

Hyperparathyroidism Excessive secretion of parathormone leads to a generalized disorder of calcium, phosphate, and bone metabolism that results in elevated serum values of calcium and phosphate. Primary hyperparathyroidism may be caused by a discrete adenoma (80%) or carcinoma (2%) or by generalized hyperplasia (18%) of all glands. Other causes include nonparathyroid tumors that secrete a parathormone-like substance and the familial

FIGURE 10-39  Hyperparathyroidism. Characteristic erosion of the distal clavicle (arrow) is shown. Metaphyseal subperiosteal resorption beneath the proximal humeral head has led to a pathologic fracture with slippage of the humeral head.

syndrome of multiple endocrine neoplasia. Secondary hyperparathyroidism occurs more frequently than the primary form and is most often attributable to chronic renal failure. Tertiary hyperparathyroidism refers to the development of autonomous functioning parathyroid glands in patients who demonstrate progressive bone disease in the presence of biochemical and clinically controlled renal disease. Imaging appearance. The radiographic findings in primary and secondary hyperparathyroidism are similar, except that in the secondary form, brown tumors (focal areas of bone destruction) are rare and osteosclerosis is more common. As a result of the predominant skeletal changes, conventional radiography is the primary image modality used for diagnosis. The earliest change is subperiosteal bone resorption, which particularly involves the radial margins of the middle phalanges (Figure 10-38), the distal clavicles (Figure 10-39), and the medial aspect of the upper third of the tibias. Loss of normal cortical definition is followed by an irregularly lacy resorption, with the endosteal margin initially remaining intact. Erosions of the terminal tufts of the fingers and loss of the lamina dura of the teeth often occur, although these findings are nonspecific and are seen in other conditions.

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FIGURE 10-41  Hyperparathyroidism. Characteristic saltand-pepper skull.

FIGURE 10-40  Hyperparathyroidism. Brown tumors have produced multiple lytic lesions about the knee.

Generalized loss of bone density may produce a groundglass appearance. So-called brown tumors may become large and expansile and even simulate a malignant process (Figure 10-40). Pathologic fractures may lead to bizarre deformities. Irregular demineralization of the calvaria produces the characteristic salt-and-pepper skull (Figure 10-41). A generalized increase in bone density (osteosclerosis) may develop in patients with hyperparathyroidism, especially when it is a result of renal failure. Thick bands of increased density adjacent to the superior and inferior margins of vertebral bodies produce the characteristic “rugger-jersey” spine (Figure 10-42). Soft tissue calcification is common, especially in secondary hyperparathyroidism. Calcific deposits may develop in vessels, articular cartilages, menisci, joint capsules, and periarticular tissues (Figure 10-43). Elevation of serum calcium and decreased excretion of calcium in the urine may result in nephrocalcinosis and urinary tract stones. Increased incidences of pancreatic calculi and pancreatitis, peptic ulcer, and gallstones have also been reported in patients with hyperparathyroidism.

FIGURE 10-42  Hyperparathyroidism. Lateral projection of the lumbar spine demonstrates osteosclerosis of the superior and inferior margins of the vertebral bodies (“rugger-jersey” spine).

The preoperative localization of a functioning parathyroid adenoma has long been a difficult imaging problem. Ultrasound can detect 80% to 85% of parathyroid abnormalities. Parathyroid carcinomas usually have a more heterogeneous internal structure than adenomas. Preoperative parathyroid localization is not required unless the patient has had previous neck surgery. Plain radiographs and barium studies are of virtually no value unless the tumor is very large. The major role of sophisticated imaging modalities in the localization of functioning parathyroid adenomas is in patients

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who remain hypercalcemic, or in whom hypercalcemia recurs (Figure 10-44), after neck surgery for hyperparathyroidism. In these patients, normal anatomic relationships are disturbed, landmarks may be absent, and scarring and adhesions distort the field and complicate the surgical technique. Also, the elusive parathyroid tumor is more likely to be situated in an ectopic position (Figure 10-45). Indeed, the success rate for parathyroid reexploration without help from imaging is less than 65%.

FIGURE 10-43  Hyperparathyroidism. A dense mass of tumoral calcification can be seen in the joint capsules and periarticular soft tissues on the lateral aspect of the foot in a patient with chronic renal disease.

Thus, CT and MRI are required to detect ectopic parathyroid tissue location (such as in the thymus). Radionuclide subtraction imaging using technetium-99m (Figure 10-46A) and thallium can detect parathyroid adenomas with a fairly high sensitivity and specificity. An adenoma takes up only the thallium (Figure 10-46B), and a residual focus of activity appears when the technetium is subtracted from the initial image (Figure 10-46C). The normal thyroid can be distinguished from the tumor because it concentrates both radionuclides. Using ultrasound or CT guidance for preoperative fine-needle aspiration biopsy can increase the specificity of localizing and confirming the exact site of a parathyroid adenoma, especially in patients who have undergone previous neck

FIGURE 10-45  Ectopic parathyroid adenoma. CT scan shows a small soft tissue mass (arrow) in the anterior mediastinum. A, Aorta; a, three major branches of the aorta (from the patient’s right to left: brachiocephalic, left carotid, and left subclavian arteries); v, right and left brachiocephalic veins.

A

B

FIGURE 10-44  Parathyroid adenoma. (A) Technetium-99m sestamibi was injected, and the patient was scanned 20 minutes later; normal distribution was noted. (B) After 4 hours, washout of the activity in the thyroid tissue and a focal area of increased activity verify that the cause of hypercalcemia is a parathyroid adenoma.

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Hypoparathyroidism Clinically, hypoparathyroidism causes sustained muscular contraction (tetany), muscle cramps in hands and feet, and numbness and tingling of the extremities. Spasm of laryngeal muscles can cause fatal obstruction of the respiratory tract. Imaging appearance. Hypoparathyroidism usually results from injury or accidental removal of the parathyroid glands during thyroidectomy, and this type of hypoparathyroidism is not associated with any significant radiographic abnormalities. In primary hypoparathyroidism, which is less common, the most common radiographic finding on plain skull radiographs or CT of the skull is cerebral calcification, especially involving the basal ganglia (Figure 10-47),

dissection. When a successful aspiration biopsy of the neck shows the presence of parathyroid cells, there is no doubt that abnormal parathyroid tissue is situated at this site, and this finding eliminates the need for extensive surgical dissection. Ultrasound, radionuclide scanning, CT, and MRI are complementary modalities for investigating the patient with hypercalcemia after parathyroid surgery. If these techniques fail to demonstrate a lesion, arteriography and venography with venous sampling may be performed for localization. Treatment. A standard bilateral neck dissection by an experienced parathyroid surgeon can be expected to have a 95% success rate in controlling hyperparathyroidism. For hypercalcemia, specific drugs such as steroids and calcium-losing diuretics may be used. A

B

Thyroid

C

Thyroid

Thyroid

Parathyroid

Parathyroid

FIGURE 10-46  Radionuclide subtraction imaging. (A) Technetium uptake. (B) Thallium uptake. (C) The residual focus of thallium activity after the technetium activity is subtracted. In this case, a substernal parathyroid is demonstrated.

A

B

FIGURE 10-47  Hypoparathyroidism. (A) Frontal projection of the skull demonstrates calcification in the basal ganglia bilaterally. (B) CT scan shows characteristic bilateral calcification in the basal ganglia (broad arrows). Note also the small calcific deposits in the tail of the caudate nuclei (thin arrows).

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the dentate (tooth-shaped) nuclei of the cerebellum, and the choroid plexus. A pattern of increased density may develop in the long bones, usually localized to the metaphyseal area. Treatment. Synthetic parathormone decreases symptoms to a tolerable level.

Pseudohypoparathyroidism and Pseudopseudohypoparathyroidism Pseudohypoparathyroidism is a hereditary disorder in which there is failure of normal end-organ response to normal levels of circulating parathyroid hormone. Most patients are obese and have short stature, with round faces, opacities in the cornea or lens of the eye, short fingers, and mental retardation.

Pseudopseudohypoparathyroidism refers to the presence of similar skeletal anomalies in other members of the patient’s family in the absence of biochemical disturbances. Imaging appearance. The most common radiographic abnormalities in pseudohypoparathyroidism are shortening of the tubular bones of the hands and feet (especially the fourth and fifth metacarpals) (see Figure 12-10) and calcific or bony deposits in the skin or subcutaneous tissues. An appearance similar to that of rickets may develop. As in idiopathic hypoparathyroidism, calcification is often found in the brain, especially the basal ganglia (best demonstrated on CT or MRI). Treatment. Therapy of pseudohypoparathyroidism consists of some form of calcium supplement, either calcium carbonate or calcitriol combined with vitamin D.

Summary of Findings for Diseases of the Parathyroid Glands Disorder

Location

Imaging Appearance

Treatment

Hyperparathyroidism

Excessive secretion of parathormone

Surgical resection by standard bilateral neck resection For hypercalcemia, steroids and calcium-losing diuretics

Hypoparathyroidism

Decreased secretion of parathormone Failure of response by target organ Similar skeletal anomalies in family members

Skeletal radiograph—subperiosteal bone resorption, erosion of distal clavicles, sclerotic stripes in vertebral bodies, saltand-pepper skull US—carcinomas produce a more heterogeneous echo than adenomas CT/MRI—detect ectopic parathyroid tissue NM subtraction imaging—thallium appears as residual focal activity on technetium subtraction scan Radiograph/CT—cerebral calcification and increased density of metaphysis Radiograph—shortening of metacarpals and metatarsals Radiograph—shortening of metacarpals and metatarsals

Pseudohypoparathyroidism Pseudopseudohypoparathyroidism

Replacement therapy— synthetic parathormone Some form of calcium supplement Some form of calcium supplement

NM, Nuclear medicine; US, ultrasound.

DIABETES MELLITUS Diabetes mellitus is a common endocrine disorder in which either beta cells in the islets of Langerhans of the pancreas fail to secrete insulin or target cells throughout the body fail to respond to this hormone. A lack of insulin prevents glucose from entering the cells, thus depriving them of the major nutrient needed for energy production. The blood glucose level rises (hyperglycemia). The severity and age at onset of diabetes vary. Juvenile-onset diabetes, which develops in childhood, and insulin-dependent diabetes require the patient to undergo daily insulin injections. Non–insulin-dependent diabetes, which tends to develop later in life, is less severe and can often be controlled by diet alone. The precise cause of diabetes is unknown, although heredity is generally considered to be an important factor. Polyuria (excessive urination) and polydipsia (drinking large quantities of liquid) are common manifestations of diabetes. The large amount of sugar filtered through the kidneys

exceeds the amount that the renal tubules can absorb. This situation leads to the excretion of glucose in the urine (glycosuria), which is a major sign of diabetes. Glucose is the major fuel of the body. However, because glucose cannot enter the cells without the action of insulin, diabetic patients are forced to metabolize a large amount of fat. This process produces a large number of acids and ketones, which can be detected in the urine. Production of fatty acids lowers the body’s pH (acidosis). Severe acidosis and dehydration in a diabetic patient who fails to take enough insulin or eats a highsugar diet can lead to diabetic coma, which may be fatal if not treated rapidly with fluids and a large dose of insulin. A major complication of diabetes is the deposition of lipids within the walls of blood vessels (atherosclerosis). It causes arterial narrowing and even occlusion, resulting in myocardial infarction (coronary artery), stroke (carotid artery), or gangrene (peripheral artery). Excess glucose in tissues provides an excellent bacterial culture medium and leads to the frequent development of infections, which tend to heal

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FIGURE 10-49  Diabetes mellitus. Bilateral calcification of the vas deferens (arrows).

FIGURE 10-48  Diabetes mellitus. Typical calcification in moderate-size vessels of the hand and wrist. Evidence of a prior surgical resection of the phalanges of the fourth digit can be seen.

poorly because of the generally poor circulation in diabetic patients. The kidneys are always affected by long-standing diabetes, and kidney failure is frequently the cause of death. Another complication is narrowing and rupture of minute retinal blood vessels, which may lead to blindness. Poor circulation to the nervous system may produce intractable pain, tingling sensations, loss of feeling, and paralysis. A patient with diabetes must also be wary of the development of insulin shock (hypoglycemic shock), which results from too much insulin, not enough food, or excessive exercise. The patient feels lightheaded and faint, trembles, and begins to perspire. In the radiology department, this condition may occur in diabetic patients who have not eaten or drunk before gastrointestinal examination or other special procedures. It is essential that this condition be rapidly recognized and that sugar be given, usually in the form of orange juice or candy. If the patient is unable to swallow, intravenous glucose may be administered.

Imaging Appearance Diabetes mellitus produces a variety of radiographic findings that involve multiple organ systems. Atherosclerotic disease and subsequent ischemia involving the coronary, extracerebral, and peripheral circulations occur earlier and are more extensive in patients with diabetes, especially those who smoke. Calcifications in peripheral vessels, especially those of the hands and feet, are virtually pathognomonic of the disease (Figure 10-48). Men with diabetes may demonstrate characteristic calcification

FIGURE 10-50  Neuropathic joint in diabetes mellitus. Severe destructive changes with calcific debris can be observed about the intertarsal joints. Note the characteristic vascular calcification posterior to the ankle joint.

of the vas deferens, which appears as bilaterally symmetrical parallel tubular densities that run medially and caudally to enter the medial aspect of the seminal vesicles at the base of the prostate gland (Figure 10-49). Diabetic persons have an increased susceptibility to infection, which especially affects the feet and may lead to severe osteomyelitis, producing bone destruction without periosteal reaction. Diabetic neuropathy with gait abnormalities and the loss of deep pain sensation may lead to repeated trauma on an unstable joint. Degeneration of cartilage, recurrent fracture and fragmentation of subchondral bone, soft tissue debris, and considerable proliferation of adjacent bone can lead to total disorganization of the joint (Charcot’s, or neuropathic, joint) (Figure 10-50). Vascular disease with

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FIGURE 10-52  Mucormycosis in a patient with diabetes. A large, thin-walled cavity (arrow) contains a smooth, elliptic, homogeneous mass (arrowheads) representing the fungus ball.

FIGURE 10-51  Diabetic gangrene. There is diffuse destruction of the phalanges and the metatarsal head of the fifth digit. Note the large amount of gas in the soft tissues of the foot.

diminished blood supply can lead to gas gangrene, in which bubbles or streaks of gas develop in the subcutaneous or deeper tissues (Figure 10-51). Diabetic neuropathy often causes radiographically evident abnormalities in the gastrointestinal tract. Findings include decreased primary peristalsis and tertiary contractions in the esophagus, delayed gastric emptying, and dilation of the small bowel. Emphysematous cholecystitis with gas in the lumen and wall of the gallbladder (see Figure 5-91) is a severe complication that occurs almost exclusively in diabetic patients. Renal disease is a common complication and a leading cause of death in persons with diabetes. Acute and chronic

pyelonephritis, renal papillary necrosis, and cystitis often occur. Diabetic neuropathy can cause dilation and atony (lack of normal tone) of the bladder with incomplete emptying. Mucormycosis infection is a devastating fungal disease that occurs virtually only in persons with uncontrolled diabetes. It usually originates in the nose and paranasal sinuses, from which it can extend to destroy the walls of the sinus and invade the substance of the brain. Pulmonary mucormycosis is a progressive severe pneumonia that is widespread and confluent and often cavitates (Figure 10-52).

Treatment The purpose of therapy in diabetes mellitus is to keep the blood glucose levels constant with a minimal variation. Oral therapy for glycemic control or short- or long-acting insulin is used when proper diet and exercise cannot maintain normal levels. In cases in which blood glucose levels are difficult to regulate, a continuous infusion pump may be used to help maintain a constant blood glucose level. Advances in therapy for this disease include islet cell transplantation and insulin gene therapy.

Summary of Findings for Diabetes Mellitus Disorder

Location

Imaging Appearance

Treatment

Diabetes mellitus

Failure of pancreas to secrete insulin or failure of target organ to respond

Skeletal radiograph—peripheral vessel calcification, severe osteomyelitis, neuropathic joints, gas gangrene, emphysematous cholecystitis

Oral medication, insulin, proper diet Advanced therapies—islet cell transplantation, insulin gene insertion

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  REVIEW QUESTIONS 1. What organ in the body is responsible for the release of insulin? a. spleen b. liver c. pancreas d. small intestine 2. What organ in the body is responsible for the release of glucagon? a. spleen b. liver c. pancreas d. small intestine 3. The _________________ glands secrete several types of steroid hormones and lie above each kidney. a. adrenal b. pituitary c. pineal d. thymus 4. What hormone has the ability to constrict some blood vessels while dilating others to shunt blood to active muscles where oxygen and nutrients are needed? a. androgen b. epinephrine c. glucocorticoids d. aldosterone 5. What hormones are known as the fight-or-flight hormones? a. androgen, epinephrine b. adrenaline, norepinephrine c. glucocorticoid, adrenaline d. androgen, glucocorticoid 6. Enlargement of the adrenal glands is best demonstrated by what diagnostic modality? a. ultrasound b. MRI c. CT d. plain image radiography 7. What pathologic condition is characterized by obesity of the trunk of the body, a fat pad behind the shoulders, and a moon-shaped face? a. Conn’s syndrome b. Cushing’s syndrome c. adrenogenital syndrome d. Addison’s syndrome 8. One complication of Cushing’s syndrome that radiographers must be cautious of is _________________. a. buffalo hump b. spontaneous fractures c. hypercalciuria d. sella erosion 9. Excessive administration of _________________ is the most common cause of adrenal insufficiency. a. adrenalin b. aldosterone c. steroids d. ACTH

10. The second most common malignancy in children is _________________. a. pheochromocytoma b. neuroblastoma c. Wilms’ tumor d. adenoma 11. The _________________ controls the hormone secretion of the pituitary gland. a. cerebellum b. pons c. medulla oblongata d. hypothalamus 12. Enlargement of the hands, feet, and face is characteristic of what pathologic condition? a. adenoma b. acromegaly c. gigantism d. none of the above 13. A pea-sized gland suspended from the base of the brain, sometimes referred to as the master gland, is called the _________________. a. thymus b. pineal c. pituitary d. pinna 14. What is the name for the butterfly-shaped gland located at the level of the larynx? a. thymus b. thyroid c. pituitary d. pineal 15. Thyroid tissue is best demonstrated by what imaging modality? a. CT b. radionuclide imaging c. ultrasound d. plain image radiography 16. Insufficient synthesis of thyroid hormone can lead to what pathologic condition? a. hyperthyroidism b. hypothyroidism c. exophthalmos d. Graves’ disease 17. What is the name for an enlargement of the thyroid gland that does not result from an inflammatory or neoplastic process? a. exophthalmos b. goiter c. myxedema d. skin thickening 18. There is a significantly higher risk of thyroid cancer in people who received _________________. a. neck irradiation in childhood b. steroid therapy in childhood c. chest radiographs in childhood d. skull radiographs in childhood

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19. If beta cells in the islets of Langerhans fail to secrete insulin, what pathologic condition results? a. goiter b. exophthalmos c. diabetes d. hypothyroidism 20. A diabetic patient who receives insulin before reporting to the radiology department for an upper gastrointestinal study should be monitored by the radiographer for any signs of developing _________________. a. ketoacidosis b. hypoglycemic shock c. acidosis d. hyperglycemic shock

21. The most common complication and leading cause of death in diabetic patients is _________________. a. hypoglycemia b. hyperglycemia c. pancreatic disease d. renal disease

11 Reproductive System OUTLINE Infectious Diseases of Both Genders Syphilis Gonorrhea Male Reproductive System Physiology of the Male Reproductive System Benign Prostatic Hyperplasia Carcinoma of the Prostate Gland Staging Undescended Testis (Cryptorchidism)

Testicular Torsion and Epididymitis Testicular Tumors Female Reproductive System Physiology of the Female Reproductive System Pelvic Inflammatory Disease Cysts and Tumors Ovarian Cysts and Tumors Dermoid Cyst (Teratoma) Uterine Fibroids

Endometrial Carcinoma Endometriosis Carcinoma of the Cervix Breast Lesions Breast Cancer Benign Breast Disease Imaging in Pregnancy Ectopic Pregnancy Trophoblastic Disease Female Infertility

menstrual phase oligohydramnios ovulation polyhydramnios primary cystadenocarcinoma primary stage of syphilis progesterone proliferative, or postmenstrual, phase prostate gland

pyosalpinx secondary stage of syphilis secretory, or postovulatory, phase seminal vesicle spermatogenesis tertiary stage of syphilis testosterone vas deferens vasectomy

KEY TERMS chorion congenital syphilis corpus luteum cystadenoma ectopic pregnancy epididymis estrogen hydrosalpinx menarche menopause

OBJECTIVES After reading this chapter, the reader will be able to: • Define and describe all boldface terms in this chapter • Describe the physiology of the reproductive system • Identify anatomic structures on both diagrams and radiographs of the reproductive system

• Differentiate various pathologic conditions affecting the reproductive system and their radiographic manifestations • Initiate alterations that must be made in routine exposure techniques to obtain optimal-quality radiographs

INFECTIOUS DISEASES OF BOTH GENDERS Syphilis Syphilis is a chronic, sexually transmitted systemic infection caused by the spirochete Treponema pallidum. The baby of an infected mother may be born with congenital syphilis. In the primary stage of infection, a chancre, or ulceration, develops on the genitals (usually the vulva of the female and the penis of the male). If untreated, the secondary stage of the disease appears as a nonitching rash that affects any part of the body. At this stage, the patient is still infectious. If still

untreated, the disease may become dormant for many years before the development of the most serious or tertiary stage of the disease, in which radiographic abnormalities become apparent. The young black male population is most often affected. Imaging appearance. Cardiovascular syphilis involves primarily the ascending aorta, which may become aneurysmally dilated and often demonstrates linear calcification of the wall (Figure 11-1). Syphilitic aortitis often involves the aortic valvular ring and produces aortic regurgitation with enlargement of the left ventricle.

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RADIOGRAPHER NOTES Because of its nonionizing character, ultrasound has become the major modality for imaging both male and female reproductive systems. Computed tomography (CT), magnetic resonance imaging (MRI), and positron emission tomography (PET) are used for staging malignant tumors when ultrasound is inconclusive, and radionuclide studies are used to differentiate testicular torsion from epididymitis. Conventional plain image radiography is virtually never indicated for disorders of the pregnant patient. The once common pelvimetry and gravid uterus examinations have been almost completely replaced by nonionizing ultrasound imaging. The two radiographic studies of the female reproductive system that are in current use are hysterosalpingography and mammography. Hysterosalpingography, which is performed with fluoroscopic guidance, evaluates the patency (openness) of the fallopian tubes. Plain radiographs are obtained only to provide a permanent record. Mammography requires dedicated equipment and a specially trained radiographer. Properly performed mammograms can detect breast cancer in the early stage, before it is symptomatic, thus decreasing the incidence of metastases and greatly improving patient survival rates. However, mammograms performed by poorly trained radiographers or with inadequate equipment may fail to demonstrate early lesions, condemning women with an otherwise curable disease to unnecessary suffering and even death. It is essential that the radiographer attempt to put the patient at ease when performing an examination of the reproductive system. Although these procedures are not actually painful, they may at times be uncomfortable and are frequently embarrassing for the patient. A good professional attitude goes a long way in reassuring the patient and making these examinations as comfortable as possible.

Syphilitic involvement of the skeletal system most commonly produces radiographic findings of chronic osteomyelitis, which usually affects the long bones and the skull. The destruction of bone incites a prominent periosteal reaction, with dense sclerosis as the most outstanding feature (Figure 11-2). Syphilis is a major cause of neuropathic joint disease (Charcot’s joint), in which bone resorption and total disorganization of the joint are associated with calcific and bony debris (Figure 11-3). Syphilitic lesions developing in the cerebral cortex can cause mental disorders, deafness, and blindness. The cerebral lesions containing syphilis bacteria (intracerebral gummata)

FIGURE 11-2  Syphilitic osteomyelitis. Diffuse lytic destruction of the proximal humerus with reactive sclerosis and periosteal new bone formation.

FIGURE 11-1  Syphilitic aortitis. Aneurysmal dilation of the ascending aorta with extensive linear calcification of the wall (black arrows). Some calcification is also seen in the distal aortic arch (white arrow).

FIGURE 11-3  Neuropathic joint disease in syphilis. Joint fragmentation, sclerosis, and calcific debris about the hip.

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385

are hypodense on nonenhanced CT. On T1-weighted MRI, the lesions appear hypointense or isointense, and they become hyperintense on T2-weighted images. The intracerebral gummata densely enhance with the administration of gadolinium. Single-photon emission computed tomography (SPECT) demonstrates the significant decrease of blood flow in the frontal and temporal cortices bilaterally. Scans obtained following therapy demonstrate a marked improvement in flow. Diffuse thickening of the gastric wall can cause narrowing of the lumen that is indistinguishable from that seen in carcinoma. Multiple bone abnormalities can occur in infants with congenital syphilis who are born to infected mothers (Figure 11-4). Mental retardation, deafness, and blindness are common complications. Treatment. In the primary and secondary stages of syphilis, antibiotic therapy cures the disease. The ulcerations in primary syphilis and the skin lesions and rash in secondary syphilis heal in a few days with penicillin, doxycycline, or tetracycline. The tertiary stage is incurable.

Gonorrhea Gonorrhea is a bacterial infection, one of the most common and most widespread of the venereal diseases, which occurs more commonly in men (1.5:1). Persons of Asian and Pacific Island descent are least likely affected, whereas the African American population is experiencing the greatest increase. Symptoms usually occur a few days after infection. An acute urethritis with copious discharge of pus develops in men. Women may be asymptomatic or may have minimal symptoms of urethral or cervical inflammation. If untreated, the inflammation may become chronic, spread upward, and produce fibrosis, leading to urethral stricture in men (Figure 11-5)

FIGURE 11-4  Congenital syphilis. Transverse bands of decreased density across the metaphyses (small arrows) associated with patchy areas of bone destruction in the diaphyses. Solid periosteal new bone formation (large arrow) is best seen about the distal humerus.

Summary of Findings for Infectious Diseases of the Reproductive System Disorder

Location

Imaging Appearance

Treatment

Syphilis

Male and female reproductive organs

Primary and secondary stages— antibiotics Tertiary stage—incurable

Gonorrhea

Male and female reproductive organs

Cardiovascular—aortic dilation with possible calcification Skeletal radiograph—chronic osteomyelitis of long bones and skull; periosteal reaction with dense sclerosis CT—intracerebral gummata are hypodense on nonenhanced scans MRI—on T1-weighted images, the lesions appear hypointense or isointense; they are hyperintense on T2-weighted images; intracerebral gummata densely enhance with contrast agent SPECT—decreased cortical flow in frontal and temporal cortices bilaterally; post-therapeutic scans demonstrate a marked improvement in flow Skeletal—septic arthritis with articular erosion and joint space narrowing PID—US or CT demonstrates thick, dilated fallopian tubes or abscess formation

GI, Gastrointestinal; PID, pelvic inflammatory disease; US, ultrasound.

Penicillin; if disease is penicillinresistant, ceftriaxone

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and pelvic inflammatory disease (PID) or sterility in women. A serious complication is fibrous scarring of the fallopian tubes that may result in sterility or an ectopic pregnancy. Imaging appearance. Gonorrheal infection can cause septic arthritis, leading to articular erosion and joint space narrowing. For patients in whom PID is suspected, ultrasound (ultrasonography) or CT is the modality of choice for demonstrating thick, dilated fallopian tubes or abscess formation. Ultrasound is superior for showing ectopic pregnancy. Treatment. Gonorrhea usually responds rapidly to antibiotic therapy (penicillin). Penicillin-resistant gonorrhea has been reported and requires a single intramuscular dose of ceftriaxone.

MALE REPRODUCTIVE SYSTEM PHYSIOLOGY OF THE MALE REPRODUCTIVE SYSTEM The major function of the male reproductive system is the formation of sperm (spermatogenesis), which begins at approximately 13 years of age and continues throughout life. Under the influence of follicle-stimulating hormone (FSH) secreted by the anterior lobe of the pituitary gland, the seminiferous tubules of the testes are stimulated to produce the male germ cells called spermatozoa. In addition to producing sperm cells, the testes secrete the male hormone testosterone. This substance stimulates the development and activity of the accessory sex organs (prostate and seminal vesicles) and is responsible for adult male sexual behavior. Testosterone causes the typical male changes that occur at puberty, including the development of facial and body hair and alterations in the larynx that result in a deepened voice. Testosterone also helps regulate metabolism by promoting growth of

skeletal muscles and is thus responsible for the greater muscular development and strength in males. The final maturation of sperm occurs in the epididymis, a tightly coiled tube enclosed in a fibrous casing (Figure 11-6). The sperm spend approximately 1 to 3 weeks in this segment of the duct system, where they become motile and capable of fertilizing an ovum. The tail of the epididymis leads into the vas deferens, a muscular tube that passes through the inguinal canal as part of the spermatic cord and joins the duct from the seminal vesicle to form the ejaculatory duct. Depending on the degree of sexual activity and frequency of ejaculation, sperm may remain in the vas deferens up to 1 month with no loss of fertility. Severing of the vas deferens (vasectomy) is an operation performed to make a man sterile. Vasectomy interrupts the route from the epididymis to the remainder of the genital tract. The seminal vesicles lie on the posterior aspect of the base of the bladder and secrete a thick liquid that is rich in fructose, a simple sugar that serves as an energy source for sperm motility after ejaculation. The seminal vesicles also secrete prostaglandin, which increases uterine contractions in the woman and helps propel the sperm toward the fallopian tubes. The prostate gland lies just below the bladder and surrounds the urethra. It secretes a thin alkaline substance that constitutes the major portion of the seminal fluid volume. The alkalinity of this material is essential to sperm motility, which would otherwise be inhibited by the highly acidic vaginal secretions. Intense sexual stimulation causes peristaltic contractions in the walls of the epididymis and vas deferens, propelling sperm into the urethra. At the same time, the seminal vesicles and prostate gland release their secretions, which mix with the mucous secretion of the bulbourethral glands to form semen. The ejaculation of semen occurs when intense

A

B

FIGURE 11-5  Gonococcal urethral stricture. (A) Initial retrograde urethrogram shows diffuse stricture of the bulbar urethra and high-grade stenoses in proximal (solid arrow) and distal (open arrow) portions of the urethra. (B) After balloon dilation, a voiding urethrogram shows considerable improvement in the appearance of the urethra.

CHAPTER 11  Reproductive System muscular contractions of erectile tissue cause the semen to be expressed through the urethral opening. Male fertility is related not only to the number of sperm ejaculated but also to their size, shape, and motility. Although only one sperm fertilizes an ovum, millions of sperm seem to be necessary for fertilization to occur. Indeed, it is estimated that sterility may result when the sperm count falls below approximately 50 million per milliliter of semen.

bladder completely, leading to partial urinary tract obstruction, bilateral ureteral dilation, and hydronephrosis. Imaging appearance. Transrectal ultrasound imaging, performed by means of a probe inserted into the rectum, demonstrates gland enlargement and heterogeneous signal intensity of the central portion (Figure 11-7). A circumferential surgical pseudocapsule, discrete nodules, and a thickened bladder wall may also be visualized. Moreover, an abdominal–pelvic scan can demonstrate residual urine volume and aids in the evaluation of the kidneys for the presence of hydronephrosis. On excretory urography, the enlarged prostate typically produces elevation and a smooth impression on the floor of the contrast material–filled bladder (Figure 11-8). Elevation of the insertion of the ureters on the trigone of the bladder produces a characteristic J-shaped, or fishhook, appearance of the distal ureters. Residual urine in the bladder provides a

BENIGN PROSTATIC HYPERPLASIA Enlargement of the prostate gland is common in men older than 60 years of age and may be detected on a digital rectal examination. The enlargement is probably related to a disturbance of hormone secretions from the sex glands that occurs as the period of reproductive activity declines. The major effect of prostatic enlargement is an inability to empty the

Bulbourethral glands

Ureter Vas (ductus) deferens

Ampulla of vas (ductus) deferens

Seminal vesicle

Urinary bladder

Ejaculatory duct

Corpus cavernosum

Prostate gland Inguinal canal

Prostatic portion of urethra

Corpus spongiosum

Cremaster muscle

Bulbourethral gland

Internal spermatic fascia Vas (ductus) deferens Testicular artery Venous plexus

Spongy portion of urethra Vas (ductus) deferens

Spermatic cord

Genital nerve

Penis

Cremaster muscle

Head of epididymis Epididymis

Body of epididymis

Tunica vaginalis Testis

Tail of epididymis Glans penis

External urinary meatus Scrotum (skin)

387

Dartos fascia and muscle

FIGURE 11-6  The male reproductive system. Illustration shows the testes, epididymis, ductus deferens, and glands of the male reproductive system.

Glans penis

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CHAPTER 11  Reproductive System

A

FIGURE 11-7  Benign prostatic hyperplasia. Transrectal ultrasound in the sagittal plane demonstrates enlargement of the central periurethral soft tissue consistent with benign prostatic hyperplasia (measurement markers). The Eiffel Tower sign is caused by an enlarged urethra (arrows).

B

FIGURE 11-9  Benign prostatic hyperplasia. (A) T1-weighted MR image shows prostatic enlargement of homogeneous low signal intensity (1). Note the high signal intensity of the large lipoma (2) in the right gluteal region. (B) On a T2-weighted image, the intermediate signal intensity of the enlarged transitional zone (1) shows increased inhomogeneity and is separated from the high–signal intensity peripheral zone (2) by a low–signal intensity rim of pseudocapsule (3).

CARCINOMA OF THE PROSTATE GLAND

FIGURE 11-8  Benign prostatic hyperplasia. Large, smooth filling defect at the base of the bladder. Note the fishhook appearance of the distal ureters and calcification in the vas deferens.

growth medium for bacterial infection, which produces cystitis; the infection may ascend from the bladder to the kidney, resulting in pyelonephritis. On MR images, benign prostatic hyperplasia causes a diffuse or nodular area of homogeneous low signal intensity on T1-weighted images and an inhomogeneous, mixed (intermediate to high) signal intensity on T2-weighted images (Figure 11-9). A pseudocapsule, representing compression of adjacent tissue visualized as a low–signal intensity rim, often accentuates focal enlargement. Diffuse enlargement shows similar intensity changes, although the pseudocapsule is not present. Unfortunately, the intensity of benign prostatic hyperplasia may often be similar to that of the normal prostate or a region of prostatitis. Treatment. Surgical resection of the prostate (transurethral resection [TUR]) can relieve the obstructive symptoms.

Carcinoma of the prostate gland is the second most common malignancy in men, with a slightly higher incidence in black men. The disease rarely occurs before 50 years of age, and the incidence increases by approximately 40% with advancing age. The tumor can be slow growing and asymptomatic for long periods or can behave aggressively with extensive metastases. Prostate carcinoma occurs most often in the peripheral zone (70%). Carcinoma of the prostate is best detected by palpation, on which it is detected as a hard, nodular, and irregular mass, on a routine rectal examination. The presence of an elevated serum PSA (prostate-specific antigen) value indicates an abnormality, although this blood test is not specific for malignancy. Imaging appearance. Radiographically, carcinoma of the prostate often elevates and impresses the floor of the contrast-filled bladder. Unlike the smooth contour seen in benign prostatic hyperplasia, the impression on the bladder floor is usually more irregular in carcinoma (Figure 11-10). Bladder neck obstruction, infiltration of the trigone, or invasive obstruction of the ureters above the bladder may produce obstruction of the upper urinary tract. Transrectal (TR) ultrasound is the preferred technique for detecting carcinoma of the prostate (Figure 11-11). The normal prostate has a generally homogeneous appearance with a moderate echo pattern. Early studies indicated that prostatic

CHAPTER 11  Reproductive System

FIGURE 11-10  Carcinoma of the prostate. A large, irregular mass elevates and impresses the floor of the contrast agent– filled bladder.

FIGURE 11-11  Cancer of the prostate. Transrectal ultrasound image demonstrates a hypoechoic mass (between cursors) with the capsule still intact.

carcinoma appeared as hyperechoic areas. However, with the development of newer and higher-frequency transducers, many carcinomas appear as areas of low echogenicity within the prostate. Up to 40% of carcinomas are isoechoic with normal prostate tissue and thus cannot be visualized on ultrasound. The latest studies have concluded that the wide range of sonographic patterns in carcinoma indicates that ultrasound cannot reliably differentiate prostatic malignancy from benign disease.

STAGING Imaging appearance. MRI can superbly delineate the prostate, seminal vesicles, and surrounding organs to provide accurate staging of pelvic neoplasms. When the spinecho technique is used, the central and peripheral zones of

389

FIGURE 11-12  Carcinoma of the prostate. Axial MR image through the pelvis demonstrates an abnormal area of increased signal intensity (black arrow) within the prostate gland (P). A Foley catheter is in place (straight white arrow), and the rectum (R) contains air and feces. Note the decreased size of the pelvic musculature on the right (curved white arrows) in this patient, who has an above-knee amputation.

the prostate are well demonstrated and distinctly separate from the surrounding levator ani muscles. In the sagittal plane, the relation of the prostate to the bladder, rectum, and seminal vesicles is clearly shown. Prostatic carcinoma is best demonstrated on long TR images, on which it appears as disruption of the normally uniform high signal intensity of the peripheral zone of the prostate (Figure 11-12). T2-weighted images demonstrate low intensity that is surrounded by the hyperintense signal of the normal tissue. The new technique of MR lymphography aids in visualizing nonenlarged pelvic lymph nodes. However, there is much controversy regarding whether MRI is reliable for detection and diagnosis of prostate cancer, and therefore a precise diagnosis requires a biopsy and histologic examination. Research findings state that the demonstration of a normal-appearing prostate gland on MRI does not exclude the presence of a neoplasm. In addition, inhomogeneity of the gland is a common nonspecific finding that can also be seen in patients with adenoma or prostatitis. Carcinoma of the prostate may spread by direct extension or by way of the lymphatics or the bloodstream. Spread of carcinoma of the prostate to the rectum can produce a large, smooth, concave pressure defect; a fungating ulcerated mass simulating primary rectal carcinoma; or a long, asymmetrical annular stricture. Both ultrasound and CT, especially the arterial phase of multislice CT, aid in defining extension of tumor into the bladder and seminal vesicles and in detecting metastases in enlarged lymph nodes (Figure 11-13). The most common hematogenous metastases are to bone. They involve primarily the pelvis, thoracolumbar spine, femurs, and ribs. These lesions are most commonly osteoblastic and appear as multiple rounded foci of sclerotic density (Figure 11-14) or occasionally as diffuse sclerosis involving

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CHAPTER 11  Reproductive System

an entire bone (“ivory vertebra”). Patients with bony metastases usually have strikingly elevated serum acid phosphatase values. Because significant bone destruction or bone reaction must occur before a lesion can be detected on plain radiographs, the radionuclide bone scan is the best screening technique for detection of asymptomatic skeletal metastases in patients with carcinoma of the prostate. However, because the radionuclide scan is very sensitive but not specific and may show increased uptake in multiple disorders of the bone, conventional radiography of the affected site should be performed when the scan is abnormal. Treatment. For a tumor confined to the prostate gland, a successful cure can be achieved by a radical prostatectomy or radiation therapy. Prostate tumors with local invasion require both a radical prostatectomy and radiation therapy. Radiation therapy may consist of implantation of iodine-125 or palladium-103 seeds. Stage D prostate cancers, the most progressive, require hormonal therapy (antiandrogen drugs)

to slow the spread of disease and palliative measures to reduce pain. In some cases, orchiectomy (removal of the testes) is performed.

UNDESCENDED TESTIS (CRYPTORCHIDISM) Near the end of gestation, the testis normally migrates from its intra-abdominal position through the inguinal canal into the scrotal sac. This condition is more common in premature males and can cause infertility. If one of the testicles cannot be palpated within the scrotum, it is important to determine whether this finding represents absence of the testis or an ectopic position of the testis. The rate of malignancy is up to 40 times higher in the undescended (intra-abdominal) testis than in the descended testicle. Imaging appearance. In the absence of a palpable testicle, ultrasound is usually used as a screening technique. This modality carries no radiation risk and has a high diagnostic

A

B

FIGURE 11-13  Metastatic carcinoma of the prostate gland. (A) CT scan shows prostatic carcinoma (p) invading the wall of the bladder (arrow) and the seminal vesicles (v). (B) CT scan on another patient shows prostatic carcinoma involving the bladder (black arrows) and seminal vesicles. The normally sharp angle between the seminal vesicles and the prostate is lost (white arrow).

B

A

FIGURE 11-14  Metastatic carcinoma of the prostate. (A) Diffuse osteoblastic metastases involving the bones about the pelvis. (B) T1-weighted spin-echo MR image illustrates osteoblastic lesions throughout the spine.

CHAPTER 11  Reproductive System accuracy in demonstrating undescended testicles that are located in the inguinal canal (Figure 11-15). However, sonography is not successful in detecting ectopic testicles in the pelvis or abdomen. If ultrasound fails to demonstrate an undescended testis, MRI or CT is indicated (Figures 11-16 and 11-17). MRI typically demonstrates a low signal mass on T1-weighted images that has high signal intensity on T2-weighted images. The uniform oval soft tissue mass of an undescended testis demonstrates contrast enhancement on CT. Treatment. Because of the extremely high rate of malignancy, the diagnosis of undescended testis usually leads to orchiopexy (surgical fixation of an undescended testis into the scrotum through the inguinal canal) in patients younger than 10 years. This may be an alternative to salvage fertility.

391

Spontaneous descent may occur in the first 6 months, and hormonal therapy may stimulate descent. Orchiectomy (surgical removal) is recommended in patients with undescended testis who are seen after puberty.

TESTICULAR TORSION AND EPIDIDYMITIS Testicular torsion refers to the twisting of the gonad on its pedicle, which leads to compromise of the circulation and the sudden onset of severe scrotal pain. Although primarily a clinical diagnosis, the scrotal pain and swelling of testicular torsion may be difficult to distinguish from those caused by inflammation of the epididymis (epididymitis). In such cases, color Doppler ultrasound or radionuclide studies are of value.

A

B

FIGURE 11-15  Undescended testes. (A) Ultrasound image in the transverse plane illustrates a normal right testis (arrows). (B) Another image in the longitudinal plane demonstrates the undescended left testis (arrows), which is smaller and less echogenic, located in the inguinal canal.

A

B

FIGURE 11-16  Malignant neoplasms developing in one of the bilateral undescended testes. (A) Undescended right testis is enlarged by carcinoma (straight arrows). The tumor has metastasized to the lymph nodes (curved arrows), which are enlarged. (B) Nontumorous intra-abdominal left testis (arrow) appears as a smaller, rounded structure adjacent to the bladder (B).

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CHAPTER 11  Reproductive System

A

B h

FIGURE 11-17  Atrophic undescended testis. (A) Coronal MR image shows a small, intermediate– signal intensity testis (arrow) associated with low–signal intensity hydrocele (h). The signal intensity of the testis is low compared with that of fat (asterisk). (B) Another image slightly posterior to that in panel A shows the normally descended contralateral testis (curved arrow), which demonstrates high signal intensity similar to that of fat (asterisk). R

L

FIGURE 11-18  Testicular torsion. Doppler ultrasound image of a 3-year-old boy demonstrates abnormal to absent blood flow in the right testicle and normal blood flow (arrows) in the left testicle. Surgical correction was performed, saving the testis.

Imaging appearance. The preferred imaging modality for testicular torsion or epididymitis depends on the patient’s age—generally, color Doppler ultrasound in adults and radionuclide studies in children. As new technology improves color and power, Doppler ultrasound is the modality of choice in most cases. Doppler ultrasound demonstrates the presence of intratesticular arterial pulsations. In testicular torsion, the arterial perfusion is diminished or absent (Figures 11-18 and 11-19), whereas in epididymitis there is increased blood flow (Figure 11-20). Similarly, the radionuclide angiogram shows isotope activity on the twisted side that is either slightly decreased or at the normal, barely perceptible level. On the uninvolved side, the perfusion should be normal.

FIGURE 11-19  Testicular torsion. Scrotal ultrasound on a 16-year-old boy demonstrates the left testicle (arrows) without arterial blood flow, a complex heterogeneous echogenicity (indicating necrotic tissue), and a thickened scrotal wall. At surgery, the testicle remained discolored and was removed.

When compared with the decreased activity on the involved side, the perfusion appears to be increased. Static nuclear scans demonstrate a rounded, cold area replacing the testicle in patients with torsion (Figure 11-21) but a hot area in those with epididymitis (Figure 11-22). A nuclear testicular scan is superior to Doppler ultrasound for distinguishing between testicular torsion and epididymitis. Treatment. Immediate surgery must be performed within 5 or 6 hours of the onset of pain to preserve the testis. For epididymitis, bed rest, scrotal support, and antibiotics are prescribed for all bacterial infections.

CHAPTER 11  Reproductive System

393

h

FIGURE 11-20  Epididymitis. A longitudinal ultrasound image from an 80-year-old man demonstrates an enlarged hypoechoic epididymis (arrows) with a moderate-sized hydrocele (h).

FIGURE 11-21  Testicular torsion. Severe diminished arterial perfusion causes the testicle to appear as a rounded, cold area (t) on a radionuclide scan. The surrounding rim of increased activity represents the blood supply to the scrotal sac (arrows).

TESTICULAR TUMORS Testicular tumors are the most common neoplasms in men between 20 and 35 years of age. Almost all testicular tumors are malignant, and they tend to metastasize to the lymphatics that follow the course of the testicular arteries and veins and drain into para-aortic lymph nodes at the level of the kidneys. There are two major types of testicular tumors. Seminomas constitute approximately 45% of germ cell tumors; the remaining 55% are nonseminomas that consist of teratomas

FIGURE 11-22  Epididymitis. Radionuclide scan shows high isotope uptake in the region of the testicle (arrows) caused by increased blood flow.

FIGURE 11-23  Seminoma. A well-circumscribed, predominantly hypoechoic, intratesticular mass (between cursors) with echogenicity markedly less than that of the normal adjacent testis (T) is characteristic of a seminoma.

and other germ cell tumors. Seminomas arise from the seminiferous tubules, whereas teratomas arise from a primitive germ cell and consist of a variety of tissues. Imaging appearance. Testicular tumors are best diagnosed on ultrasound examination (with 98% to 100% accuracy). The normal testis has a homogeneous, medium-level echogenicity. A localized testicular tumor appears as a circumscribed mass with either increased or decreased echogenicity in an otherwise uniform-echo testicular structure. Seminomas appear as uniform hypoechoic masses without calcification or cystic areas (Figure 11-23). A teratoma appears inhomogeneous with cystic and solid areas of calcification and cartilage (Figure 11-24). Testicular tumors can also be detected

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CHAPTER 11  Reproductive System

on MRI (Figure 11-25), which is required when ultrasound findings are equivocal or when there is discrepancy between the ultrasound findings and the physical examination. Lymphatic metastases from testicular tumors typically occur at the level of the renal hilum (where the gonadal veins drain) and are best detected by CT (Figure 11-26). This modality also can detect spread of tumor to the lung or liver.

Treatment. All testicular cancers are removed (orchiectomy). Seminomas are radiosensitive, and early diagnosis and irradiation have resulted in many cures. Teratomas are surgically removed; if malignant, surgery is followed by radiation therapy and chemotherapy (consisting of several cytotoxic drugs in combination). Follow-up examinations are required to rule out metastasis.

Summary of Findings for Diseases of the Male Reproductive System Disorder

Location

Imaging Appearance

Treatment

Benign prostatic hyperplasia

Enlargement of prostate gland

Surgical resection to relieve symptoms

Carcinoma of the prostate gland

Prostate gland

Undescended testis

Inguinal or ectopic testicle

US—transrectal inner gland enlargement (relatively hypoechoic compared with the peripheral zone) IVU—elevation and smooth impression of floor in a contrast agent–filled bladder; distal ureters have a characteristic J-shaped appearance MRI—diffuse or nodular area of homogeneous low signal intensity on T1-weighted images and an inhomogeneous, mixed (intermediate to high) signal intensity on T2-weighted images IVU—irregular elevation of the floor of a contrast agent–filled bladder with possible obstruction US—transrectal wide range of sonographic patterns, depending on glandular area involved MRI—on long TR images, loss of uniform high signal intensity of the peripheral zone US—demonstrates inguinal testicle MRI—demonstrates ectopic undescended testis; low signal mass on T1-weighted images that has high signal on T2-weighted images CT—uniformly enhanced, oval soft tissue mass

Testicular torsion

Testes

Epididymitis

Inflammation of the epididymis

Testicular tumors

Seminoma (seminiferous tubules) Teratoma (primitive germ cell)

Color Doppler US—arterial perfusion is diminished or absent Radionuclide angiogram—slightly decreased normal intake, cold areas on static scan Color Doppler US—increased blood flow Radionuclide angiogram—appears as a hot area on a static scan US—seminoma appears uniformly hypoechoic without calcifications; teratoma is an inhomogeneous mass with cystic and solid areas MRI—T2-weighted image demonstrates inhomogeneous signal intensity CT—demonstrates lymphatic involvement as lowattenuation nodules

Radical prostatectomy Local invasion—surgery and radiation therapy (seeds) Stage D—hormonal therapy, palliative measures Spontaneous descent Hormonal therapy Orchiopexy—surgical attachment in the scrotum Orchiectomy Immediate surgery to preserve testis

Bed rest, scrotal support, and antibiotics Orchiectomy Seminoma—radiosensitive Cancerous teratoma—surgery, radiation therapy, and chemotherapy

IVU, Intravenous urography; US, ultrasound.

FEMALE REPRODUCTIVE SYSTEM PHYSIOLOGY OF THE FEMALE REPRODUCTIVE SYSTEM The ovaries, the female equivalent of the testes, are responsible for the production of ova and the secretion of female hormones. A woman’s reproductive life begins with the onset of menstruation, menarche, which generally occurs between 11 and 15 years of age. Once each month, on approximately the

first day of menstruation, several primitive graafian follicles and their enclosed ova begin to grow and develop, and the follicular cells start to secrete estrogen. In most cycles, only one follicle matures and migrates to the surface of the ovary, where it ruptures and expels the mature ovum into the pelvic cavity (ovulation). After the release of the ovum, the remaining cells of the ruptured follicle enlarge and a golden-colored pigment (lutein) is deposited in their cytoplasm. This corpus luteum continues to grow for 7 or 8 days and secretes progesterone

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CHAPTER 11  Reproductive System in increasing amounts. If fertilization of the ovum has not occurred, the size and secretions of the corpus luteum gradually diminish until the nonfunctional structure is reduced to a white scar (corpus albicans) that moves into the central portion of the ovary and eventually disappears. If fertilization does occur, however, the corpus luteum remains intact throughout pregnancy. The cyclic changes in the ovaries are controlled by a variety of substances secreted by the anterior pituitary gland. Growth of the primitive graafian follicles and ova and the secretion of

estrogen are controlled by FSH, whereas rupture of the follicle, expulsion of its ripe ovum, and the secretion of progesterone are under the control of luteinizing hormone (LH). The fallopian tubes serve as ducts for the ovaries, even though they are not directly attached to them (Figure 11-27). The union of an ovum and a spermatozoon (fertilization) normally occurs in the fallopian tubes. In the next few days, the resulting embryo reaches the uterus, where it begins to implant itself in the endometrium. Occasionally, implantation occurs in the fallopian tube or pelvic cavity instead of the uterus, resulting in an ectopic pregnancy. Within 10 days, there is the earliest development of the placenta, which is derived in part from both the developing embryo and the maternal tissues and serves to nourish the fetus and anchor it to the uterus. Although they are closely related, maternal blood and fetal blood do not mix, and the exchange of nutrients occurs across the important fetal membrane termed the chorion. Menstrual cycle refers to the changes in the endometrium of the uterus that occur in women throughout the childbearing years. Each cycle

FIGURE 11-24  Malignant teratoma. A transverse testicular scan demonstrates a large malignant teratoma replacing most of the testis. Cystic (C) and solid elements with small echogenic foci (arrows) from small calcifications are present. T, Residual normal testis.

FIGURE 11-26  Metastatic testicular seminoma. CT scan through the level of the kidneys shows diffuse nodal metastases (M) containing characteristic low-attenuation areas. Extrinsic pressure on the lower left ureter has caused severe hydronephrosis with dilation of the renal pelvis (h).

A

B

FIGURE 11-25  Testicular seminoma. (A) T2-weighted MR image shows that the signal intensity of the seminoma (S) in the left testis is inhomogeneous, and its contrast is markedly different from that of the adjacent hydrocele (H). (B) Inhomogeneous intermediate signal intensity of intratesticular tumor (S) extends into the epididymis (E). Note that the normal contralateral testis (T) demonstrates a much higher signal intensity.

396

CHAPTER 11  Reproductive System Isthmus of uterine tube Ovarian ligament

Fundus of uterus

Ampulla of uterine tube Body of uterus

Uterine body cavity

Ovary

Endometrium Myometrium Cervix of uterus

Internal os of cervix Cervical canal

Infundibulum of uterine tube Infundibulopelvic ligament Fimbriae

Broad ligament Uterine artery and vein

Fornix of vagina External os of vaginal cervix Vagina

FIGURE 11-27  The female reproductive system.

lasts approximately 28 days and is divided into three phases: proliferative, secretory, and menstrual. Although the first day of menstruation is normally regarded as the first day of the cycle, for ease of description the menstrual phase is described last. The proliferative, or postmenstrual, phase occurs between the end of the menses and ovulation. Production of estrogen by ovarian follicular cells under the influence of FSH causes proliferation of the endometrium of the uterus. In a typical 28-day cycle, the proliferative phase usually includes cycle days 6 to 13 or 14. However, there is far more variability in the length of this phase than in the others. The secretory, or postovulatory, phase occurs between ovulation and the onset of the menses. The high level of estrogen in the blood after ovulation inhibits the secretion of FSH, and the anterior lobe of the pituitary gland begins to secrete LH. The LH stimulates the corpus luteum to produce the hormone progesterone, which stimulates a further increase in the thickness of the endometrium and prepares the uterus for implantation of the ovum should fertilization occur. The length of the secretory phase is fairly constant, usually 14 days. If fertilization of the ovum does not occur, the high level of progesterone in the blood inhibits the secretion of LH so that the corpus luteum begins to degenerate and ceases to produce progesterone. As the superficial layers of the hypertrophied endometrium begin to break down, denuded bleeding areas are exposed. The flow of blood, mucus, and sloughed endometrium from the uterus is called the menstrual flow. This menstrual phase of the cycle lasts approximately 4 to 6 days, until the low level of progesterone causes the pituitary gland to again secrete FSH and a new menstrual cycle begins. Of course, if the ovum is fertilized, the corpus luteum does not degenerate, and the endometrium remains intact throughout pregnancy. The reproductive years terminate with the cessation of menstrual periods (menopause), which usually begins when a woman is in her late 40s or early 50s.

PELVIC INFLAMMATORY DISEASE Inflammation of the pelvic reproductive organs is usually the result of venereal disease (especially gonorrhea) in women of childbearing age, with the peak incidence between ages 20 and 24 years. It can also develop from an unsterile abortion or delivery or multiple sexual partners, or it may be a complication of intrauterine devices. If PID is not promptly and adequately treated, spread of infection to the fallopian tubes may cause fibrous adhesions that obstruct the inner portion near the uterus. If the outer ends of the tubes remain open, the spill of purulent material can lead to peritonitis and the formation of a pelvic abscess. More commonly, the outer ends close, and the fallopian tubes fill with pus (pyosalpinx). After antibiotic therapy, the infection subsides, and the tubes may remain filled with a watery fluid (hydrosalpinx). Obstruction of the fallopian tubes can result in infertility or ectopic pregnancy. Spread of infection to involve the ovaries can produce tubo-ovarian abscesses, which are usually bilateral. Imaging appearance. Ultrasound is the imaging procedure of choice for detecting PID and pelvic abscesses. The transabdominal approach best demonstrates the extent of the disease process, whereas the endovaginal approach is most sensitive for detecting dilated tubes, inflammatory changes, and abscesses. The fluid-filled urinary bladder provides an excellent acoustic window by displacing confusing loops of small bowel. Endometritis may occur after childbirth or in association with PID. Ultrasound demonstrates a thickened endometrium, possibly with irregularity that may contain fluid (Figure 11-28). Pyosalpinx and tubo-ovarian abscesses typically are seen as tubular adnexal masses that are sonolucent and compatible with fluid collections (Figure 11-29). However, abscesses may also have thick and irregular (or “shaggy”) walls or may contain echoes or fluid levels representing the layering of purulent debris (Figure 11-30). In severe cases, CT may aid in assessing the full extent of the disease. MRI is unnecessary unless the patient has an iodine allergy.

CHAPTER 11  Reproductive System

397

FIGURE 11-28  Endometritis. Ultrasound image illustrates an enlarged endometrial cavity with a heterogeneous echogenicity (between cursors) associated with a therapeutic abortion. FIGURE 11-30  Chronic pelvic inflammatory disease. Transverse sonogram demonstrates large, complex cystic and echogenic masses (arrows) posterior to the echo-free bladder.

c

c

f

Lt

Rt Cx

FIGURE 11-29  Tubo-ovarian abscess. Ultrasound image demonstrates a large sonolucent mass (M) posterior to the bladder (B).

The status of the fallopian tubes can be assessed radiographically by hysterosalpingography, in which the uterine cavity and fallopian tubes are opacified after the injection of contrast material into the uterus. In the woman with normal patent fallopian tubes, contrast material extravasating into the pelvic peritoneal cavity outlines the peritoneal surfaces and, often, loops of bowel within the pelvis (Figure 11-31). If the fallopian tubes are occluded by fibrosis from PID or developmental anomalies, there is no evidence of the contrast material reaching the peritoneal cavity (Figure 11-32). Plain abdominal or pelvic radiographs are of little value in detecting PID and pelvic abscesses. Abnormal gas collections can be masked by fecal material in the rectum and in loops of small bowel. Treatment. Antibiotic therapy and abstaining from sexual intercourse until the inflammation subsides are the

f

FIGURE 11-31  Normal hysterosalpingogram. Arrows point to a bilateral spill of contrast material into the peritoneal cavity. c, Cornua of the uterus; Cx, internal cervical os; f, fimbriated portion of fallopian tube; Rt and Lt, right and left fallopian tubes, respectively.

usual treatments for PID. In more complex cases, ultrasound-guided aspiration and drainage may be required. Thick purulent materials require catheter drainage; most nonpurulent abscesses need only aspiration. The healing phase may leave the fallopian tubes scarred and obstructed, resulting in an inability to conceive. Invitro fertilization is an alternative method to become pregnant in these cases.

CYSTS AND TUMORS Ovarian Cysts and Tumors Physiologic ovarian cysts are most common in female infants and in women of childbearing age. They include follicular cysts (unruptured, enlarged follicles) and corpus luteum cysts, which occur after continued hemorrhage or lack of

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CHAPTER 11  Reproductive System

A

B

FIGURE 11-32  Hydrosalpinx. Unilateral (A) and bilateral (B) gross dilation of fallopian tubes without evidence of free spill of contrast material into the peritoneal cavity.

B

A

B

M

E

FIGURE 11-33  Ovarian cysts. (A) Ultrasound image demonstrates a large (5 × 6 cm) sonolucent mass (M) with back wall enhancement (E) involving the right ovary. (B) In another patient, the longitudinal image of the right ovary demonstrates a septated (arrows) mass (between cursors) with homogeneous sonolucent components measuring 5 × 6.7 cm located posterior to the bladder (B).

resolution of the corpus luteum. Polycystic ovarian syndrome (PCOS) is characterized by multiple ovarian cysts, which may interfere with the physiology of the ovary. This is considered the most common genital disorder found in young women. The most common malignancies involving the ovaries are metastatic tumors, which arise principally from carcinomas of the breast, colon, and stomach. They are frequently bilateral and often asymptomatic. Imaging appearance. On ultrasound, ovarian cysts appear as rounded, anechoic adnexal masses (Figure 11-33). On MRI, which is used only when ultrasound findings are indeterminate, the cysts appear hyperintense on T2-weighted pelvic images (Figure 11-34). On ultrasound, PCOS appears as 10 or more cysts located peripherally in the echodense stroma. Primary cystadenocarcinoma of the ovary often contains psammomatous bodies, depositions of calcium carbonate located in the fibrous stroma of the tumor that can be detected on plain abdominal radiographs. These psammomatous calcifications appear as scattered, fine, amorphous shadows that are barely denser than the normal soft tissues and can therefore be easily missed unless they are extensive

(Figure 11-35). On ultrasound examination, cystadenocarcinoma typically appears as a large cystic mass with internal septa. It may be difficult to distinguish cystadenocarcinoma (Figure 11-36) from cystadenoma (Figure 11-37), its benign counterpart. The more solid and irregular the areas within the mass on ultrasound images, the more likely that it represents a malignant tumor. In addition, the association of ascites with an ovarian mass is strongly suggestive of underlying malignancy. MRI is a more definitive study to determine whether the tumor has benign or malignant characteristics. Ovarian carcinomas usually spread by implanting widely on the omental and peritoneal surfaces. This pattern can produce the characteristic CT appearance of an “omental cake,” an irregular sheet of soft tissue densities beneath the anterior abdominal wall (Figure 11-38). CT is also of value in detecting tumor adherence to bowel, ureteral involvement, and retroperitoneal adenopathy, making CT the modality of choice for staging and surgical planning. PET may be used in determining recurrence of ovarian carcinoma (Figure 11-39). Treatment. Simple ovarian cysts are common, and many resolve without treatment. Cysts that are larger than 10 mm

CHAPTER 11  Reproductive System

399

FIGURE 11-34  Ovarian cysts. On a T2-weighted axial MR image with fat saturation, multiple ovarian cysts (arrows) appear as high signal intensities because of the fluid within them.

FIGURE 11-35  Psammomatous calcifications. Diffuse, ill-defined collections of granular amorphous calcification are visible within this cystadenocarcinoma of the ovary.

A

B

FIGURE 11-36  Endovaginal sonogram of a cystadenocarcinoma. (A) The transverse image demonstrates a thickened wall and septations within the ovary, the left measuring 9 × 7 × 10 cm. (B) The longitudinal image illustrates an enlarged uterus with a large, complex mass. The CT scan had shown posterior wall thickening in the cyst and irregular densities within the liver—highly suggestive of cystadenocarcinoma.

A

B

FIGURE 11-37  Cystadenoma. Longitudinal (A) and transverse (B) sonograms demonstrate a complex, predominantly cystic mass (sonolucent) containing several thin and well-defined septations (arrows), which suggest a benign lesion—a mucinous cystadenoma.

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CHAPTER 11  Reproductive System

or are complex may require drainage or surgery. With surgical treatment, ovarian carcinoma currently has a 25% to 30% survival rate.

Dermoid Cyst (Teratoma) A dermoid cyst, the most common type of germ cell tumor, contains skin, hair, teeth, and fatty elements, all of which typically derive from ectodermal tissue. These cysts are of no clinical significance unless they grow so large that they produce symptoms by compressing adjacent structures. Approximately half of all ovarian dermoid cysts contain some calcification. This is usually in the form of a partially or completely formed tooth (Figure 11-40); less frequently, the wall of the cyst is partially calcified. Imaging appearance. The characteristic calcification combined with the relative radiolucency of the lipid material within the lesion is pathognomonic of an ovarian dermoid cyst. The most common ultrasound appearance of a dermoid cyst is a complex, primarily solid mass containing high-level

echoes arising from hair or calcification within the mass ­(Figures 11-41 and 11-42). The highly echogenic nature of these masses may make it difficult to delineate them completely and to distinguish them from surrounding gas-containing loops of bowel. Treatment. Surgical removal is recommended because a dermoid cyst may undergo transformation and become malignant.

Uterine Fibroids Fibroids (leiomyomas) of the uterus are benign smooth-­ muscle tumors that are very common; they are often multiple and vary greatly in size. Growth of fibroid tumors is stimulated by estrogen. They develop only during the reproductive years and tend to shrink after menopause. Abnormal bleeding between periods or excessively heavy menstrual flow is the most common symptom. Large tumors may project from the uterus, causing pressure on surrounding organs, which results in pelvic pain. They can also interfere with delivery or, if on a stalk (pedunculated), protrude into the vagina.

M

FIGURE 11-38  “Omental cake.” Metastases (M) resulting from cystadenocarcinoma of the ovary cause an irregular sheet of soft tissue densities beneath the anterior abdominal wall that posteriorly displaces the adjacent, contrast-filled bowel loops. Coronal

FIGURE 11-40  Dermoid cyst containing multiple wellformed teeth. Note the relative lucency of the mass (arrows), which is composed largely of fatty tissue. Transverse

Sagittal

FIGURE 11-39  Recurrence of ovarian carcinoma. PET scan revealed a solitary focus of intense fluorodeoxyglucose (FDG) uptake in the right paramidline retrocystic location, suggestive of an active neoplasm and consistent with regional recurrence of the patient’s ovarian carcinoma. The finding resulted in a change in treatment: The tumor focus, identified by PET–FDG to be in the right posterior pelvis, was successfully resected.

CHAPTER 11  Reproductive System

FIGURE 11-41  Dermoid cyst. Sagittal sonogram demonstrates only the near wall of the dermoid because of acoustic shadowing from a hairball (arrows), producing the so-called tip of the iceberg sign.

401

FIGURE 11-43  Calcified uterine fibroid. The calcified mass extends well beyond the confines of the pelvis.

A

B

FIGURE 11-42  Dermoid cyst. (A) Kidney–ureter–bladder study demonstrates two toothlike densities (arrow) beside the coccyx. (B) A transverse sonogram shows a heterogeneous mass (between cursors) with a high-amplitude echogenic focus (arrows) as a result of the toothlike densities.

FIGURE 11-44  Uterine fibroid. Excretory urogram demonstrates persistent dense opacification of a huge uterine leiomyoma (arrows).

Imaging appearance. Uterine fibroids are by far the most common calcified lesions of the female genital tract. They have a characteristic mottled, mulberry, or popcorn type of calcification and appear on plain abdominal radiographs as smooth or lobulated nodules with a stippled or whorled appearance. A very large calcified fibroid occasionally occupies the entire pelvis or even extends out of the pelvis to lie in the lower abdomen (Figure 11-43). During excretory urography, persistent uterine opacification is often seen in patients with an underlying uterine fibroid tumor (Figure 11-44). The tumor typically presses on the fundus of the bladder, causing a lobulated extrinsic impression

402

CHAPTER 11  Reproductive System

that differs from the smooth impression usually seen with ovarian cysts. Extension of a fibroid into the adjacent tissues (parametrium) may cause medial displacement of the pelvic ureter or ureteral compression leading to hydronephrosis. The classic ultrasound appearance of a uterine fibroid is a hypoechoic, solid, contour-deforming mass in an enlarged, inhomogeneous uterus (Figure 11-45). Fatty degeneration and calcification cause focal increased echogenicity; the calcification may result in acoustic shadowing. A subserosal fibroid projecting from the uterus, but attached to it by a large stalk, may occasionally simulate an adnexal mass or an ovarian tumor. Endovaginal (transvaginal) ultrasound is the best modality to demonstrate small and submucosal uterine fibroids (Figure 11-46). MRI is more sensitive than CT or ultrasound but is indicated only when ultrasound is inconclusive in differentiating between uterine and adnexal masses or between leiomyoma and adenomyosis, or to search for submucosal fibroids in the patient with unexplained bleeding (Figure 11-47). Treatment. In many cases, no treatment is required for uterine fibroids. Medications can induce a temporary chemical menopause that causes a temporary shrinkage of a fibroid. If bleeding and fibroid size cannot be controlled with medications, surgery is performed. In younger women and for

superficial fibroids, a myomectomy (removal of the leiomyoma) is performed to preserve the uterus. Large or multiple tumors usually require hysterectomy, especially in a woman for whom childbearing is undesirable or complete. Many newer therapeutic techniques are available—multilaser technique, myolysis (electrical coagulation of the myoma), and uterine artery embolization—and various medications have proved to be effective.

Endometrial Carcinoma Adenocarcinoma of the endometrium is the predominant neoplasm of the uterine body and is the most common invasive gynecologic neoplasm. It usually occurs in postmenopausal women, especially those who have never had children. Approximately 75% of patients in whom this tumor is found are 50 years or older and are being seen clinically for postmenopausal bleeding. Imaging appearance. Excretory urography may demonstrate an enlarged uterus impressing or invading the posterior wall and fundus of the bladder. The typical ultrasound appearance of endometrial carcinoma is an enlarged uterus with irregular areas of low-level echoes and bizarre clusters of high-intensity echoes (Figure 11-48). Unless evidence of local invasion can be demonstrated, the ultrasound findings are indistinguishable from those of fibroid tumors, which often occur in patients with endometrial carcinoma. The endovaginal approach is generally preferred to measure endometrial thickness and to determine whether dilation and curettage (D&C—dilation of the cervix to allow scraping of the uterine wall) is required for histologic examination. CT demonstrates focal or diffuse enlargement of the body of the uterus (Figure 11-49). This modality is especially

FIGURE 11-45  Uterine fibroid. Longitudinal sonogram demonstrates a pedunculated leiomyoma as a hypoechoic mass (M) projecting from the fundus of the uterus (U). Decreased sound transmission through the mass indicates its solid nature.

FIGURE 11-46  Submucosal uterine fibroid. Endovaginal ultrasound image of the uterus in the sagittal plane demonstrates a fibroid filling the superior endometrial cavity (arrow).

FIGURE 11-47  Uterine fibroid. T2-weighted MR sagittal image demonstrates a sharply marginated fibroid in the uterine fundus that contains both high and low signal intensity.

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CHAPTER 11  Reproductive System useful for detecting clinically unsuspected omental and nodal metastases in patients with advanced disease, for evaluating patients with suspected neoplastic recurrence, and for checking the response to chemotherapy or radiation treatment. MRI allows differentiation of the endometrium (the inner lining) from the myometrium (the muscle layer) of the uterus and has been shown to be useful for demonstrating focal or diffuse endometrial tumors (Figure 11-50). The excellent contrast resolution of this technique may allow determination of the depth of myometrial invasion. For staging purposes, MRI is superior to CT for demonstrating extension of the tumor into the cervix, broad ligaments, and ovaries. Lymphatic involvement of the pelvis and retroperitoneal lymph nodes can also be visualized; the use of a contrast agent improves the contrast resolution.

FIGURE 11-48  Endometrial carcinoma. Endovaginal sonogram localizing irregular endometrial thickening (arrows) with echogenic polypoid projections into the fluid-filled endometrial canal (F).

Treatment. The first option for treatment of endometrial carcinoma is a hysterectomy with resection of the enlarged lymph nodes. Radiation therapy may follow surgery, especially in cases of advanced disease or an incomplete resection. For inoperable cancers, the preferred choice is chemotherapy.

Endometriosis Endometriosis is the presence of normal-appearing endometrium in sites other than their normal location inside the uterus. Although tissues next to the uterus (ovaries, uterine ligaments, rectovaginal septum, and pelvic peritoneum) are most frequently involved in endometriosis, the gastrointestinal and urinary tracts can also be affected. Current theories of the cause of endometriosis include (1) reflux of endometrial fragments backward through the fallopian tubes during menstruation, with implantation into the pelvis; (2) transformation of multipotential cells in the abdomen and pelvis; (3) implantation of endometrial fragments during surgery or delivery; and (4) spread of endometrial tissue by way of the bloodstream or lymphatic system. Imaging appearance. Although the endometrial tissue lies outside the uterus, it still responds to hormonal changes and undergoes proliferative and secretory phases along with sloughing and subsequent bleeding. Thus, an endometrial implant within a closed space can continue to grow with each menstrual cycle (Figure 11-51). Clinical symptoms include abnormal bleeding, painful menstruation (dysmenorrhea), and pain during sexual intercourse (dyspareunia). Because endometriosis is usually clinically apparent only when ovarian function is active, most women who are symptomatic for

6

1 4

b

2

M 5

3

FIGURE 11-49  Bladder invasion by endometrial carcinoma. CT scan shows a mass (M) obliterating the fat planes between the bladder (b) and the uterus. Urine within the bladder outlines thickening of the posterior bladder wall. Nodular extension into the ischiorectal fossa indicates local extension of the tumor.

5

FIGURE 11-50  Endometrial carcinoma. Sagittal T2-weighted MR image shows extensive tumor of mixed s­ ignal intensity (1) that has invaded the endocervix and permits identification only of the ectocervix (2). Tumor has extended inferiorly along the serosal surface of the uterus into the vesicovaginal septum (3) and bladder wall (4). Low-intensity foci in the vagina represent radiotherapy implants (5). Note the normal urinary bladder wall superiorly (6).

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CHAPTER 11  Reproductive System

FIGURE 11-51  Endometrioma. Endovaginal sonogram demonstrating diffuse, homogeneous, low-level echoes throughout the cystic mass (arrows).

endometriosis are between 20 and 45 years of age. Ultrasound may demonstrate cystic masses filled with old blood. However, differentiation of endometriosis from other adnexal masses requires MRI. Endometriosis involving the urinary tract most commonly produces ureteral obstruction below the level of the pelvic brim. The condition mimics a ureteral tumor and may appear as an intraluminal mass or stricture or as a smooth, rounded, or multilobular filling defect in the bladder. In the gastrointestinal tract, endometriosis primarily affects those segments that are situated in the pelvis (especially the rectosigmoid colon). It typically causes abdominal cramps and diarrhea during the menstrual period and may appear as single or multiple masses in the colon (Figure 11-52). Repeated shedding of endometrial tissue and blood into the peritoneal cavity can lead to the development of dense adhesive bands causing small bowel obstruction. A rare complication of endometriosis with intrathoracic implants of endometrial tissue is recurrent catamenial pneumothorax, which is usually right-sided and occurs during menstrual flow. Treatment. The main functions of treatment for endometriosis include pain management, reduction of disease progression, and prevention or reversal of infertility. To manage pain and reduce disease progression, drugs can be used to interrupt the menstrual cycle by stopping proliferation and secretion of extrauterine cells. A conservative surgical treatment, laser surgery, is used to remove visible endometrial implants that obstruct the fallopian tubes. When the pain of the disease is unbearable, the radical surgical treatment is a complete hysterectomy.

Carcinoma of the Cervix Carcinoma of the cervix is the third most common form of cancer in women. Development of the tumor appears to be

FIGURE 11-52  Endometriosis. Three separate endometrial implants (arrows and arrowheads) are seen in the sigmoid colon. The most distal lesion has a smooth interface with the bowel wall, indicating no intramural invasion. The two more proximal lesions have irregular borders, indicating intramural or submucosal invasion.

related to chronic irritation, infection, and poor hygiene. A higher incidence occurs in women who have begun sexual activity at an early age and have had multiple sexual partners. The development of the Papanicolaou smear examination has permitted detection of cervical carcinoma at a very early stage (carcinoma in situ—confined to the site of origin), when it has not yet invaded the underlying tissues and is surgically curable. Widespread cervical cancer becomes inoperable, and radiation therapy is the usual treatment. Imaging appearance. At the time of the initial staging, one third of patients with carcinoma of the cervix have unilateral or bilateral hydronephrosis, which can be demonstrated by excretory urography or ultrasound. Indeed, the most common cause of death in patients with carcinoma of the cervix is impairment of renal function caused by ureteral obstruction. Extension of the tumor to the bladder may cause an irregular filling defect; direct infiltration of the perirectal tissues may produce irregular narrowing of the rectosigmoid colon and widening of the retrorectal space. Distant metastases to the skeleton or lungs are uncommon, even in patients with advanced disease. Ultrasound usually demonstrates a cervical carcinoma as a solid mass behind the bladder (Figure 11-53). CT is more accurate in detecting pelvic side wall invasion and therefore is usually the initial staging procedure in patients in whom there is a clinical suspicion of advanced disease (Figures 11-54 and 11-55). This modality is also the procedure of choice for monitoring tumor response to treatment and for assessing suspected recurrence. MRI is superior to CT and is the preferred study to distinguish the cervix from the uterus and vagina. Thus, MRI is of value in detecting and staging cervical carcinoma (Figures 11-56 and 11-57). CT cannot always differentiate tumor from adjacent normal tissue. After radiation therapy for carcinoma of the cervix (and other types of pelvic carcinoma), it may be difficult to distinguish chronic rectal narrowing and widening of the retrorectal

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CHAPTER 11  Reproductive System

FIGURE 11-53  Carcinoma of cervix. Sonogram demonstrates a solid, echogenic mass (asterisk) lying behind the bladder (Bl) that is indistinguishable from a benign cervical myoma.

FIGURE 11-56  Cervical carcinoma. On this sagittal T1-weighted MR image, posterior cervical lobulation (1) is the only primary sign of an infiltrating cervical neoplasm. Note the considerable widening of the central uterine high-intensity zone (2) caused by an accumulation of menstrual products in the endometrial canal resulting from tumor occlusion of the endocervical canal. Urine (3) within the vagina produces low signal intensity on this imaging sequence.

3

1

FIGURE 11-54  Carcinoma of cervix. CT scan demonstrates the inhomogeneity of an enlarged cervix (Cx) without evidence of bladder invasion.

2 5

2

4

FIGURE 11-55  Bladder invasion by carcinoma of the cervix. CT scan shows irregularity (arrow) of the posterior margin of a contrast-filled urinary bladder (Bl) and the adjacent inhomogeneous cervical mass (M).

FIGURE 11-57  Carcinoma of the cervix. Sagittal T2-weighted MR image shows a bulky cervical neoplasm (1) with mottled high signal intensity. The lesion has invaded the upper third of the vaginal stroma (2) anteriorly and posteriorly, but it has spared the uterus (3). The urethra (4) and urinary bladder (5) are anteriorly displaced by the tumor.

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CHAPTER 11  Reproductive System

space caused by radiation effects from that caused by recurrence of tumor. Radiation therapy can also lead to the development of fibrous inflammatory adhesions between loops of bowel and the bladder, resulting in the development of fistulas between bowel loops (enteric–enteric fistula) and between a bowel loop and the urinary bladder (enteric–vesicular fistula).

Treatment. A hysterectomy with resection of the involved nodes and surrounding tissues and followed by radiation is recommended for stage I and stage II cervical cancers. Advanced lesions require surgery with a combination of radiation and chemotherapy. A pelvic exenteration (removal of all the pelvic organs to debulk the tumor) is used as a last resort.

Summary of Findings for Diseases of the Female Reproductive System Disorder

Location

Imaging Appearance

Treatment

Pelvic inflammatory disease

Infection of uterus and fallopian tubes

Antibiotics Drainage or aspiration of abscesses

Ovarian cysts

Follicular or in corpus luteum

Polycystic ovarian syndrome Ovarian tumors

Multiple cysts

US—uterus with a thickened endometrium; fallo­pian tubes appear as adnexal masses that are sonolucent; multiloculated, irregular mass with scattered internal echoes CT—shows full extent of severe disease Hysterosalpingography—nonvisualized fallopian tubes US—round, anechoic adnexal masses MRI—cysts produce high signal intensity on T2-weighted images US—10 or more cysts peripherally

Dermoid cyst (teratoma)

Fibrous stroma Omental and peritoneal surface Germ cell tumor of ovary

Uterine fibroids (leiomyomas)

Uterine smooth muscle

Endometrial carcinoma

Uterine body

Endometriosis

Endometrium outside normal location

Carcinoma of the cervix

Cervix

Ovarian metastasis

KUB—scattered tumor calcifications US—solid irregular mass with associated ascites CT—irregular sheet of soft tissue densities b ­ eneath the anterior abdominal wall—omental cake PET—determines recurrence Radiograph—calcifications US—complex, primarily solid mass containing highlevel echoes KUB—mottled mulberry, popcorn calcification IVU—lobulated extrinsic impressions of fundus of bladder US—hypoechoic, solid, contour-deforming mass in an enlarged inhomogeneous uterus (endovaginal demonstrates small and submucosal fibroids) MRI—to differentiate anatomy and distinguish fibroid from adenomyosis; mixed signal intensity on images IVU—cancer invading posterior wall and fundus of bladder US—enlarged uterus with irregular hypoechoic ­areas and bizarre clusters of high–signal intensity echoes CT—diffuse enlargement of the uterine body; omental and nodal metastases MRI—to determine depth of myometrial invasion US—sonolucent masses MRI—differentiates endometriosis from other adnexal masses

US—solid mass posterior to bladder CT—demonstrates pelvic side-wall invasion MRI—differentiates uterus from vagina; used for staging

IVU, Intravenous urography; KUB, kidney–ureter–bladder radiograph; US, ultrasound.

Self-resolution Aspiration and drainage Surgery Insert drugs to induce ovulation Surgery Surgery

Surgery

Medications Myomectomy Myolysis Hysterectomy

Hysterectomy Radiation therapy for incomplete resection Chemotherapy for inoperable tumors

Medications to interrupt menstrual cycle Conservative surgery—laser technique Radical surgery—­ hysterectomy Stage I and II—hysterectomy followed by radiation Advanced stages—surgery with radiation and che­ motherapy

CHAPTER 11  Reproductive System

BREAST LESIONS Breast Cancer Breast cancer is the most common malignancy among women between ages 44 and 50 years. Most tumors are classified as infiltrating duct carcinomas, which occur most frequently in the upper lateral quadrant (Figure 11-58). Current surgical and radiation therapy techniques provide highly effective treatment, but only if the cancers are detected when localized to the breast itself. Today, many breast tumors are diagnosed before they are palpable because routine screening is available (especially in the United States). In these instances, the prognosis is considerably better because the mass has not extended into surrounding tissue or beyond the breast. Breast cancers diagnosed in stage I have a patient survival rate of approximately 98%. Unfortunately, most breast tumors are discovered accidentally rather than in the course of regular survey examinations. By this time, the majority have spread either to regional lymph nodes or systemically, accounting for the current high mortality (approximately 50%) that makes breast cancer the leading cause of cancer death in women. Periodic careful physical examination of the breast, done either by a trained health professional (clinical breast examination [CBE]) or by the patient (breast self-examination [BSE]), will discover cancers that are small and more likely to be localized. Even smaller, nonpalpable, and potentially more curable lesions can be detected by mammography, a radiographic examination that is by far the most effective diagnostic procedure for breast cancer. Indeed, routine mammography combined with physical examination is the only approach currently available that promises to significantly reduce breast cancer mortality. Following a general clinical

407

history, the accepted assessment of a suspected breast mass is a three-pronged approach, comprising physical examination, imaging (usually mammography), and needle biopsy. With screening mammography, 7% to 10% of the patients are recalled for more extensive imaging. Of these, 15% to 20% require a biopsy, and in 5% to 7% cancer is detected. On screening examinations, 40% of the cancers detected are in situ (at the origin), and approximately 75% have no nodal involvement. Imaging appearance. Full-field digital systems have replaced the traditional film-screen system in mammographic imaging. The digital system uses a lower dose and produces an image with increased contrast resolution that enables radiologists to better visualize anatomic structures, thus improving the sensitivity and specificity. In many cases, the digital image is interpreted by the radiologist and reviewed by computer-­ aided diagnosis (CAD) to improve sensitivity and specificity. Almost every breast cancer is seen mammographically as a tumor mass, clustered calcifications, or both. Either feature, when clearly demonstrated, is so indicative of malignancy that prompt biopsy is required whether the lesion is palpable or not. Secondary changes of breast carcinoma include skin thickening and nipple retraction. Magnification imaging and compression techniques greatly improve the diagnostic value of the image. The typical malignant tumor mass is poorly defined with areas of distortion, has irregular margins, and demonstrates numerous fine linear strands or spicules radiating out from the mass (Figure 11-59). This appearance is characteristic but not diagnostic of malignancy and is in stark contrast to the typical mammographic picture of a benign mass, which has well-defined, smooth margins and a round, oval, or gently lobulated contour (Figure 11-60).

Clavicle Intercostal muscle Fascia of pectoral muscles Pectoralis major muscle Alveolus

Pectoralis major muscle

Ductule

A

Duct

Alveoli

Lactiferous duct Areola Lactiferous sinus Nipple Nipple pores Adipose tissue Suspensory ligaments (of Cooper)

FIGURE 11-58  The female breast.

B

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CHAPTER 11  Reproductive System

A

B

FIGURE 11-59  Breast cancer. Full (A) and magnified coned (B) views of the breast demonstrate an ill-defined, irregular mass with radiating spicules (arrowheads).

FIGURE 11-60  Benign breast mass. Screen-film mammogram demonstrates smooth, round fibroadenoma with clearly defined margins.

Clustered calcifications in breast cancer are typically numerous, very small, and localized to one segment of the breast. They demonstrate a wide variety of shapes, including fine linear, curvilinear, and branching forms (Figure 11-61). Although only approximately half of breast cancers are seen mammographically as clusters of calcifications, typical calcifications are seen in many of the nonpalpable intraductal cancers that often do not form mass lesions and may otherwise escape detection. Ultrasound provides a secondary diagnostic tool that can differentiate a benign cyst from a solid mass, and thus it substantially reduces the number of biopsies performed for benign cysts (Figures 11-62 and 11-63) and normal fibroglandular tissue. Ultrasound is best in determining the size of a mass, and Doppler ultrasound permits visualization of blood flow patterns. However, ultrasound is of limited value in detecting nonpalpable cancers, particularly

FIGURE 11-61  Malignant calcifications in breast cancer. Numerous tiny calcific particles with linear (straight arrows), curvilinear (solid arrowhead), and branching (open arrowhead) forms characteristic of malignancy. Note the benign calcification in the arterial wall, which is easily recognized from its large size and tubular distribution (curved arrow).

those that have calcifications alone, and thus it cannot substitute for mammography as a screening examination. In cases of ruptured silicone implants, an inflammatory process causes the development of silicone granulomas. These produce a “snowstorm” appearance (Figure 11-64), causing posterior shadowing that obscures the posterior border. MRI with multiple sequences and contrast enhancement now has the ability to help differentiate between benign adenomas and carcinomas (Figure 11-65). The use of image subtraction (noncontrast image subtracted from the enhanced image) assists in highlighting the contrast-­ enhanced regions. Benign masses tend to have smooth borders, whereas malignancies appear as high–signal intensity

CHAPTER 11  Reproductive System

A

m

m

409

implant twisting or rupture, which may not be visible on other imaging techniques. Although not used routinely, CT can assist in determining extension of the disease (Figure 11-67). SPECT fusion imaging aids in determining lymphatic involvement for breast malignancies (Figure 11-68). The most sensitive imaging modality is PET. Although PET is the least used modality because of its expense and limited availability, as a molecular imaging technique it can demonstrate the metabolic activity and vascularization of the tumor at its earliest stages. Currently, PET is used to detect recurrences in scarred breasts because postoperative scarring makes mammography less effective for visualizing new lesions. Although relatively infrequent (1 in 100), breast cancer also can develop in men. Breast cancer in men usually has a poor prognosis because it is often diagnosed in a later stage. Breast enlargement in men results from a proliferation of the glandular component and is known as gynecomastia. Treatment. Imaging also plays a role in surgical planning by providing guidance (with ultrasound or mammography) for needle localization (Figure 11-69). A conservative surgical approach is lumpectomy, which is used for isolated lesions. Mastectomy, a more aggressive surgical approach, involves the removal of all breast tissue and a dissection of the lymph nodes. If the lymph nodes contain cancerous cells, the axillary nodes are removed (radical mastectomy). Chemotherapy and radiation therapy are used in more advanced cases, depending on the type of cancer cells and whether the axillary nodes are involved. Hormonal chemotherapy with synthetic antiestrogens may be used if the tumor contains estrogen receptors.

Benign Breast Disease B

FIGURE 11-62  Sonography for breast disease. (A) Mammogram shows several rounded masses (m) that could be solid or cystic in a breast that is very dense anteriorly. (B) Sonogram clearly shows that the largest mass (M) is cystic because it contains no internal echoes and shows considerable posterior enhancement (arrows).

lesions with spiculation. Using longer sequences, carcinomas produce high signal intensity, whereas adenomas assume a lower signal intensity (and are not apparent). Fat suppression using water excitation best demonstrates the functional parenchyma, and this technique helps differentiate among various lesions. MRI is used in questionable cases for surgical preplanning to determine whether lumpectomy or mastectomy is the best operative approach. For patients with breast implants, MRI may best demonstrate the surrounding breast tissue (Figure 11-66). This modality also demonstrates

Fibrocystic disease of the breast is a common benign condition that occurs in approximately 20% of premenopausal women. It is usually bilateral, with cysts of various sizes distributed throughout the breasts that also contain an increased amount of fibrous tissue. The size of a cyst usually changes with the menstrual cycle, as does the amount or type of fluid in it. Imaging appearance. A fibroadenoma is the most common benign breast tumor. It generally appears as a smooth, well-circumscribed mass with no invasion of surrounding tissue (see Figure 11-60). Ultrasound permits differentiation of a solid fibroadenoma from a fluid-filled breast cyst. Sonographically, a simple cyst has an anechoic center with a thin echogenic capsule (see Figure 11-62). High-risk patients require monitoring of the cystic lesions for possible conversion to a cancerous process. Equivocal lesions may require imaging with other modalities. Treatment. The most conservative treatment of a benign cyst addresses pain management, usually through dietary modifications and reduction of caffeine intake. If dietary changes do not decrease pain to a tolerable level, drainage of the cyst may be performed. Hormonal therapy with synthetic antiestrogens that block estrogen and progesterone is used in cases of cyclical pain. However, these drugs may produce intolerable side effects. Surgery is not the most effective treatment unless there is only a single cyst (and most patients have multiple cysts).

A

B

FIGURE 11-63  Spiculated lesion. (A) Mammography using magnification–spot compression demonstrates microcalcifications and a spiculated lesion. (B) Breast sonography shows finger-like projections emanating from the lesion measuring 1.8 × 1.25 cm.

A

B

FIGURE 11-64  Ruptured silicone breast implants. (A) Mammogram shows retroglandular implant with extracapsular silicone (arrows). (B) Ultrasound image of the same patient shows the typical “snowstorm” appearance of free extracapsular silicone (arrowheads).

A

B

FIGURE 11-65  Breast carcinoma. (A) Unilateral sagittal T1-weighted fat-saturated postcontrast MR image demonstrates a single mass. (B) Postcontrast MR subtraction image illustrates a spiculated mass.

CHAPTER 11  Reproductive System

411

FIGURE 11-66  Breast implants. MRI distinguishes between breast tissue and implant. A fold in one implant is also visualized (arrow).

A

B

C

D

FIGURE 11-67  Breast cancer. CT scans demonstrate an enhancing breast lesion (arrow) in the axial (A) and coronal projections (B). The lymph nodes (arrows) are enlarged, as seen on the coronal (C) and sagittal projections (D). On lung window scans, pulmonary metastatic nodules were demonstrated.

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CHAPTER 11  Reproductive System A

B

C

FIGURE 11-68  Right sentinel lymph node studied with SPECT and CT fusion imaging. (A) A triplanar anatomic CT image. (B) A triplanar SPECT physiologic image. (C) A triplanar fusion image. One sentinel node is located and marked for intraoperative removal.

Lesion

A

Lesion

STEREO SCOUTS

Lesion

Lesion

B

Prebiopsy stereos with needle through lesion

Area of lesion removal

Area of lesion removal

C

Postbiopsy Stereos

Biopsy needle pulled back for imaging

FIGURE 11-69  Stereotaxic needle biopsy. (A) Stereotaxic scout images (stereos) of breast lesion. (B) Stereotaxic images showing needle localization. (C) Postbiopsy images of lesion with the needle pulled back to demonstrate lesion removal.

Summary of Findings for Breast Lesions Disorder

Location

Imaging Appearance

Treatment

Breast carcinoma

Breast tissue

Lumpectomy Mastectomy Radical mastectomy Chemotherapy or hormonal therapy

Benign breast disease

Fibrocystic breast or single cysts

Mammography—poorly defined with areas of distortion, irregular margins with numerous fine linear strands or spicules radiating from the mass US—differentiates benign cysts from a solid mass and its size; blood flow patterns assessed with Doppler imaging; ruptured silicone implants produce “snowstorm” appearance MRI (subtraction imaging)—benign masses tend to have smooth borders, whereas malignancies demonstrate high signal intensity with spiculation; fat suppression best demonstrates the functional parenchyma and helps differentiate lesions; best demonstrates the surrounding breast tissue in patients with implants PET—demonstrates metabolic activity and vascularization of the tumor at the earliest stages; utilized to detect recurrences in scarred breast tissue Mammography—smooth, well-circumscribed mass without invasion of surrounding tissue US—simple cyst appears as an anechoic center with a thin echogenic capsule

US, Ultrasound.

Pain management through diet Hormonal therapy Surgery for single cysts

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IMAGING IN PREGNANCY Because of its noninvasive and nonionizing character, ultrasound is the modality of choice in the evaluation of possible complications of pregnancy. A major role of ultrasound is to assess the gestational age, a measurement that is often highly inaccurate when based on the date of the last menstrual period. Knowledge of the true gestational age may be critically important for obstetric decisions because the length of pregnancy is a major factor in interpreting the graphs that indicate the status of the fetus. Measurements of fetal age by ultrasound include the longest biparietal diameter (BPD), the crown-to-rump length, and the length of the fetal femur. The BPD is measured from the outer margin of the skull on one side to the inner margin on the other side at the level of the thalami (Figure 11-70). A single measurement of the BPD has its greatest accuracy between 12 and 26 weeks; after this time, the size of the head and thus the BPD may be affected by a growth disturbance. Crown-to-rump length refers to the distance between the tip of the head and the bottom of the fetal trunk (Figure 11-71). This measurement is highly accurate for assessing gestational age in early pregnancy (less than 11 weeks). Fetal femoral length (Figure 11-72) aids in determining fetal age in the

second and third trimesters by identifying epiphyseal cartilage at the knee, which indicates a gestational age beyond 33 to 35 weeks. An early diagnosis of multiple pregnancies can be made by ultrasound (Figure 11-73). This is essential so that therapeutic measures can be taken to reduce the high complication rate associated with twin (or more) fetuses. Ultrasound can be used to detect an abnormal volume of amniotic fluid, which is often associated with underlying fetal anomalies. Polyhydramnios refers to an excessive accumulation of amniotic fluid that may be caused by maternal disorders such as diabetes mellitus and Rh isoimmunization (Figure 11-74). Polyhydramnios is also caused by fetal abnormalities, especially those related to the central nervous system, the gastrointestinal tract, the circulatory system, and dwarfism. Oligohydramnios refers to a very small volume

A FIGURE 11-71  Crown-to-rump length measurement. Cursors delineate the length of the fetus from the top of the head to the bottom of the torso.

B

FIGURE 11-70  Biparietal diameter (BPD) in a 27-week fetus. (A) Cursors delineate BPD, which is measured from the outer margin of skull on one side to the inner margin on other side. Arrows point to the midline falx. (B) Dotted line indicates the head circumference.

FIGURE 11-72  Fetal femur. Cursors demonstrate a femur length of 3.96 cm, and cartilage is not demonstrated, indicating a fetal age earlier than 33 weeks.

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A

415

of amniotic fluid. This condition results primarily from fetal urinary tract disorders, such as renal aplasia, renal dysplasia, and urethral obstruction. Oligohydramnios is also associated with intrauterine growth retardation. Clinically significant errors of morphologic development occur in up to 5% of all children. The in utero detection of these anomalies by ultrasound may permit in utero medical or surgical therapy, may provide an indication for termination of the pregnancy, or may influence the mode of delivery. Although a detailed description of the rapidly expanding field of prenatal sonography is beyond the scope of this book, some of the abnormalities that can be detected, and often treated, in utero are osseous (bony) and neural anomalies of the fetal cranium (Figures 11-75 and 11-76) and spine, gastrointestinal atresias and developmental cysts, cystic and obstructive

B

FIGURE 11-73  Multiple pregnancies. (A) Endovaginal sonogram shows two gestational sacs surrounded by the echogenic chorionic ring (c) composed of the decidua capsularis and the chorion laeve within the decidua vera (d). A yolk sac (small arrow) and live embryo (arrowhead) are present within each gestational sac. The crown-to-rump lengths measure 5.4 mm and 4.7 mm, corresponding to a gestational age of 6.5 weeks. (B) Lateral abdominal radiograph of a woman with quadruplets clearly shows four separate fetal skulls and spines.

FIGURE 11-74  Polyhydramnios. Excessive accumulation of amniotic fluid (hypoechoic area) surrounds the fetus in a mother of advanced age for pregnancy.

FIGURE 11-75  Anencephaly. Long-axis image of a third-­ trimester fetus shows that the head (H) is irregularly shaped, echogenic, and much smaller than the body (arrowheads). B, Maternal bladder.

FIGURE 11-76  Ventriculomegaly. Cranial axial ultrasound image at 27 menstrual weeks shows obvious ventricular enlargement with convex surface of the lateral ventricle wall that parallels the bony calvaria. Note the dangling choroids (c).

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CHAPTER 11  Reproductive System

LEGS FOOT

FIGURE 11-77  Clubfoot. Prenatal ultrasound image shows one foot at a right angle to the leg.

lesions of the genitourinary tract, and congenital cardiac diseases and skeletal anomalies (Figure 11-77). Because ultrasound examinations can demonstrate the fetus and placenta with no apparent risk to the mother or unborn child, ultrasonography is unquestionably the imaging study of choice for evaluating the gravid (pregnant) woman. In extremely rare instances, there may be justification for performing radiographic pelvimetry to demonstrate the architecture of the maternal pelvis and to compare the size of the fetal head with the size of the maternal bony pelvic outlet to determine whether the pelvic diameters are adequate for normal delivery or a cesarean section will be required. In almost all cases, however, the combination of careful clinical evaluation and ultrasonography is sufficient to make these decisions without the need to resort to radiographic pelvimetry with its high radiation dose. There is absolutely no indication ever to perform fetography, the radiographic demonstration of the fetus in utero. Ultrasound can provide far better diagnostic information and is not associated with the danger of radiation-induced fetal malformations.

Ectopic Pregnancy Although ectopic pregnancy is a life-threatening condition, responsible for up to one fourth of maternal deaths, the diagnosis is missed by the initial examining physician in up to three fourths of cases. More than 95% of ectopic pregnancies occur within the fallopian tubes, and more than half the patients with this complication of pregnancy have a history or pathologic evidence of PID. Ectopic pregnancies are often associated with urine or plasma levels of human chorionic gonadotropin (HCG) that are substantially lower for the expected date of gestation than those in patients with normal intrauterine pregnancies. Imaging appearance. Ultrasound is the major imaging modality for diagnosing ectopic pregnancy. The classic appearance consists of an enlarged uterus that does not contain a gestational sac and is associated with an irregular adnexal mass, an “ectopic fetal head,” or fluid in the culde-sac (Figure 11-78). The unequivocal demonstration of an

FIGURE 11-78  Ectopic pregnancy with a live embryo in the adnexa. Endovaginal sonography shows the tubal ring (arrowheads) and gestational sac, containing the yolk sac and live embryo (e). Asterisk indicates free fluid. U, Uterus.

intrauterine pregnancy virtually excludes an ectopic pregnancy because the incidence of coexisting ectopic and intrauterine pregnancies is only 1 in 30,000. Treatment. Emergency surgical intervention before a fatal hemorrhage occurs is required.

Trophoblastic Disease Trophoblastic disease refers to a spectrum of pregnancy-­related disorders ranging from benign hydatidiform mole to the more malignant and frequently metastatic choriocarcinoma. A hydatidiform mole results from abnormal fertilization when there is an absence of the female chromosome. Approximately half of choriocarcinomas follow pregnancies complicated by hydatidiform mole. The remainder occur after spontaneous abortion, ectopic pregnancy, or normal deliveries. Imaging appearance. A hydatidiform mole typically appears on an ultrasound image as a large, soft tissue mass of placental (trophoblastic) tissue filling the uterine cavity and containing echoes of low to moderate amplitude (“bunch of grapes”) (Figure 11-79) without any signs of fetal movement. Endovaginal sonography confirms that there is no evidence of a developing fetus. On ultrasound images, choriocarcinoma resembles benign hydatidiform mole and usually appears as a large complex mass of central hemorrhage, with necrosis found in the expected position of the uterus. Choriocarcinoma tends to metastasize to the lungs, where it typically produces multiple large masses that rapidly regress once appropriate chemotherapy is instituted. Treatment. Hydatidiform moles are treated by removal of all placental tissue by suction curettage of the uterus. If suction curettage does not lower the patient’s human chorionic gonadotropin level, the disease progresses, and the patient requires chemotherapy. For choriocarcinoma, folic acid antagonists have a cure rate of approximately 80% if treatment begins before brain metastasis occurs.

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Summary of Findings for Pregnancy Disorder

Location

Imaging Appearance

Treatment

Uterine pregnancy Ectopic pregnancy

Fetus within the uterus Fertilization outside the uterus Abnormal fertilization

US—demonstrates the fetus and placenta US—enlarged uterus without gestational sac and an appearance of an irregular adnexal mass US—large soft tissue mass with “bunch of grapes” appearance

Normal birth Surgical intervention Suction curettage

Malignant transformation of hydatidiform mole

US—large complex mass with necrosis

Lack of fertilization or implantation

Radiograph—hysterosalpingography to demonstrate the ovaries, fallopian tubes, and uterus US—screening for congenital anomalies and to monitor treatment

Chemotherapy of folic acid antagonist Ovulationinduction agents

Trophoblastic disease Hydatidiform mole Choriocarcinoma

Female infertility

US, Ultrasound.

A

B FIGURE 11-79  Hydatidiform mole. Longitudinal sonogram in a patient in her second trimester of pregnancy demonstrates a large, moderately echogenic mass filling the central uterine cavity. Note the numerous small cystic spaces (arrows), which represent greatly hydropic chorionic villi.

FEMALE INFERTILITY The causes of infertility in young women include anomalies in the reproductive organs, such as an abnormal uterus that cannot hold a fetus (Figure 11-80), obstructed fallopian tubes, ovaries that are unable to produce mature ova, and disruption of the path the ova normally follow to the uterus. Imaging appearance. The major radiographic procedure for evaluating infertile women is hysterosalpingography, in which the uterine cavity and fallopian tubes are opacified after the injection of contrast material into the uterus. In a woman with normal patent fallopian tubes, contrast material extravasating into the pelvic peritoneal cavity outlines the peritoneal surfaces (see Figure 11-31). Developmental anomalies or fibrosis from PID may cause occlusion of one or both of the fallopian tubes; in such cases, there is no evidence of the contrast material reaching the peritoneal cavity (see Figure 11-32). In addition to assessing tubal patency,

C

FIGURE 11-80  Uterine agenesis. Ultrasound images of a 16-year-old girl who has never had a menstrual cycle. Midline sagittal view (A) demonstrates the bladder (dark area) with no uterus found posteriorly. Normal left (B) and right (C) ovaries are shown in the parasagittal plane.

hysterosalpingography can also demonstrate uterine abnormalities that contribute to infertility, such as intrauterine fibroids, severe uterine flexion or retroversion, and other congenital and acquired malformations. Treatment. For women who receive ovulation-induction agents as treatment for infertility, ultrasound can be used to monitor the maturation of ovarian follicles. Low-level internal

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echoes in mature ovarian follicles appear to be a prognostic indicator of fertility. They may represent a periovulatory state, which is an appropriate time for artificial insemination or invitro fertilization. Ultrasound can also demonstrate the

characteristic bilateral multicystic ovarian enlargement in the ovarian hyperstimulation syndrome, which may develop in women receiving menotropins ­ (Pergonal) therapy for ­infertility.

  REVIEW QUESTIONS 1. Why has ultrasound become the major imaging modality for both the male and the female reproductive systems? 2. In addition to ultrasound, what are the main radiographic studies currently used for the female reproductive system? 3. The formation of sperm is known as _________________. 4. What male hormone helps to regulate metabolism by promoting growth of skeletal muscles and is considered responsible for the greater degree of muscle development in men? 5. Severing of the vas deferens to create sterility is termed _________________. 6. The second most common cause of malignancy in men is _________________. 7. What imaging modality for demonstrating the prostate gland uses a probe inserted into the rectum? 8. True or false: Ultrasound studies of the prostate gland cannot always determine the malignant or benign status of prostatic disease. 9. Prostatic carcinoma can often spread through the bloodstream to the bone and can sometimes cause sclerosis of an entire vertebra. This pathologic condition is termed _________________. 10. What screening technique is usually employed to identify the location of an undescended testicle?

11. What is the term used to describe the twisting of the male gonad on its pedicle? 12. The most common neoplasms in men between 20 and 35 years of age are tumors that tend to metastasize through the _________________ system. 13. The rupture and expulsion of the mature ovum into the pelvic cavity is termed _________________. 14. A pregnancy that occurs in a fallopian tube or in the pelvic cavity is termed _________________. 15. What is the name of the radiographic procedure used to demonstrate the patency or status of the fallopian tubes? 16. Untreated _________________ can lead to cerebral cortical lesions, causing mental disorders, and involvement of the skeletal system and affects infants born to infected mothers. 17. The most common type of germ cell tumor, often containing teeth, hair, and fatty material, is called a(n) _________________. 18. Leiomyomas, which are more commonly referred to as _________________, are benign smooth-muscle tumors of the uterus. 19. The most common malignancy among women occurs in the _________________. 20. The second most common form of cancer in women is _________________.

12 Miscellaneous Diseases OUTLINE Nutritional Diseases Vitamin Deficiencies Hypervitaminosis Protein–Calorie Malnutrition (Kwashiorkor) Obesity

Systemic Lupus Erythematosus Melanoma Muscular Dystrophy

Hereditary Diseases Chromosomal Aberrations Genetic Amino Acid Disorders

niacin nutritional deficiency osteomalacia pectus excavatum Pelken spur syndrome

testicular dysgenesis thiamine vitamins water-soluble vitamins Wimberger’s sign of scurvy

KEY TERMS arachnodactyly ascorbic acid aseptic necrosis fat-soluble vitamins gonadal dysgenesis microcephaly

OBJECTIVES After reading this chapter, the reader will be able to: • Describe nutritional disorders and their possible relationship to disorders of other organs • Define terminology relating to nutritional disorders • Define and describe all boldface terms in this chapter • Distinguish the pathologic conditions caused by various vitamin deficiencies

• Describe the pathologic conditions associated with muscular dystrophy, melanoma, and systemic lupus erythematosus • Differentiate hereditary abnormalities, including chromosomal aberrations and genetic amino acid disorders

NUTRITIONAL DISEASES

Vitamin Deficiencies

Disorders of nutrition range from malnutrition and vitamin deficiency to obesity and hypervitaminosis. In addition to inadequate intake, nutritional deficiency may be related to disorders of the liver, pancreas, and gastrointestinal tract that result in an inability of the body to digest and properly use proteins, carbohydrates, and lipids. In diabetes mellitus, the absence of insulin prevents entry of glucose into the cells and thus deprives the body of its major source of energy. Abnormalities of the pancreas, liver, and gastrointestinal tract that cause nutritional diseases are discussed elsewhere; this section deals with diseases caused by vitamin deficiency, malnutrition, and obesity.

Vitamins are an essential part of the enzymatic systems that are vital to the body’s cellular metabolism. Vitamins are formed (synthesized) only by plants, not by animals. Therefore, humans’ supply of vitamins comes directly from eating fruits and vegetables or from animals (including fish) that have eaten plants and have stored the vitamins. Vitamins are generally divided into two categories: fat soluble and water soluble. The fat-soluble vitamins (A, D, E, and K) can be stored within body tissues. Water-soluble vitamins (B and C) cannot be stored and must be a regular part of the diet to prevent a deficiency. The major B vitamins are thiamine, riboflavin, niacin, pantothenic acid, cobalamin (vitamin B12), and folic acid.

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RADIOGRAPHER NOTES Radiography of patients with various nutritional diseases can be challenging because of the many effects these diseases have on all body systems. Some produce deformities; others can cause mental disorders. Obese patients can present unique problems in positioning and in selection of radiographic settings. The radiographer must be especially empathetic when dealing with these patients, who often are embarrassed because of their size and thus difficult to deal with. The manifestations of systemic lupus erythematosus cause considerable discomfort for patients. Patients with melanoma that has already metastasized or those who are facing extensive surgical intervention are usually very depressed and sometimes require special handling. Patients with muscular dystrophy can be easily agitated and are usually frustrated by their inability to control themselves. Hereditary diseases that cause abnormalities require special understanding on the part of the technologist to attain optimal patient cooperation that will result in good diagnostic radiographs. In general, patients suffering from the various diseases in the miscellaneous category in this chapter can be very demanding and require considerable patience on the part of the radiographer.

Vitamin deficiency diseases are rare in the United States but are prevalent in underdeveloped countries.

Beriberi (Thiamine Deficiency) Beriberi results from a deficiency in thiamine (vitamin B1), a coenzyme essential for carbohydrate metabolism that promotes growth and maintains muscle tone and heart function. Beriberi occurs primarily in rice-eating countries, such as China, where the main staple is polished rice from which the vitamin-containing skin and germ have been removed. Infantile beriberi is common in breast-fed infants 2 to 4 months of age whose mothers have thiamine deficiency. Noninflammatory degeneration of the myelin sheath caused by thiamine deficiency produces a peripheral neuropathy characterized by weakness of the limbs and a “pins and needles” sensation in the extremities. Imaging appearance. Initially, peripheral vasodilation in beriberi increases cardiac output, which then produces a generalized enlargement of the cardiac silhouette and increased pulmonary vascular markings. With progression of disease, the myocardium becomes edematous and flabby and cannot function properly, leading to congestive heart failure and generalized edema (Figure 12-1). Pellagra (Niacin Deficiency) Pellagra, caused by a deficiency of niacin (vitamin B3), is characterized by reddening and scaling of the skin on exposed parts of the body, vomiting and severe diarrhea, and nervous and mental disorders (ranging from chronic depression to violent, irrational behavior). The body requires niacin to complete the cellular process called respiration, in which nutrients and oxygen reach the cells through a series of chemical reactions. As a result of dietary supplements, epidemics of pellagra no longer exist; however, sporadic incidences occur among chronic alcoholics and people suffering from malabsorption.

FIGURE 12-1  Beriberi. Diffuse pulmonary edema caused by severe high-output heart failure.

Scurvy (Vitamin C Deficiency) In patients with scurvy, the deficiency of ascorbic acid (vitamin C) leads to an inability of the supporting tissues to produce and maintain vascular endothelium and the cementing substances that hold epithelial cells together (collagen, osteoid, and dentin). Scurvy was classically a disease of sailors and explorers deprived of fresh fruit and vegetables containing vitamin C. Weakening of capillary walls in scurvy often results in bleeding into the skin, joints, and internal organs. The gums are especially affected and bleed easily. The open lesions provide an entry for bacteria, leading to necrosis of gum tissue and tooth loosening and loss. Impaired synthesis of collagen leads to poor and delayed wound healing. Imaging appearance. In children, disordered chon­ droblastic and osteoblastic activity cause radiographic bone changes that are most prevalent where growth is normally most rapid (especially about the knee and wrist). The bones are generally osteoporotic with blurring or disappearance of trabecular markings and severe cortical thinning. Widening and increased density of the zone of provisional calcification produce the characteristic “white line” of scurvy (Figure 12-2). A relatively lucent osteoporotic zone forms on the diaphyseal side of the white line. This osteoporotic zone is easily fractured, permitting the dense bone to become impacted on the shaft and to jut laterally beyond it, thus giving rise to characteristic marginal spur formation (Pelken spur). The epiphyseal ossification centers are demineralized and surrounded by dense, sharply demarcated rings of calcification (Wimberger’s sign of scurvy). If epiphyseal dislocations have not occurred, the appearance of the skeletal structures usually returns to normal after appropriate therapy. Subperiosteal hemorrhage often occurs along the shafts of the long bones. Calcification of the elevated periosteum and underlying hematoma is a radiographic sign of healing. Rickets (Vitamin D Deficiency) Rickets is a bone disease of young children in which a lack of vitamin D leads to decreased absorption of calcium from

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421

FIGURE 12-2  Scurvy. Frontal projections of both knees demonstrate widening and increased density of the zone of provisional calcification, producing the characteristic “white line” of scurvy. Note also the submetaphyseal zone of lucency and characteristic marginal spur formation (Pelken spur). Epiphyseal ossification centers are surrounded by a dense, sharply demarcated ring of calcification (Wimberger’s sign).

the gastrointestinal tract, resulting in weak, deformed bones. In adults, lack of vitamin D causes generalized softening of bones (osteomalacia). The radiographic findings of rickets and osteomalacia are found in Chapter 4.

Vitamin A Deficiency Vitamin A, or retinol, is essential for vision because it is a vital component of the pigment that absorbs light in the rods of the retina. A lack of vitamin A results in night blindness, an inability to see in dim light. Vitamin A also is important for maintaining the integrity of the mucous membranes lining the respiratory, gastrointestinal, and urogenital tracts. A lack of vitamin A makes these membranes dry and susceptible to cracking, permitting infectious organisms to enter the underlying tissues. Vitamin A is derived from β-carotene, a yellow plant pigment that is converted into vitamin A by the liver. Good sources of vitamin A include dairy products, egg yolks, fish, and vegetables such as carrots, spinach, and sweet potatoes. Vitamin K Deficiency Vitamin K, a fat-soluble vitamin, is necessary for the formation of prothrombin, an essential ingredient in the blood-clotting mechanism. It is primarily found in green leafy vegetables. A deficiency of vitamin K results in excessive bleeding.

Treatment of Vitamin Deficiencies Any of the following three approaches can be used to treat vitamin deficiencies: (1) The patient’s diet is modified to include foods that contain the recommended daily requirements, (2) the patient is given synthetic oral supplements, and (3) vitamins are injected. Some deficiencies may be associated with absorption abnormalities resulting from a lack of the specific vitamins needed to absorb and process vitamins. Dietary modifications for vitamin B deficiencies include increasing the intake of protein (meat), green leafy vegetables, and milk. For vitamin C deficiencies, an increase in consumption of fresh fruits and green leafy vegetables may help. Vitamin D deficiencies require the addition of cod liver oil, egg yolks, butter, and oily fish to the diet. Fortified milk and exposure to sunlight also provide vitamin D. To increase vitamin A, a diet including more liver, meat, eggs, milk, and dark green and yellow vegetables is of value. Eating more spinach, lettuce, broccoli, Brussels sprouts, and cabbage increases dietary vitamin K.

Hypervitaminosis Long-term excessive intake of vitamin A produces a syndrome characterized by bone and joint pain, hair loss, itching, anorexia, dryness and fissuring of the lips, hepatosplenomegaly, and yellow tinting of the skin. This condition usually affects young children, who become irritable and fail to gain weight. Imaging appearance. Excess vitamin D causes too much calcium to be absorbed from the gastrointestinal tract. The

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resulting hypercalcemia leads to the deposition of calcium in the kidney, heart, lungs, and wall of the stomach (Figure 12-3). Treatment. Because there is an excess of vitamins, treatment requires a decrease in vitamin intake and monitoring of the patient to ensure that the levels are stable.

Protein–Calorie Malnutrition (Kwashiorkor) Severe protein–calorie malnutrition (kwashiorkor) affects millions of young children (younger than 5 years) in developing countries (approximately 182 million in 2000) and produces abnormalities involving the gastrointestinal tract and nervous system. In those affected, an imbalance between the body’s supply of nutrients and its demand for energy causes a wasting away or emaciation. Fatty replacement of liver tissue and the resulting decreased levels of albumin lead to diffuse edema and ascites and the characteristic clinical appearance of a considerably protuberant abdomen. Damage to the pancreas and intestinal mucosa prevents proper digestion and absorption of nutrients.

FIGURE 12-3  Hypervitaminosis D. Huge masses of calcification near the shoulder joints bilaterally.

Imaging appearance. Retarded bone growth with thinned cortices usually occurs in protein–calorie malnutrition. Atrophy of the thymus gland and lymphoid tissues diminishes the child’s resistance to infection from organisms that enter the body through skin lesions and the damaged mucous membranes of the gastrointestinal tract. Mental development is also impaired, and brain atrophy can be demonstrated radiographically. Treatment. The initial approach to protein–calorie malnutrition is to correct the child’s fluid and electrolyte balance. Milk and supplementary vitamins are added to the diet. The mortality rate, which is 15% to 40%, results from the dangerous fluid imbalance.

Obesity Obesity refers to an excess of adipose (fatty) tissue that develops when the caloric intake (from food) consistently exceeds the amount of calories required by the body to perform its daily activities. The condition may be related simply to personal habits of excessive eating combined with a lack of activity, or it may be a result of such conditions as hypothyroidism, Cushing’s disease, insulinoma, and hypothalamic disorders. Imaging appearance. Excess adipose tissue can cause displacement of normal abdominal structures, producing such radiographic patterns as widening of the retrogastric (Figure 12-4) and retrorectal spaces. An extreme increase in the intra-abdominal volume causes diffuse elevation of the diaphragm with a relatively transverse position of the heart (simulating cardiomegaly), prominence of pulmonary markings, and atelectatic changes at the lung bases. In the most severe form of obesity (pickwickian syndrome), the excursion of the diaphragm is limited, and the lungs can barely expand with breathing. This results in profound hypoventilation, hypoxia, retention of carbon dioxide, secondary polycythemia, and pulmonary hypertension with right heart failure. An excessive deposition of fatty tissue can also appear radiographically as widening of the mediastinum and prominence of the pericardial fat pads.

FIGURE 12-4  Obesity. Enlargement of the retrogastric space caused by a massive deposition of fatty tissue.

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423

Summary of Findings for Nutritional Diseases Disorder

Cause

Imaging Appearance

Beriberi

Deficiency in vitamin B1 Decrease in carbohydrate ­metabolism Deficiency in vitamin B3 Deficiency in vitamin C

Enlarged cardiac silhouette with increased pulmonary markings

Pellagra Scurvy

Rickets

Vitamin A deficiency

Vitamin K deficiency

Hypervitaminosis

Deficiency of vitamin D Leads to decrease in absorption of calcium Deficiency of vitamin A Visual deficiencies and ­ decreased integrity of mucous membranes Deficiency of vitamin K Decreased prothrombin ­production Usually excessive vitamin A or D

Protein–calorie ­malnutrition

Severe protein–calorie deficiency

Obesity

Excessive adipose tissue—due to caloric intake consistently exceeding calories required

Not specific Osteoporosis with blurring of ­trabecular markings and severe cortical thinning Widening and increased density of the zone of provisional calcification, producing a white line See “Osteomalacia” in Chapter 4

Not specific

Treatment

Increased intake by diet modification Increased intake with ­synthetic supplements Injections of the specific vitamin Increased absorption of ­vitamin through ­association with other dietary products

Not specific

Vitamin A—not specific Vitamin D—hypercalcemia leads to deposition of calcium in the kidney, heart, lungs, and wall of the stomach Retarded bone growth Thinned cortices Brain atrophy Displacement of anatomic structures Elevated diaphragm Widened mediastinum

Treatment. The simplest treatments for obesity include weight management by dieting, use of nutritional counseling and behavioral therapy, and dietary drugs. Patients with morbid obesity may undergo surgical procedures in an attempt to lose large amounts of weight. Gastric restrictive operations attempt to limit gastric capacity and limit gastric outflow, thus making the patient feel full after a small meal. This effect causes the patient to limit his or her oral intake and results in weight control. The major procedure is a gastroplasty, in which a small upper gastric remnant is connected to a larger lower gastric pouch by a narrow channel. Another procedure, gastric banding, is the placement of an adjustable band (accessed by an external port) that can be inflated to control gastric emptying. Complications of gastric restrictive procedures, which can occur in the early and late postoperative periods, include leakage, perforation, widening of the channel, and obstruction.

Decreased vitamin intake

Balance of fluids and electrolytes Provision of milk and ­supplemental vitamins Weight management by dieting Nutritional counseling and behavioral therapy Dietary drugs Surgical resection to limit gastric capacity

SYSTEMIC LUPUS ERYTHEMATOSUS Systemic lupus erythematosus is a connective tissue disorder that affects primarily young or middle-aged women and most likely represents an immune complex disease. The cell activation is thought to be connected to genetic, environmental, and hormonal factors. The presentation and course of the disease are highly variable, from limited skin involvement to tragic systemic disease. Characteristic findings include a butterfly-shaped rash over the nose and cheeks and extreme sensitivity of the skin to sunlight. Imaging appearance. Pain in multiple muscles and joints is the most frequent clinical complaint in patients with systemic lupus erythematosus. A characteristic finding is subluxations and malalignment of joints in the absence of erosions (Figure 12-5). Cardiopulmonary abnormalities also frequently develop. Pleural effusions, usually bilateral and small but occasionally

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FIGURE 12-5  Systemic lupus erythematosus. Frontal and oblique projections of the hand show subluxation of the phalanges at the metacarpal articulations and hyperextension deformities of the proximal interphalangeal joints. Note the absence of erosive changes.

approximately one-fourth of patients. In the gastrointestinal system, a necrotizing inflammation of blood vessels can result in massive bleeding, multiple infarctions, and bowel perforation. Many of the radiographic manifestations of systemic lupus erythematosus tend to disappear during spontaneous remissions or after steroid therapy. Treatment. Anti-inflammatory drugs are used to treat pain in the muscles and joints in patients with systemic lupus erythematosus. Systemic corticosteroids help prevent pathologic conditions involving the renal and central nervous system. If skin lesions occur, antimalarial drugs are prescribed.

MELANOMA FIGURE 12-6  Systemic lupus erythematosus. Bilateral pleural effusions, more pronounced on the right, with some streaks of basilar atelectasis. Massive cardiomegaly is attribu­ table to a combination of pericarditis and pericardial effusion.

massive, occur in approximately half of patients with the disease (Figure 12-6). Enlargement of the cardiac silhouette is generally the result of pericarditis and pericardial effusion. Although kidney involvement (often leading to renal failure) is one of the most serious manifestations of systemic lupus erythematosus, no specific urographic findings are seen. Enlargement of the liver, spleen, and lymph nodes occurs in

Melanoma is an extremely malignant skin cancer that metastasizes widely throughout the body. The tumor develops from a benign mole (nevus), which changes size and color and becomes itchy and sore. The incidence of melanoma is rising, having increased in the United States approximately 2000% since 1930. Globally, cancer statistics from 2002 show that incidences in Australia and New Zealand are approximately six times higher in males and two times higher in females. Although melanoma represents only 4% of all skin cancers, the mortality rate is greater than 70%. Imaging appearance. Metastases from malignant melanoma frequently involve the gastrointestinal tract, usually sparing the large bowel. They are typically well circumscribed, round, or oval nodules that may develop central

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425

FIGURE 12-7  Metastatic melanoma. Large central ulcerations in two sharply defined filling defects in the small bowel (arrows).

necrosis and ulceration; in a barium study, such a nodule appears as a dense, barium-filled central crater surrounded by a sharply marginated nodular mass (bull’s-eye, or target, lesion) (Figure 12-7). Gastrointestinal metastases can be the first clinical manifestation of metastatic melanoma; at times, it can be impossible to identify the primary tumor site. Metastatic melanoma can also produce multiple nodules in the lung and destructive bone lesions with neither new bone formation nor reactive sclerosis. Treatment. Carefully watching for changes in moles or in the skin and having a biopsy to assess the lesion is the best prevention of melanoma and is highly recommended. Also, continuous protection from the sun may reduce the development of these lesions. Surgical excision of the tumor and surrounding tissue may be all that is required. A lymph node biopsy determines whether chemotherapy is required for metastases. The prognosis depends on the size of the lesion and the results of the lymph node biopsy.

MUSCULAR DYSTROPHY Muscular dystrophy refers to a group of chronic inherited conditions in which fat replaces muscle, leading to generalized weakness and eventually death due to respiratory muscle failure or pneumonia. Males are more commonly affected because of the X-linked inheritance pattern. Of the many types, the most common is Duchenne’s muscular dystrophy (DMD), which has been identified on the DMD gene as the Xp21 band. A milder form is Becker’s muscular dystrophy. Imaging appearance. On radiographs of the extremities, the extensive accumulation of fat within the remaining muscle bundles produces a fine striated, or striped, appearance (Figure 12-8). Because most of the muscle tissue is replaced by fat, the fascial sheath bounding the muscles may stand out as a thin shadow or as increased density when it is visualized on edge. Decreased muscular tone can lead to osteoporosis, bone atrophy with cortical thinning, scoliosis, and joint contractures.

Summary of Findings for Miscellaneous Disorders Disorder

Cause

Imaging Appearance

Treatment

Systemic lupus ­erythematosus

Immune complex ­ disease (a connective tissue disorder)

Skeletal—subluxations and malalignment of joints Chest—pleural effusions, small and bilateral; cardiac enlargement

Melanoma

Widely metastasizing malignant skin cancer

Metastatic involvement of the ­gastrointestinal tract; round or oval ­nodules with necrosis and ulceration

Muscular dystrophy

Replacement of muscle by fat

Extremities—fine striated (striped) ­appearance of remaining muscle bundles

Anti-inflammatory drugs for muscle and joint pain Systemic corticosteroids help prevent renal and central nervous system pathology Antimalarial drugs for skin lesions Prevention—monitoring for changes in skin and reduction of sun exposure Surgical excision of lesion and surrounding tissue; biopsy needed to determine whether chemotherapy is necessary Nonstrenuous exercise to maintain mobility and function Drug therapy to protect muscle mass and function

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An abnormal swallowing mechanism in muscular dystrophy can result in the failure to clear barium adequately from the pharynx; this problem may lead to tracheal aspiration and nasal regurgitation of contrast material (or other ingested substances). Treatment. No curative therapy for muscular dystrophy is known. Gene therapy and cell therapy are currently under investigation as possible treatments. Currently, drug therapy is used to protect muscle mass and function. A regimen of nonstrenuous exercise is recommended to maintain mobility and function for as long as possible.

FIGURE 12-8  Muscular dystrophy. Thin, demineralized bones of the lower leg. Increased lucency, representing fatty infiltration in muscle bundles, makes fascial sheaths appear as thin shadows of increased density (arrows) surrounded by fat.

HEREDITARY DISEASES Chromosomal Aberrations The chromosomes may mutate in many different ways and cause a multitude of disease processes. The following describes chromosomal aberrations in two trisomy disorders (Down syndrome and Klinefelter’s syndrome), a monosomy disorder (Turner’s syndrome), and an autosomal dominant disorder (Marfan’s syndrome). A syndrome indicates the presence of a combination of symptoms that commonly occur together and are related to a single cause.

Down Syndrome Down syndrome, the most common of the trisomy disorders (trisomy 21), is caused by an extra-autosomal chromosome that results in an individual having three strands of chromosome 21 instead of the normal two. Down syndrome is usually diagnosed at birth because of the characteristic clinical appearance: mental deficiency, short stature, poor muscle tone, short neck, and a straight skin crease extending across the palm of the hand. The typical facial appearance includes widely set eyes, a short and flat nose, and a coarse tongue that often protrudes through a partially open mouth. Congenital heart disease, especially septal defects, occurs in approximately 40% of patients with Down syndrome. There is also a greater-than-normal incidence of duodenal obstruction (duodenal atresia or annular pancreas) and Hirschsprung’s disease and a substantially increased likelihood of development of leukemia. Laboratory tests (chorionic villus sampling [CVS], amniocentesis, and percutaneous umbilical blood sampling [PUBS]) and the age of the mother are used to determine the risk of Down syndrome for prospective parents. Ultrasound (ultrasonography) can provide additional information. Even with these sophisticated tests, false-positive results may occur, and an accurate diagnosis can be made only after birth. Imaging appearance. The major skeletal abnormality in infancy in a child with Down syndrome is in the pelvis, where there is a decrease in the acetabular and iliac angles with hypoplasia and noticeable lateral flaring of the iliac wings (Figure 12-9). Other common skeletal abnormalities are shortening of the middle phalanx of the fifth finger, squaring of the

A

I

FIGURE 12-9  Down syndrome. Two examples of a typical pelvis in Down syndrome show flared iliac wings and diminished acetabular (A) and iliac (I) angles.

CHAPTER 12  Miscellaneous Diseases vertebral bodies (superoinferior length becoming equal to or greater than the anteroposterior measurement), hypoplasia of the nasal sinuses, and delayed closure of the cranial sutures. Treatment. The many different anomalies of Down syndrome require various treatments, which generally provide a better quality of life for the affected person. Experimental dietary supplements (dimethyl sulfoxide [DMSO]–amino acid formula) are believed by some authorities to slow the retardation process, but the U.S. Food and Drug Administration has not approved these drugs.

Klinefelter’s Syndrome Klinefelter’s syndrome (testicular dysgenesis) is a disorder characterized by small testes that fail to mature and to produce sperm and testosterone. The fundamental defect is the presence in a male of two or more X chromosomes, indicating that this disorder is another sex chromosome trisomy. The pituitary gland sends a signal for the body to produce testosterone, but the testes do not respond. At puberty, the breasts enlarge, and a female distribution of hair develops. The affected individual is tall, mentally deficient (often with language impairment), and sterile. Imaging appearance. Radiographically, skeletal changes are both less common and less pronounced in Klinefelter’s syndrome than in Turner’s syndrome, its female counterpart. The metacarpal sign is present in fewer than 25% of the patients. Hypogonadism may lead to delayed epiphyseal fusion and retarded bone maturation. Treatment. Hormonal therapy provides treatment of the symptoms of Klinefelter’s syndrome. When the patient enters puberty, testosterone therapy assists the body in developing normal male attributes (male distribution of hair growth and muscular body type). Turner’s Syndrome Turner’s syndrome (gonadal dysgenesis), a sex chromosome monosomy disorder, is characterized by primary amenorrhea (no ovulation or menstruation), sexual infantilism, short stature, and bilateral tiny gonads. Although the patient appears to be female, she has only one X chromosome as a result of faulty cellular division. Various urinary tract anomalies, especially horseshoe kidney and other types of malrotation, are often seen in patients with gonadal dysgenesis. Coarctation of the aorta is the most common cardiovascular anomaly. Because coarctation of the aorta most often affects men, its appearance in a woman should indicate the possibility of underlying gonadal dysgenesis. Imaging appearance. A characteristic, but nonspecific, skeletal abnormality in Turner’s syndrome is shortening of the fourth metacarpal and sometimes also the fifth metacarpal (Figure 12-10). This produces the metacarpal sign, in which a line drawn tangentially to the distal ends of the heads of the fourth and fifth metacarpals passes through the head of the third metacarpal (indicating the disproportionate shortening of the fourth and fifth metacarpals), rather than extending distally to the head of the third metacarpal as in an unaffected person. Skeletal surveys performed serially at

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specified intervals during adolescence demonstrate changes in bone growth. Treatment. Patients with Turner’s syndrome can receive treatment for their short stature and for gonadal dysfunction. Human growth hormones have been available since 1994. Hormone replacement therapy of progesterone and/or estrogen may be prescribed to treat gonadal dysfunction (lack of ovulation) and to promote female physical attributes (hair distribution and breast growth).

Marfan’s Syndrome Marfan’s syndrome is an inherited generalized disorder of connective tissue with ocular, skeletal, and cardiovascular manifestations. Most patients with this autosomal dominant disorder are tall and slender, appearing emaciated because of the decrease in subcutaneous fat. A typical feature of Marfan’s syndrome is bilateral dislocation of the lens of the eye caused by weakness of its supporting tissues. A laxity of ligaments about the joints leads to loose-jointedness (or double-jointedness), recurrent dislocations, and flat feet. Almost all patients with Marfan’s syndrome have abnormalities of the cardiovascular system. Necrosis of the medial portion of the aortic wall causes a progressive dilation of the ascending aorta that produces a bulging of the upper right portion of the cardiac silhouette (Figure 12-11) and an unusual prominence of the pulmonary outflow tract as it is displaced by the dilated aorta. Dissecting aneurysm, a serious complication, may kill the patient in early life.

FIGURE 12-10  Turner’s syndrome. Frontal projection of a hand shows the short fourth metacarpal.

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CHAPTER 12  Miscellaneous Diseases

Summary of Findings for Hereditary Diseases Disorder

Cause

Imaging Appearance

Treatment

Down syndrome

Extra autosomal chromosome—­ trisomy 21

Various treatments to provide a better quality of life

Klinefelter’s syndrome (testicular dysgenesis)

Sex chromosome trisomy disorder—male with two or more X chromosomes Sex chromosome trisomy disorder—female with one X chromosome Autosomal dominant disorder of connective tissue

Pelvis—decreased acetabular and iliac angles with hypoplasia and lateral flaring of iliac wings Possible delayed epiphyseal fusion and retarded bone maturation Shortening of the fourth and fifth metacarpals

Growth hormones for stature Hormonal therapy for gonadal dysfunction No cure

Turner’s syndrome (gonadal dysgenesis) Marfan’s syndrome

Imaging appearance. The major radiographic abnormality is elongation and thinning of the tubular bones (Figure 12-12), most pronounced in the hands and feet and seen clinically as arachnodactyly (spider-like digits). Patients may exhibit pectus excavatum (concave sternum) on a lateral chest radiograph (Figure 12-13). Treatment. Currently, no cure exists for Marfan’s syndrome. The laxity of the joints makes affected patients susceptible to scoliosis; monitoring the spine and treating any curvature early help prevent spinal deformities. These patients are vulnerable to endocarditis resulting from dental procedures and commonly receive prophylactic antibiotics.

Genetic Amino Acid Disorders

Elongation and thinning of tubular bones (hands and feet), arachnodactyly

Hormonal therapy

function. This genetic defect causes a decrease or an interruption in amino acid metabolism.

Homocystinuria Homocystinuria, an inborn error of the metabolism of the amino acid methionine, causes a defect in the structure of collagen or elastin. The absence of the enzyme cystathionine B-synthase causes an elevation in methionine by not allowing the metabolic cycle to complete its process. Homocystinuria occurs only if both parents carry the gene (i.e., it is an autosomal recessive trait). Patients with homocystinuria have a tendency to demonstrate arterial and venous thrombosis, and premature occlusive vascular

The genetic amino acid disorders result from the absence of an enzyme required to produce a biochemical reaction that the body requires for normal growth and physiologic

FIGURE 12-11  Marfan’s syndrome. Arteriogram shows the enormous dilation of the aneurysmal ascending aorta.

FIGURE 12-12  Arachnodactyly in Marfan’s syndrome. Metacarpals and phalanges are unusually long and slender.

CHAPTER 12  Miscellaneous Diseases disease is the major cause of death. Other common signs are similar to those of Marfan’s syndrome (long limbs, arachnodactyly, and scoliosis). Additional symptoms are myopia (nearsightedness), dislocation of the lens of the eye, and mental retardation. Imaging appearance. The most common and striking radiographic feature of homocystinuria is osteoporosis of the spine, which is often associated with biconcave deformities of the vertebral bodies (Figure 12-14). Treatment. Because no cure has been found, treatment available consists of a low-methionine diet and increased doses of vitamin B6 and folic acid or cysteine supplements. Not all patients have found this treatment effective.

Phenylketonuria Phenylketonuria (PKU) is an inborn error of metabolism in which an enzyme deficiency results in the impaired conversion of phenylalanine to tyrosine. Fortunately, routine screening enables diagnosis of this disease at birth. If the condition is not diagnosed and treated early, the excessive phenylalanine in the blood usually causes the patient to suffer profound retardation (microcephaly), hyperactivity, and seizures, all related to brain atrophy. Because of an inadequate amount of tyrosine, there is impaired production of the pigment melanin, and the patient is very light in color.

FIGURE 12-13  Pectus excavatum. Lateral chest radiograph demonstrates a concave sternum.

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Imaging appearance. The brain atrophy of PKU appears as dilation of the ventricles and sulci on computed tomog­ raphy (CT) or magnetic resonance imaging (MRI). Treatment. Treatment of PKU involves a diet low in phenylalanine and protein. Dietary measures can prevent the disease process from progressing if the treatment begins before age 1 year. Treatment instituted later in life will not improve any destructive damage that has already occurred.

Alkaptonuria and Ochronosis Alkaptonuria is a rare inborn error of metabolism in which an enzyme deficiency leads to an abnormal accumulation of homogentisic acid in the blood and urine. The urine is either very dark on voiding or becomes black after standing or being alkalinized. The disorder often goes unrecognized until middle age, when deposition of the black pigment of oxidized homogentisic acid in cartilage and other connective tissue produces a distinctive form of degenerative arthritis (ochronosis). Imaging appearance. The pathognomonic radiographic finding in alkaptonuria is dense, laminated calcification in multiple intervertebral disks (Figure 12-15); the calcification begins in the lumbar spine and may extend to involve the dorsal and cervical regions. Treatment. Medical therapy can inhibit the rate of pigment deposit. A low-protein diet and added vitamin C may retard the accumulation of homogentisic acid in older children and adults.

FIGURE 12-14  Homocystinuria. Striking osteoporosis of the spine is associated with biconcave deformities of the vertebral bodies.

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CHAPTER 12  Miscellaneous Diseases

FIGURE 12-16  Glycogen storage disease. Generalized globular cardiac enlargement with left ventricular prominence. FIGURE 12-15  Ochronosis. Frontal projection of the lumbar spine shows the dense laminated calcification of multiple intervertebral disks (arrows).

Cystinuria Cystinuria is an inborn error of amino acid transport characterized by impaired tubular absorption and excessive urinary excretion of several amino acids. Large amounts of cystine in the urine predispose to the formation of renal, ureteral, and bladder stones. It is common to see multiple and bilateral stones, even large staghorn calculi. Imaging appearance. Pure cystine stones are not radiopaque and can be demonstrated only on excretory urography, where they appear as filling defects in the urinary tract. Stones containing the calcium salts of cystine appear radiopaque and can be detected on plain abdominal radiographs. Abdominal CT may define the filling defect better than intravenous urography. Treatment. Currently, there is no cure for cystinuria. However, therapy is available to provide relief from symptoms and to prevent new stones from developing. One approach is to increase water intake to six to eight glasses a day to dilute the increased excretion of cystine in the urine. Thiol drugs may be of value in dissolving the cystine for excretion. Glycogen Storage Diseases The glycogen storage diseases are a group of genetic disorders that involve the pathways for the storage of carbohydrates as glycogen (in the liver) and for its use in maintaining blood glucose and providing energy. Normal or abnormal glycogen in an excess amount infiltrates and enlarges multiple organs, especially the heart and liver (Figure 12-16). Gaucher’s Disease Gaucher’s disease is an inborn error of metabolism characterized by the accumulation of abnormal quantities of complex lipids in the reticuloendothelial cells of the spleen, liver, and

FIGURE 12-17  Gaucher’s disease. The distal ends of the femurs show typical marrow infiltration of the distal femur causing abnormal modeling, flaring, and the characteristic (but nonspecific) Erlenmeyer flask deformity.

bone marrow. The adult (chronic) form of Gaucher’s disease is most common; some cases arise in children or infants. Aseptic necrosis (especially involving the femoral heads) is a common complication. The spleen is usually greatly enlarged, and hepatomegaly is common. Imaging appearance. The most striking changes in Gaucher’s disease occur in the skeletal system. Infiltration of the bone marrow with abnormal lipid-containing cells causes a loss of bone density with expansion and cortical thickening of the long bones, especially the femur. Marrow infiltration of the distal femur causes abnormal modeling, flaring, and the characteristic (but nonspecific) Erlenmeyer flask deformity (Figure 12-17). Treatment. In the past, the traditional treatment for Gaucher’s disease was splenectomy. Today, new experimental treatments are used in an attempt to inhibit the accumulation of complex lipids. Enzyme replacement is still under investigation, although initial trials have demonstrated reversal of extraskeletal symptoms.

CHAPTER 12  Miscellaneous Diseases

431

Summary of Findings for Genetic Amino Acid Disorders Disorder

Cause

Imaging Appearance

Treatment

Homocystinuria

Absence of cystathionine B synthase

Phenylketonuria

Enzyme deficiency leading to excessive phenylalanine Enzyme deficiency leading to excessive homogentisic acid Error of amino acid transport

Osteoporosis of the spine—­ biconcave deformities of vertebral bodies CT or MRI—brain atrophy with ­ dilation of ventricles and sulci Dense laminated calcification of ­ multiple intervertebral disks CT—defines cystine stones in the urinary tract

Low methionine diet; increased ­vitamin B6 and folic acid or ­cysteine supplements Low phenylalanine and protein diet to control progression Therapy to inhibit rate of deposit

Alkaptonuria/­ ochronosis Cystinuria

Gaucher’s disease

Abnormal accumulation of complex lipids

Extremity—loss of bone density, with expansion and cortical thickening of long bones

No cure—increased water intake to help prevent stone formation Thiol drugs to aid in dissolving the cystine Treatment to inhibit the accumulation of complex lipids Enzyme replacement to reverse extraskeletal symptoms

  REVIEW QUESTIONS 1. A vitamin C deficiency that years ago was common among sailors because of their lack of fresh fruit and vegetables is termed _________________. 2. _________________ is a vitamin deficiency disease that occurs primarily in countries in which polished rice is the main staple. 3. A deficiency of niacin, characterized by reddening and scaling of exposed skin, vomiting, diarrhea, and nervous and mental disorders, is termed _________________. 4. Vitamin _________________ is necessary in the blood-­ clotting mechanism. 5. A lack of vitamin _________________ can result in night blindness. 6. When caloric intake consistently exceeds the amount needed for the body to function, _________________ occurs. 7. A disease of young to middle-aged women that is most likely an immune complex disease, that can affect several systems of the body, and that is characterized by a butterfly-shaped rash across the nose and cheeks is _________________.

8. A very malignant form of skin cancer, capable of metastasizing throughout the body, is _________________. 9. An inherited muscular disease characterized by severe weakness and eventual death from respiratory muscle failure or pneumonia is _________________. 10. The radiographer should be very alert to the possibility of _________________ in patients with muscular dystrophy who lack normal swallowing ability. 11. Name three trisomy disorders: _________________, _________________, and _________________. 12. _________________ syndrome occurs when a female has only one X chromosome. 13. Arachnodactyly, or spider-like digits, occurs in which two hereditary disorders?

ANSWERS TO REVIEW QUESTIONS CHAPTER 1 1. edema 2. phagocytosis 3. keloid 4. suppurative 5. ischemia 6. infarct 7. hematoma 8. atrophy 9. neoplasia 10. adenoma 11. epidemiology 12. mortality 13. morbidity 14. personal protective equipment (PPE) 15. transmission-based precautions 16. etiology 17. diagnosis 18. syndrome 19. asymptomatic 20. prognosis

CHAPTER 2 1. location 2. b 3. shape 4. a 5. d 6. b 7. a 8. a 9. c 10. d 11. a 12. a 13. c 14. c 15. c

CHAPTER 3 1. pneumothorax, pneumomediastinum 2. Swan–Ganz 3. superior vena cava 4. generator, electrodes 5. infarction 6. In AP and PA radiographs, the tip may appear to be in the proper position, but a lateral view is needed to ensure that the tip is in the anterior portion of the right ventricle—the correct position. 7. hyaline membrane disease

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8. cystic fibrosis 9. croup 10. epiglottitis 11. alveolar pneumonia 12. lung abscess 13. bronchography 14. emphysema 15. silicosis, asbestosis, anthracosis 16. sarcoidosis 17. pulmonary arteriovenous fistula 18. tension pneumothorax 19. empyema 20. pneumonia 21. histoplasmosis, coccidioidomycosis 22. coughing, droplets 23. pneumothorax 24. emphysema 25. pneumoconiosis 26. mesothelioma 27. septic embolism 28. atelectasis 29. larger and more vertical mainstem bronchi 30. subcutaneous emphysema 31. c 32. mediastinal emphysema (pneumomediastinum) 33. c

CHAPTER 4 1. b 2. a 3. d 4. d 5. b 6. transitional vertebra 7. increase 8. b 9. a 10. b 11. c 12. c 13. a 14. d 15. b 16. d 17. c 18. d 19. b 20. c 21. b 22. d 23. b 24. c

Answers to Review Questions 25. a 26. c 27. d 28. d 29. a 30. b 31. b

CHAPTER 5 1. b 2. c 3. a 4. b 5. c 6. a 7. b 8. d 9. c 10. c 11. c 12. b 13. b 14. d 15. d 16. a 17. b 18. a 19. d 20. c 21. c 22. b 23. b 24. d 25. b 26. c 27. a 28. d 29. b 30. a

CHAPTER 6 1. d 2. d 3. b 4. a 5. c 6. d 7. c 8. a 9. c 10. a 11. b 12. a, c, e 13. urinary calculi, strictures of normal narrowing (UVJ and UPJ), ureterocele

14. hydroureter 15. polycystic kidney disease

CHAPTER 7 1. d 2. a 3. b 4. d 5. d 6. c 7. b 8. d 9. a 10. a 11. c 12. c 13. a 14. b 15. a 16. c 17. b 18. c 19. b 20. b 21. b 22. b 23. d 24. d

CHAPTER 8 1. c 2. c 3. b 4. d 5. d 6. b 7. a 8. c 9. b 10. c 11. CT 12. CT, MRI 13. transient ischemic attack 14. MRI 15. epilepsy 16. Alzheimer’s disease 17. Parkinson’s disease 18. horizontal, erect 19. hydrocephalus 20. cross-table lateral, horizontal

CHAPTER 9 1. c 2. a

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434

Answers to Review Questions

3. c 4. b 5. b 6. c 7. c 8. c 9. a 10. c 11. b 12. b

CHAPTER 10 1. c 2. c 3. a 4. b 5. b 6. c 7. b 8. b 9. c 10. b 11. d 12. b 13. c 14. b 15. b 16. b 17. b 18. a 19. c 20. b 21. d

CHAPTER 11 1. nonionizing imaging source, high-frequency sound waves 2. hysterosalpingography, mammography 3. spermatogenesis 4. testosterone

5. vasectomy 6. cancer of the prostate 7. ultrasound 8. true 9. ivory vertebra 10. ultrasound 11. testicular torsion 12. testicular, lymphatic 13. ovulation 14. ectopic 15. hysterosalpingography 16. syphilis 17. dermoid/teratoma 18. fibroids 19. breast 20. carcinoma of the cervix

CHAPTER 12 1. scurvy 2. beriberi 3. pellagra 4. K 5. A 6. obesity 7. systemic lupus erythematosus 8. melanoma 9. muscular dystrophy 10. aspiration 11. Down syndrome, Turner’s syndrome, Klinefelter’s syndrome 12. Turner’s 13. Marfan’s syndrome, homocystinuria

I L L U S T R AT I O N C R E D I T S CHAPTER 1 Figure 1-6 from Bryk D etal: Kaposi’s sarcoma of the intestinal tract: roentgen manifestations, Gastrointest Radiol 3:425, 1978.

CHAPTER 3 Figures 3-1 and 3-2 from Thibodeau GA, Patton KT: Anatomy and physiology, ed 7, St. Louis, 2010, Mosby. Figures 3-4 and 3-8 from Dunbar RD: Radiologic appearance of compromised thoracic catheters, tubes, and wires, Radiol Clin North Am 22:699-722, 1984. Figures 3-5, 3-7, 3-9 from Eisenberg RL: Diagnostic imaging in internal medicine, New York, 1985, McGraw-Hill. Figure 3-10 from Swischuk LE: Radiology of the newborn and young infant, Baltimore, 1980, Williams & Wilkins. Figure 3-14 from Podgore JK, Bass JW: J Pediatr 88:154-155, 1976. Figures 3-18, 3-35, and 3-82 from Eisenberg R: Atlas of signs in radiology, Philadelphia, 1984, Lippincott. Figures 3-41 and 3-68 from Fraser RG, Paré JAP: Diagnosis of diseases of the chest, Philadelphia, 1979, Saunders. Figure 3-42 from Eisenberg R: Atlas of signs in radiology, Philadelphia, 1984, Lippincott. Figure 3-62 from Lee JKT, Sagel SS, Stanley RJ, editors: Computed body tomography, New York, 1989, Raven Press. Figure 3-80 from Cappitanio MA etal: Radiology 103: 460-461, 1972. Figure 3-91 from Vix VA: Semin Roentgenol 12:277-286, 1977. Figure 3-92 from Eisenberg RL: Diagnostic imaging in surgery, New York, 1987, McGraw-Hill.

CHAPTER 4 Figure 4-1 from Thibodeau GA, Patton KT: Anatomy and physiology, ed 7, St. Louis, 2010, Mosby. Figure 4-14 from Brown JC, Forrester DM: Arthritis. In Eisenberg RL, Amberg JR, editors: Critical diagnostic pathways in radiology, Philadelphia, 1981, Lippincott. Figure 4-27 from Forrester DM, Brown JC, Nesson JW: The radiology of joint disease, Philadelphia, 1978, Saunders. Figures 4-29 and 4-35 from Rumack C, Wilson S, Charboneau JW, editors: Diagnostic ultrasound, ed 2, St Louis, 1998, Mosby. Figure 4-31 from Greenspan A: Orthopedic radiology, Philadelphia, 1988, Lippincott. Figure 4-56 from Eisenberg RL: Diagnostic imaging in internal medicine, New York, 1985, McGraw-Hill. Figure 4-57 from Eisenberg RL: Gastrointestinal radiology: a pattern approach, Philadelphia, 1990, Lippincott.

Figure 4-71 from deSantos LA, Bernardino ME, Murray JA: Computed tomography in the evaluation of osteosarcoma: experience with 25 cases, AJR Am J Roentgenol 132:535-540, 1979. Figures 4-72 and 4-86A from Stark DD, Bradley WG Jr: Magnetic resonance imaging, ed 2, St. Louis, 1991, Mosby. Figures 4-87 and 4-123 from Eisenberg R: Diagnostic imaging in surgery, New York, 1987, McGraw-Hill. Figure 4-99 from Sty JR, Starshak RJ: The role of bone scintigraphy in the evaluation of the suspected abused child, Radiology 146:369-375, 1983. Figure 4-102 from Silverman FN: Caffey’s pediatric x-ray imaging, St. Louis, 1985, Mosby. Figure 4-110 from Bassett LW, Gold RH, Epstein HC: Anterior hip dislocation: atypical superolateral displacement of the femoral head, AJR Am J Roentgenol 141:385-386, 1983. Figure 4-115 from Osborn AG: Head trauma. In Eisenberg RL, Amberg JR, editors: Critical diagnostic pathways in radiology, Philadelphia, 1981, Lippincott.

CHAPTER 5 Figures 5-1 and 5-2 from Thibodeau GA, Patton KT: Anatomy and physiology, ed 6, St. Louis, 2007. Figure 5-3 and 5-4 from Thibodeau GA, Patton KT: Anatomy and physiology, ed 7, St. Louis, 2010, Mosby. Figures 5-18, 5-19, 5-20, 5-24, 5-25, and 5-92 from Eisenberg RL: Gastrointestinal radiology: a pattern approach, Philadelphia, 1990, Lippincott. Figure 5-31 from Rumack C, Wilson S, Charboneau JW, editors: Diagnostic ultrasound, ed 4, St. Louis, 2010, Mosby. Figure 5-35 from Margulis AR, Burhenne JH, editors: Alimentary tract radiology, ed 4, St. Louis, 1989, Mosby. Figure 5-45 from Rumack C, Wilson S, Charboneau JW, editors: Diagnostic ultrasound, ed 3, St. Louis, 2004, Mosby. Figure 5-52 from Jeffrey RB: CT and sonography of the acute abdomen, New York, 1989, Raven Press. Figure 5-61 from Rice RP etal: Radiographics 4:393-409, 1984. Figure 5-73 from Caroline DF, Evers K: Colitis: radiographic features and differentiation of idiopathic inflammatory bowel disease, Radiol Clin North Am 25:47-66, 1987. Figure 5-74 from Lichtenstein JE: Radiologic-pathologic correlation of inflammatory bowel disease, Radiol Clin North Am 25:3-23, 1987. Figure 5-79 from Butch RJ: In Taveras JM, Ferruci JT, editors: Radiology: diagnosis, imaging, intervention, Philadelphia, 1987, Lippincott. Figure 5-101 from Jeffrey RB, Federle MP, Laing FC: Computed tomography of mesenteric involvement in fulminant pancreatitis, Radiology 147:185-192, 1983. Figure 5-108 from Federle MP, Goldberg HL: In Moss AA, Gamsu G, Genant HK, editors: Computed tomography of the body, Philadelphia, 1992, Saunders.

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Illustration Credits

Figure 5-115 from Koehler RE: Spleen. In Lee JKT, Sagel SS, Stanley RJ, editors: Computed body tomography, New York, 1983, Raven Press.

CHAPTER 6 Figure 6-1 from Thibodeau GA, Patton KT: Anatomy and physiology, ed 7, St. Louis, 2010, Mosby. Figure 6-2 from Brundage DJ: Renal disorders, St. Louis, 1992, Mosby. Figure 6-3 from Thibodeau GA, Patton KT: Anatomy and physiology, ed 7, St. Louis, 2010, Mosby. Figure 6-14 from Friedland GW etal: Clin Radiol 27:367-373, 1976. Figures 6-18 and 6-19 from Tonkin AK, Witten DM: Genitourinary tuberculosis, Semin Roentgenol 14:305-318, 1979. Figure 6-25 from Eisenberg R: Gastrointestinal radiology: a pattern approach, Philadelphia, 1990, Lippincott. Figure 6-39 from Bosniak MA, Ambos MA: Polycystic kidney disease, Semin Roentgenol 10:133-143, 1975. Figure 6-44 from Bosniak MA, Faegenburg D: Radiology 84:692-698, 1965. Figure 6-47 from McClennan BL, Lee JKT: Kidney. In Lee JKT, Sagel SS, Stanley RJ, editors: Computed body tomography, New York, 1983, Raven Press. Figure 6-49 and 6-55 from Friedland GW etal, editors: Uroradiology: an integrated approach, New York, 1983, Churchill Livingstone. Figure 6-52 from Merten DE, Kirks DR: In Eisenberg RL, editor: Diagnostic imaging: an algorithmic approach, Philadelphia, 1988, Lippincott. Figure 6-57 from Cohn LH etal: The treatment of bilateral renal vein thrombosis and nephrotic syndrome, Surgery 64:387-396, 1968.

CHAPTER 7 Figures 7-1 and 7-2 from Thibodeau GA, Patton KT: Anatomy and physiology, ed 6, St. Louis, 2007, Mosby. Figure 7-3 from Thibodeau GA, Patton KT: Anatomy and physiology, ed 7, St. Louis, 2010, Mosby. Figures 7-5, 7-6, and 7-7 from Cooley RN, Schreiber MH: Radiology of the heart and great vessels, Baltimore, 1978, Williams & Wilkins. Figure 7-8 from Rumack etal: Diagnostic ultrasound, ed 3, vol 2, St. Louis, 2005, Mosby. Figure 7-10 from Swischuk LE: Plain film interpretation in congenital heart disease, Baltimore, 1979, Williams & Wilkins. Figure 7-13 from Schoepf UJ, Becker BM, etal. CT of coronary artery disease, Radiology 2004; 232: 18-37. Figure 7-14 from Stark DD, Bradley WG, editors: Magnetic resonance imaging, St. Louis, 1988, Mosby. Figure 7-17 from Fischell TA, Block PC: Cardiovasc Reviews Reports 6:89-99, 1985. Figure 7-22 from Fraser RG, Pare JAP: Diagnosis of diseases of the chest, Philadelphia, 1979, Saunders.

Figure 7-26 from Burko H etal: In Eisenberg RL, Amberg JR, editors: Critical diagnostic pathways in radiology: an algorithmic approach, Philadelphia, 1981, Lippincott. Figure 7-29 from Waltman AC: In Athanasoulis CA etal, editors: Interventional radiology, Philadelphia, 1982, Saunders. Figure 7-32 from Eisenberg R: Gastrointestinal radiology: a pattern approach, Philadelphia, 1990, Lippincott. Figure 7-34 from Thoeni RF, Margulis AR: In Eisenberg RL, editor: Diagnostic imaging: an algorithmic approach, Philadelphia, 1988, Lippincott. Figure 7-36 from Fisher RG, Hadlock FP, Ben-Menachem Y: Radiol Clin North Am 19:91-112, 1981. Figure 7-37 from Woodring JH, Pulmano CM, Stevens RK: The right paratracheal stripe in blunt chest trauma, Radiology 143:605-608, 1982. Figure 7-40 from Ovenfors CO, Godwin JD: In Eisenberg RL, editor: Diagnostic imaging: an algorithmic approach, Philadelphia, 1988, Lippincott. Figure 7-45 from Waltman AC: In Athanasoulis CA etal, editors: Interventional radiology, Philadelphia, 1982, Saunders. Figure 7-47 from Katzen BT, van Breda A: Low dose streptokinase in the treatment of arterial occlusions, AJR Am J Roentgenol 136:1171-1178, 1981. Figure 7-50 from Vickers SCW etal: Radiology 72:569-575, 1959. Figure 7-60 from Miller SW, Gillian LD: In Eisenberg RL, editor: Diagnostic Imaging: An algorithmic approach, Philadelphia, 1988, Lippincott. Figure 7-61 from Holden RW, Mail JT, Becker GJ: In Eisenberg RL, editor: Diagnostic imaging: an algorithmic approach, Philadelphia, 1988, Lippincott.

CHAPTER 8 Figure 8-1 from Thibodeau GA, Patton KT: Anatomy and physiology, ed 7, St. Louis, 2010, Elsevier. Figure 8-2 courtesy of Vidic B, Suarez F: Photographic atlas for the human body, St. Louis, 1984, Mosby in Thibodeau GA, Patton KT: Anatomy and physiology, ed 7, St. Louis, 2010, Elsevier. Figure 8-3 from Thibodeau GA, Patton KT: Anatomy and physiology, ed 7, St. Louis, 2010, Elsevier. Figure 8-4 from Ross MR, Davis DO, Mark AS: MRI Decisions 4:24-33, 1990. Figure 8-5 from Edelman RR, Hesselink JR, editors: Clinical magnetic resonance imaging, Philadelphia, 1990, Saunders. Figures 8-7, 8-8, and 8-75 from Stark DD, Bradley WG: Magnetic resonance imaging, ed 2, St. Louis, 1991, Mosby. Figures 8-20 and 8-24 from Williams AL, Haughton VM: Cranial computed tomography, St. Louis, 1985, Mosby. Figures 8-26 and 8-77 from Eisenberg RL: Clinical imaging: an atlas of differential diagnosis, Gaithersburg, Md, 1992, Aspen. Figure 8-28B from Levine HL, Kleefield J, Rao KCVG: In Lee SH, Rao KCVG, editors: Cranial computed tomography, New York, 1983, McGraw-Hill.

Illustration Credits Figure 8-29 from Bilaniuk LT: Adult infratentorial tumors, Semin Roentgenol 25:155-173, 1990. Figures 8-34A and 8-39 from Pressman BD: In Eisenberg RL, editor: Diagnostic imaging: an algorithmic approach, Philadelphia, 1988, Lippincott. Figure 8-41 from Eisenberg RL: Diagnostic imaging in surgery, New York, 1987, McGraw-Hill. Figures 8-46 and 8-48 from Dolan K, Jacoby C, Smoker W: Radiographics 4:576-663, 1984. Figure 8-47 from Rogers LF: Radiology of skeletal trauma, New York, 1982, Churchill Livingstone. Figure 8-58 from Drayer BP: Neuroradiology. In Rosenberg RN, Heinz ER, editors: The clinical neurosciences, New York, 1984, Churchill Livingstone. Figure 8-65 from Bronen RA: Epilepsy: the role of MR imaging, AJR Am J Roentgenol 159:1165-1174, 1992. Figure 8-73 from Johnson CE, Zimmerman RD: MRI Decisions 3:2-16, 1989.

CHAPTER 9 Figures 9-1 and 9-2 and Unnumbered Figure 9-1 from Thibodeau GA, Patton KT: Anatomy and physiology, ed 7, St. Louis, 2010, Elsevier. Figure 9-5 from Leight TF: Radiol Clin North Am 1:377-393, 1963. Figure 9-8 from Moseley JE: Semin Roentgenol 9:169-184, 1984. Figure 9-25 from Stoker DJ, Murray RO: Skeletal changes in hemophilia and other bleeding disorders, Semin Roentgenol 9:185-193, 1974.

CHAPTER 10 Figure 10-1 from Thibodeau GA, Patton KT: Anatomy and physiology, ed 7, St. Louis, 2010, Elsevier. Figure 10-3 from Lee JKT, Sagel SS, Stanley RJ, editors: Computed body tomography, New York, 1983, Raven Press. Figures 10-5 and 10-6 from Karstaedt N etal: Computed tomography of the adrenal gland, Radiology 129:723-730, 1978. Figure 10-9 and 10-14 from Stark DD, Bradley WG: Magnetic resonance imaging, ed 2, St. Louis, 1991, Mosby. Figure 10-13 from Welch TJ etal: Pheochromocytoma: value of computed tomography, Radiology 148:501-503, 1983. Figure 10-15 from Eisenberg RL: Diagnostic imaging in surgery, New York, 1987, McGraw-Hill. Figure 10-17 from Friedland GW etal: Uroradiology: an integrated approach, New York, 1983, Churchill Livingstone. Figure 10-19 from Thibodeau GA, Patton KT: Anatomy and physiology, ed 6, St. Louis, 2007, Mosby. Figure 10-24 from Jacob S in Thibodeau GA, Patton KT: Anatomy and physiology, ed 6, St. Louis, 2007, Mosby. Figure 10-26 from Palmer EL, Scott JA, Strauss HW: Practical nuclear medicine, Philadelphia, 1992, Saunders. Figure 10-45 from Stark DD etal: Parathyroid scanning by computed tomography, Radiology 148:297-303, 1983.

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CHAPTER 11 Figure 11-5 from Russinovich NA etal: Balloon dilatation of urethral strictures, Urol Radiol 2:33-37, 1980. Figure 11-6 from Thibodeau GA, Patton KT: Anatomy and physiology, ed 7, St. Louis, 2010, Mosby. Figure 11-9 from McCarthy S, Fritzsche PJ: In Stark DD, Bradley WG, editors: Magnetic resonance imaging, St. Louis, 1988, Mosby. Figure 11-13 from Thoeni RF: In Moss AA, Gamsu G, Genant HK, editors: Computed tomography of the body, Philadelphia, 1983, Saunders. Figure 11-16 from Jeffrey RB: In Moss AA, Gamsu G, Genant HK, editors: Computed tomography of the body, Philadelphia, 1983, Saunders. Figure 11-17 from Fritzsche PJ, etal: Undescended testis: value of MR imaging, Radiology 164:169-173, 1987. Figures 11-23, 11-24, 11-48, 11-51, 11-70, 11-71, 11-73A, 11-76, and 11-78 from Rumack CM, Wilson SR, Charboneau JW: Diagnostic ultrasound, St. Louis, 1998, Mosby. Figure 11-25 from Baker LL etal: MR imaging of the scrotum: pathologic conditions, Radiology 163:93-98, 1987. Figures 11-27 and 11-58 from Thibodeau GA, Patton KT: Anatomy and physiology, ed 6, St. Louis, 2007, Mosby. Figures 11-30, 11-45, 11-53, 11-55, and 11-79 from Callen PW, editor: Ultrasonography in obstetrics and gynecology, Philadelphia, 1983, Saunders. Figure 11-31 from Yune HY etal: Hysterosalpingography in infertility, Am J Roentgenol Radium Ther Nucl Med 122:642-651, 1974. Figure 11-35 from Eisenberg RL: Diagnostic imaging in surgery, New York, 1987, McGraw-Hill. Figure 11-38 from Lee JKT, Sagel SS, Stanley RJ, editors: Computed body tomography, New York, 1983, Raven Press. Figure 11-41 from Eisenberg R: Atlas of signs in radiology, Philadelphia, 1984, Lippincott. Figures 11-50, 11-56, and 11-57 from Lupetin AR: In Stark DD, Bradley WG, editors: Magnetic resonance imaging, St. Louis, 1988, Mosby. Figure 11-52 from Gedgaudas RK, etal: The value of the preoperative barium-enema examination in the assessment of pelvic masses, Radiology 146:609-616, 1983. Figure 11-54 from Gross BH etal: Computed tomography of gynecologic diseases, AJR Am J Roentgenol 141:765-773, 1983. Figure 11-64 from Hagen-Ansert S: Textbook of diagnostic ultrasound, St. Louis, 2001, Mosby. Figure 11-75 from Pasto ME, Kurtz AM: Semin Ultrasound CT MR 5:170-193, 1984.

CHAPTER 12 Figure 12-2 from Eisenberg R: Atlas of signs in radiology, Philadelphia, 1984, Lippincott. Figure 12-5 from Brown JC, Forrester DM: In Eisenberg RL, Amberg JR, editors: Critical diagnostic pathways in radiology: an algorithmic approach, Philadelphia, 1981, Lippincott.

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Illustration Credits

Figure 12-9 from James AE Jr etal: Radiological features of the most common autosomal disorders: trisomy 21-22 (mongolism or Down’s syndrome), trisomy 18, trisomy 13-15, and the cri du chat syndrome, Clin Radiol 22:417-433, 1971. Figure 12-11 from Ovenfors CO, Godwin JD: In Eisenberg RL, Amberg JR, editors: Critical diagnostic pathways in radiology: an algorithmic approach, Philadelphia, 1981, Lippincott.

Figure 12-14 from Thomas PS, Carson NA: Homocystinuria. The evolution of skeletal changes in relation to treatment, Ann Radiol 21:95-104, 1978. Figure 12-17 from Levin B: Gaucher’s disease: Clinical and roentgenologic manifestations, AJR Am J Roentgenol 85:685-696, 1961.

APPENDIX

A

Prefixes/Suffixes/Roots Prefix/Suffix/Root

Meaning

Example

a-, aba-, anad-algia anaanteanti-, antautobi-blast cardicaudal cephalchondro-clast contracranicyanocyto-dactyldecidermdysectoendo-, entoerythrgastr-genic gyn-, gynecohem-, haemhemiheterohomohyperhypoiatroinfraintraipsiiso-itis juxtakiloleuko-, leucolipo-lysis, -lytic

away from without, not toward pain up, back again before, in front of against, antibody self two budding heart tail head cartilage destroyer, breaker opposite skull dark blue cell finger, toe tenth skin bad, difficult outside of within red stomach causing woman blood half different same over, excessive under, too little healer, healing below within same equal inflammation near, next to thousand white fat dissolve

abduction asymmetric, anencephalic adduction arthralgia anaplastic antecubital antitoxin autoimmune bilateral, bidirectional osteoblast cardiology, cardiac; pericardium caudal cephalic; hydrocephaly chondroma, chondrosarcoma osteoclast contralateral cranium, cranial cyanotic cytoplasm; erythrocyte, leukocyte polydactyly, arachnodactyly decimal dermatology; epidermis dysplasia, dysuria ectoderm, ectopic endoderm, endometrium erythrocyte gastric carcinogenic, pathogenic gynecology hemorrhage, hemolytic hemisphere, hemidiaphragm heterogeneous homogeneous hyperthyroidism, hypertension, hyperintense hypothyroidism, hypotension, hypointense iatrogenic; psychiatry infratemporal intramural, intradermal ipsilateral isointense appendicitis, diverticulitis juxta-articular kilogram leukocyte, leukemia lipoma, liposarcoma lytic, osteolytic

439

440

APPENDIX A  Prefixes/Suffixes/Roots

Prefix/Suffix/Root

macromagnmalmega-, megalomelanmicromillimonomultimyelomyonecroneononoculoligo-ology oncoophthalm-osis osteopanpar-, parapathoperiplasm-, plastpleurpneumopolypostprepseudopsychreretro-rrhea schizosclerosemisubsuper-, suprasyn-, symtachytechntertitetrathermotomo-, -tome transtriultrauni-

Meaning

large great, large bad, ill large black small thousandth one many marrow muscle dead new not eye few study of tumor eye condition of bone all beside disease around shape, form rib, side air, breath many after, later, behind before, in front of false mind, spirit again, anew backward, behind flow, gush split hard half under, below above; more than with, together fast art, skill third four heat cut across three beyond one

Example

macroadenoma magnify, magnum (foramen) malunion, malalignment megadose melanoma, melanin microscope, microadenoma, microcirculation milligram, milliliter monostotic, monoclonal multilocular, multifaceted myelogram; osteomyelitis myoma, myositis necrosis neovascularity, neoplasm nonunion, nonviable ocular, oculomotor (nerve) oligemia radiology, pathology oncology ophthalmology diverticulosis osteomyelitis, osteosarcoma pansinusitis, pancytopenia para-aortic, paravertebral pathology; adenopathy periarticular, periventricular, pericardium neoplasm; anaplastic pleural, pleurisy pneumothorax, pneumonia polycystic, polyostotic post-traumatic, postsurgical, postoperative premenstrual, prepontine pseudotumor, pseudopolyp psychiatry, psychology reoperate, recalcify retroperitoneum diarrhea schizophrenia sclerotic, atherosclerosis semicircular suborbital, subphrenic, subhepatic suprarenal, supraorbital synthesis, symmetric tachycardia technology, technique tertiary tetralogy (of Fallot) thermometer tomography; microtome transverse (colon), transvenous (pacer) trimalleolar, trisomy ultrasound unilateral

APPENDIX

B

Laboratory Values and Their Significance Laboratory Values

Significance of Laboratory Values

↑ Lactic dehydrogenase (LDH) ↑ Serum glutamic-oxaloacetic transaminase (SGOT) ↑ Serum glutamic-pyruvic transaminase (SGPT) ↑ Total protein ↑ Uric acid ↓ Calcium ↓ Glucose ↓ Total protein

Prostate cancer, metastatic to bone Liver disease, Paget’s disease, bone tumor Pancreatitis Liver disease Liver disease Hyperparathyroidism, bone destruction Tendency toward atherosclerosis Kidney disease Myocardial infarction, pulmonary infarction Diabetes mellitus, Cushing’s syndrome, glucagon-secreting pancreatic tumor Myocardial infarction, pulmonary infarction, liver disease Liver disease Myocardial infarction, liver disease Dehydration, immunoglobinopathy Gout, antidiuretic therapy Hypoparathyroidism, malabsorption, osteomalacia/rickets Insulin-secreting pancreatic tumor, liver disease, hypopituitarism Chronic liver disease, malnutrition, nephrotic syndrome

↑ Acid phosphatase ↑ Alkaline phosphatase ↑ Amylase ↑ Bilirubin ↑ Blood urea nitrogen (BUN) ↑ Calcium ↑ Cholesterol ↑ Creatinine ↑ Creatinine phosphokinase (CPK) ↑ Glucose

441

G LO S S A RY A aberration  Deviation from normal abscess  Encapsulated collection of pus achalasia  Failure of the lower esophageal

sphincter to relax because of absence or destruction of cells in the myenteric nerve plexus, which results in difficulty swallowing acid–base balance  Stable concentration in body fluids acinus  Cluster of alveoli acquired immunodeficiency syndrome (AIDS)  Impairment of cellular immunity acromegaly  Gradual marked enlargement

and thickening of the bones of the face and jaw active immunity  A person forms antibodies

to counteract an antigen in the form of a vaccine or a toxoid adenocarcinoma  Malignancies of glandular tissue adenoma  Benign epithelial neoplasm that grows in a glandlike structure adenopathy  Enlargement of the lymphatic glands adnexal  Pertaining to the uterine appendages (ovaries, fallopian tubes, and ligaments) adult respiratory distress syndrome (ARDS)  Severe pulmonary congestion due

to diffuse injury to the alveolar–capillary membrane afferent  To carry toward the center agenesis  Absence of an organ alcoholic gastritis  Inflammation of the stomach lining caused by alcohol alveolar, or air-space, pneumonia  Inflammatory exudates that replace air and cause the affected lung to become solid amorphous  Without shape or definite form anaphylactic  Reactions are characterized by hypotension and vascular collapse (shock) with urticaria (hives), bronchiolar spasm, and laryngeal edema anaplastic  Without form androgens  Any steroid hormone that increases male characteristics anechoic  Not producing internal echoes (on ultrasound) anemia  Decreased hemoglobin in the blood below normal levels aneurysmal bone cyst  Consists of numerous blood-filled arteriovenous communications angioma  Tumor composed of blood vessels angulation  Indicates an angular deformity between the axes of the major fracture fragments ankylosing spondylitis  Chronic inflammation affecting the spine ankylosis  Immobility and consolidation of a joint caused by disease, injury, or surgical procedure annihilation  Interaction produces two high-­ energy photons (gamma rays) in opposite ­directions (separated by 180 degrees) antibodies  Body’s counteraction to control antigens

442

anticoagulant  Substance that suppresses or

bougienage  Passage of an instrument through

delays coagulation of the blood antigens  Body’s ability to recognize foreign substances aortic valve  Valve between the left ventricle and aorta aplasia  Lack of normal development resulting in a small size or developmental failure resulting in the absence of an organ or tissue appositional growth  Flat bones growth in size by the addition of osseous tissue to their outer surfaces arachnodactyly  Congenital condition of long, thin, spider-like fingers and toes arachnoid membrane Middle meningeal covering arachnoid villa  Projections of fibrous tissue from the arachnoid membrane arteriovenous malformation  Abnormal communication between an artery and a vein ascites  Accumulation of fluid in the abdominal cavity ascorbic acid  Vitamin C aseptic necrosis  Cystic and sclerotic degeneration due to injury, not infection asthma  Widespread narrowing of the airways as a result of exposure to stimuli astrocytoma  Primary tumor of the brain composed of astrocytes asymptomatic  A patient showing no evidence of diseases atresia  Congenital absence or closure of a normal body orifice or tubular organ atrial septal defect  Congenital anomaly resulting in an opening between the atria atrophy  Diminished size due to wasting away autonomic nervous system  Regulates involuntary body functions autosomes  All chromosomes except gender avulsion fracture  Small fragments torn from bony prominences

a tubular structure to increase its caliber (as in the treatment of a stricture of the esophagus) bowing fracture  Plastic deformation caused by a stress Bowman’s capsule  Cup-shaped end of renal tubule boxer’s fracture  Fracture of the neck of the fifth metatarsal with a dorsal angulation bronchial adenomas  Neoplastic growth of glandular structures in the bronchi bronchiectasis  Chronic dilatation of the bronchi or bronchioles bronchioalveolar carcinoma  Adenocarcinoma of epithelial cells projecting into the alveolar spaces bronchiolar (alveolar cell) carcinoma  Malignant neoplastic growth of the bronchioli spreading into the alveolar spaces bronchogenic carcinoma  Primary malignancy arising from the mucosa of the bronchial tree bullae  Large air-containing space butterfly fragment  Elongated triangular fragment of cortical bone generally detached from two other larger fragments of bone

B bacteremia  Bacteria spread through the circu-

latory system bacterial (phlegmonous) gastritis  Inflam-

mation of the stomach lining caused by a bacterial infection bacterial meningitis  Infection of the membranes covering the brain and spinal cord caused by bacteria basal ganglia  Islands of gray matter largely composed of cell bodies basophil  Granulocyte white blood cell Bence Jones protein  Abnormal protein typically found in the blood of patients with multiple myeloma benign  Tumors that closely resemble their cells of origin in structure and function and remain localized blowout fracture  Break in the floor of the orbit bone islands  Solitary, sharply demarcated areas of dense compact bone

C cachexia  Ill health and malnutrition marked

by weakness and emaciation that is usually associated with severe disease processes callus  New bone tissue that reunites the parts of a fracture cancellous bone  Spongy bone of the medullary cavity and bony trabeculae cancer  Collectively malignant tumors carcinoma  Malignant neoplasm of epithelial cell origins caseation  Form of necrosis in which the tissue is changed into a dry, amorphous mass resembling cheese catamenial  Pertaining to menstruation cavitation  Formation of cavities, as in pulmonary tuberculosis or neoplasm centesis  Puncture and aspiration central nervous system (CNS)  Consisting of the brain and spinal cord cerebellum  Posterior portion of the brain located behind the brainstem cerebrovascular disease  Any process that is caused by an abnormality of the blood vessels or blood supply to the brain cerebrum  Left and right larger superior portion of the brain cervical rib  An extra rib that articulates with a cervical vertebra chest physiotherapy  Chest percussions (tapping) to keep lung secretions moving chondroblastic  Forming cartilaginous tissue chondrosarcoma  Malignant tumor of cartilaginous origin chordae tendineae  Thin cords that connect each cusp of the two atrioventricular valves to papillary muscles in the heart ventricles

GLOSSARY chorion  Important fetal membrane for ex-

change of nutrients choroids plexus  Tangled mass of tine blood vessels within the ventricles that produce cerebrospinal fluid chromophobe adenomas  Pituitary tumor of nonstaining cells (acid or basic dyes) chronic bronchitis  Excessive tracheobronchial mucus production leading to the obstruction of small airways chyme  Gastric contents that have become mixed with hydrochloric acid and the proteolytic enzyme pepsin, resulting in a milky white product clay shoveler’s fracture  An avulsion fracture of a spinous process in the lower cervical or upper thoracic spine closed fracture  Fracture that does not disrupt the skin coagulation factors  Responsible for the process of blood clotting coalesce  To merge into a single mass coeur en sabot  Appearance resembling the curved-toe portion of a wooden shoe colic  Intermittent abdominal pain whose fluctuation corresponds to smooth muscle peristalsis collaterals  Blood vessels that develop or enlarge to provide an alternative route around an obstruction collecting tubule  Funnels urine into the papillary ducts in the renal pelvis Colles’ fracture  Transverse fracture of the distal radial metaphysic proximal to the wrist with a dorsal displacement of the distal fragment collimator  Containing multiple parallel channels to allow the rays to pass colonic ileus  Selective or disproportionate gaseous distention of the large bowel without an obstruction comminuted fracture  Composed of more than two fragments communicating hydrocephalus Increased cerebrospinal fluid involving the entire ventricular system and subarchnoid space community-acquired  Infected by exposure in the public domain compact bone  Outer layer consists of which to the naked eye appears dense and structureless complete fracture  Discontinuity between two or more fragments complete fusion  Occurs in the kidneys and produces a single irregular mass that has no resemblance to a renal structure compound fracture  Overlying skin is disrupted with tissue destruction compression fracture  Compaction of bone trabeculae and results in decreased bone length or width computed tomography Produces cross-­ sectional tomographic images by first scanning a slice of tissue from multiple angles with a narrow x-ray beam congenital  Existing at birth congenital syphilis  The baby of an infected mother may be born with this form of syphilis

congenital tracheoesophageal (TE) fistulas  Result from the failure of a satisfactory

esophageal lumen to develop completely separate from the trachea conjunctivitis  Inflammation of the delicate membrane that lines the eyelids and covers the exposed surface of the sclera (white part) of the eye constipation  Extra water is absorbed from the fecal mass to produce a hardened stool contracture  Shortening or shrinkage of a muscle or tendon resulting in persistent flexion or distortion at a joint corpus callosum  Mass of white matter connecting the two cerebral hemispheres corpus luteum  Anatomic structure on the ovary surface corrosive gastritis  Inflammation of the stomach caused by corrosive agents cortex  Outer portion of a bone or internal organ (kidney, adrenal gland, and brain) crossed ectopic  Ectopic kidney located on the same side as the normal kidney CT number  Attenuation of a specific tissue relative to that of water curvilinear  Having a curved configuration cyst  Saclike structure usually filled with fluid cystadenoma  Benign tumor forming a large cystic mass cytology  Microscopic examination to determine cell structure D deglutition  Swallowing demarcate  To set or mark the limits of de novo  From the beginning; anew depressed fracture  Portions of the fracture

fragments driven inward, such as the skull or tibial plateau diagnosis  The precise disease process affecting the patient diaphysis  Shaft of a long bone diarrhea  Results from increased motility of the small bowel, which floods the colon with an excessive amount of water that cannot be completely absorbed diarrheogenic islet cell tumors  Produce the WDHA syndrome diastatic fracture  Linear fracture intersecting a suture and courses along it to cause sutural separation diastole  Heart relaxation phase when blood enters the heart diencephalon  Lies between the cerebrum and the midbrain and consists of the third ventricle, thalamus, and hypothalamus diffusion imaging  Relies on the movement of molecules and random thermal motion dilation and curettage  Dilation of the cervix to allow the scraping of the uterine wall diploic space  Loose osseous tissue between the two tables of the skull direct fusion  Equipment designed to image two modalities simultaneously and integrate the images dislocation  Displacement of a bone no longer in contact with its normal articulation displacement  Separation of bone fragments

443

dissection  Separation of layers dominant  Genes that always produce an effect duplication (duplex kidney) A common

anomaly that may vary from a simple bifid pelvis to a completely double pelvis ureter and ureterovesical orifice dura mater  Tough outermost meningeal covering dysarthria  Difficulty speaking dysphagia  Difficulty swallowing dysplasia  Disordered growth or faulty development of various tissues or body parts dyspnea  Shortness of breath E echogenic  Producing a relatively strong re-

flection in ultrasound ectopic  Abnormally positioned ectopic kidney  Abnormally positioned kid-

neys that may be found in various locations, from the true pelvis (pelvic kidney) to above the diaphragm (intrathoracic kidney) ectopic pacemaker  Initiates abnormal heartbeats ectopic pregnancy  Implantation occurring in the fallopian tube or pelvic cavity edema  Accumulation of abnormal amounts of fluid in the intercellular tissue spaces or body cavities effaced  Wiped out or obliterated efferent  To carry away from the center or part effusion  Accumulation of fluid Eisenmenger’s syndrome  Ventricular septal defect associated with pulmonary hypertension and cyanosis resulting from right-to-left shunting electrolyte  Element or compound that dissociates in fluid into ions electrolyte balance  Equilibrium of electrolytes in the body embolus  Any foreign matter, such as a blood clot or an air bubble, carried in the bloodstream emphysema  Pathologic accumulation of air in tissues or organs (especially as applied to a disease of the lungs) empyema  Accumulation of pus in a cavity emulsifier  Substance that acts like soap by dispersing the fat into very small droplets that permit it to mix with water endemic  Present in a particular country, nation, or region endogenous  Originating from within the body endosteum  Inner membrane lining the medullary cavity of a bone en face  Face to face, looking at engorgement  Congestion of a blood vessel or tissue with blood or other fluid eosinophils  Granulocytic bilobed leukocyte ependymoma  Tumor arising from the wall of the fourth ventricle, especially in children, and the lateral ventricles in adults epidemiology  A study of determinants that is compiled for a specific disease in a given population upon determining the type of neoplastic involvement epididymis  Tightly coiled tube enclosed in a fibrous casing in which final maturation of the sperm occurs

444

GLOSSARY

epiphrenic diverticula  Outpouching found

in the distal 10 cm of the esophagus epiphyseal cartilage  Cartilaginous plate separating the epiphysis from the diaphysis epiphyses  End of a long bone that at first is separated from the main part by cartilage but later fuses with it by ossification erythrocytes  Red blood cells erythropoietin  Protein serving as the humoral regulator of red blood cell formation estrogen  Hormonal steroid compound that promotes secondary sex characteristics in female development etiology  The study of disease causes (not a synonym for cause) eventration  Diaphragmatic—elevation of the diaphragm; abdominal—protrusion of the bowel or removal of abdominal viscera exacerbation  Increase in the severity of a disease or any of its symptoms exenteration  Removal of all organs to debulk a tumor exogenous  Arising from outside the body exophthalmos  Abnormal protrusion of the eyeball external fixation  Accomplished by the use of casts and splints external reduction  Fracture is manipulated without surgical incision extramedullary hematopoiesis Formation of red blood cells outside the bone marrow extrinsic asthma  Environmental allergens exudate  Material (fluid, cells, or cellular debris) that has escaped from blood vessels and has been deposited in tissues or on tissue surfaces, usually as a result of inflammation F fat-soluble vitamins Include vitamins A,

D, E, and K and can be stored within body tissues fat-suppressed images  Requires “saturation or full magnetization” on the T1 sequence to ensure a large contrast difference between fat and water fecalith  Intestinal stone formed around a center of fecal material fibrin  Essential portion of a blood clot fibrinolysis  Breaking up of a blood clot fibromuscular dysplasia Arterial disorder characterized by intramural folds of fibrous endothelial tissue fissures  Deep grooves divide each cerebral hemisphere into lobes fistula  Abnormal connection, usually between two internal organs or from an internal organ to the surface of the body focal  Localized follicular carcinoma  Neoplasm with a follicular arrangement of cells functional MR (fMR)  Allows the localization of specific regions of the brain that correspond to various functions fundoplication  Taking tucks in the fundus of the stomach and distal esophagus fusiform  Spindle-shaped fusiform aneurysm  Bulging of the entire circumference of the vessel wall

G Galeazzi fracture  Combination fracture of

the shaft of the radius with a posterior dislocation of the ulna gamma camera  A sodium iodide crystal detects the ionizing radiation emitted from the patient giant cell tumor (osteoclastoma)  Frequently occurring at the end of a long bone as a mass surrounded by a thin shell of new periosteal bone gigantism  Excessive size and stature glioblastomas  Neoplasm consisting of embryonic epithelial cells developing around the neural tube, transforming to supportive connective tissue of the nerve cells or ventricle lining gliomas  Largest group of primary brain tumors, composed of malignant glial cells glomerulus  Tuft or cluster glucocorticoid  Regulate carbohydrate metabolism and is regulated by the adrenocorticotropic hormone glycogen  Excess glucose absorbed is stored as gonadal dysgenesis  Variety of conditions related to abnormal development of the gonads grading  Assessment of malignant tumor to determine the degree of aggressiveness or malignancy Gram’s method  Technique for staining micro­ organisms (i.e., Gram stain) grand mal seizure  Epileptic seizure characterized by generalized involuntary muscular contractions and cessation of respiration that precedes tonic and clonic spasms of the muscles granulation tissue  Combination of young developing capillaries and actively proliferating fibroblasts producing connective tissue fibers granuloma  Tumor-like mass of tissue caused by a chronic inflammatory process greenstick fracture  Incomplete fracture of one cortex gyri  Winding convolutions of the cerebral hemispheres H hangman’s fracture  Fracture of the arch of

C2 anterior to the inferior facet; associated with anterior subluxation of C2 and C3 Heberden’s nodes  Small, hard nodules at the distal interphalangeal joints of the fingers produced by calcific spurs of the articular cartilage and associated with osteoarthritis helical  Spiral continuous motion hematogenous spread  Travels by means of the bloodstream hematoma  Hemorrhage trapped in body tissues hemiparesis  Weakness of one side of the body hemiplegia  Paralysis on one side of the body hemodynamic  Pertaining to the movements involved in the circulation of the blood hemoglobin  Complex protein–iron compound in the blood that carries oxygen hemoptysis  Coughing up blood or bloodstained sputum

hemorrhage  Rupture of a blood vessel hepatitis  Inflammatory disease of the liver hereditary  Transmitted to offspring through

genes heterogeneous  Composed of materials that

have different structures or qualities histology  Microscopic examination to deter-

mine tissue structure homogeneous  Composed of material of simi-

lar or identical structure or quality horseshoe kidney  Fusion of the lower poles

of the kidneys hydrocephalus  Enlargement of the head re-

sulting from an abnormal increase in fluid within the ventricular system hydronephrosis  Distention of the pelvis and calyces of the kidney hydrosalpinx  Fallopian tube cystically enlarged filled with clear fluid hydroureter  Dilatation of the ureter hyperactive  Increased activity hyperechoic  A term used to make comparisons of echo intensities between adjacent structures hyperglycemia  Greater amount of glucose than normal in the blood hyperlucency  Overly black appearance on a radiograph hypernephroma  Most common renal cell carcinoma hyperplasia  Abnormal increase in the number of cells composing a tissue or organ hypertension  High blood pressure hypoactive  Decreased activity hypocalciuria  Abnormally low calcium in the urine hypoplastic kidney  Underdeveloped kidney hypotension  Low blood pressure hypothalamus  Activates, controls, and integrates peripheral autonomic nervous system, endocrine system, and somatic functions hypoxia  Deficiency (lack) of oxygen I iatrogenic  Resulting from the activity of diag-

nosis or treatment by medical personnel idiopathic  Having an unknown cause for un-

derlying disease immune  Reaction of the body provides a pow-

erful defense against invading organisms incomplete fracture  Opposite cortex is intact incontinence  Loss of urinary bladder control indolent  Causing little or no pain; slow to

heal infarct  Localized area of ischemic necrosis

within a tissue or organ produced by occlusion of either its arterial supply or its venous drainage infarction  Death of tissue because of interruption of the normal blood supply infectious gastritis Inflammation of the stomach lining caused by a microorganism infiltrating  Spreading into surrounding tissue inflammation  Initial response of body tissue to local injury infundibulum  Funnel-shaped organ or passage inguinal  Pertaining to the groin

GLOSSARY insidious  Developing in a slow or unapparent

localized ileus  Isolated distended loop of

manner; more dangerous than seems evident (e.g., an insidious disease) in situ  Confined to the site of origin insufficiency  Less than the normal amount insulinoma  Hormone-secreting neoplasm most frequently in the tail of the pancreas, usually benign integrated imaging  Requires software to fuse to imaging modalities internal fixation Surgically placed metal plates and screws, wires, rods, or nails to maintain reduction interstitial pneumonia  Inflammatory process predominantly involving the walls and lining of the alveoli, its septa, and interstitial supporting structures intima  Innermost layer of an organ or blood vessel intraluminal  Within the empty space (lumen) of a hollow viscus intramembranous ossification  Bone formation from connective tissue intramural  Within the wall of an organ intrathoracic kidney  Kidney located in the thoracic cavity intrinsic  Belonging to the real nature of a thing intrinsic asthma  Reaction to exercise, heat or cold exposure, and emotional upset intrinsic rhythm  Specialized pacemaker cells in the sinoatrial node that initiate impulses at regular intervals ipsilateral  Relating to the same side (antonym: contralateral) irritable bowel syndrome  Refers to several conditions that have an alteration in intestinal motility ischemia  Lack of blood supply in an organ or tissue islands of Langerhans  Another name for islets of Langerhans isoechoic  A term used to describe two structures that have the same echogenicity even though the tissue may not be the same

small or large bowel loop of Henle  U-shaped portion of the renal tubule lordosis  Anterior concavity in the curvature of the lumbar and cervical spine, as viewed from the side lymphangitic  Spread by means of the lymphatic system lymphatic leukemia Malignancy of the lymph nodes in which the lymphocytes are the only white blood cells to increase lymphatic spread  The major metastatic route of carcinomas, especially those of the lung and breast lymphoma  Neoplastic disorder of lymphoid tissue lytic  Destructive

J Jefferson fracture  Comminuted fracture of

the ring of the atlas involving both anterior and posterior arches Jones fracture  Transverse fracture at the base of the fifth metatarsal juxta-articular  Adjacent to a joint K kyphosis  Anterior convexity in the curvature

of the thoracic spine, sacrum, and coccyx, as viewed from the side L left-to-right shunt  Diversion of blood from

the left side of the heart to the right through a septal defect leukocytes  White blood cells leukocytosis  Abnormal amount of white blood cells in the blood linear skull fracture  Jagged or irregular sharp lucent line lipoma  Tumor composed of fat

M magnetic

resonance imaging (MRI) A strong magnet producing radiofrequencies at specified intervals and receives a return signal to produce an image malabsorption disorder  Multitude of conditions in which there is defective absorption in the small bowel malaise  Vague feeling of physical discomfort or uneasiness, as early in an illness malignant  Neoplasm that invades and destroys adjacent structures and spreads to distant sites Mallory–Weiss syndrome Subsequent inflammation of the distal esophagus due to a laceration associated with bleeding and mediastinal penetration caused by severe retching and vomiting mandibular fractures  The angle of the mandible is the most common site of fracture, although fractures can involve any portion of the body and the condylar and coronoid processes marrow  Hollow, tube-like structure within the diaphysis mast cell  Connective tissue containing large basophilic granules containing heparin, serotonin, bradykinin, and histamine, which are released in response to injury or infection mastication  Chewing matrix  Basic material from which a substance (e.g., tissue) develops medulla  Inner substance of a bone (bone marrow) or an internal organ (kidney, adrenal gland) medullary carcinoma  Soft malignant neoplasm of the epithelium that contains little or no fibrous tissue medullary cavity  Hollow, tube-like structure within the diaphysis medulloblastoma  Poorly differentiated malignancy consisting of tightly packed spongioblastic and neuroblastic cells megahertz (MHz)  One million waves per second menarche  Commencement of the cyclic menstrual function meninges  Three membranes covering the brain and spinal cord meningitis  Inflammation of the coverings of the brain and spinal cord

445

meningocele  Protrusion of the meninges

through the skin menopause  Cessation of the menstrual cycle menstrual phase  Menstruation occurs, the

final phase of the three mesentery  Peritoneal folds that attach the

small and large bowel to the back wall of the peritoneal cavity mesothelioma  Tumor that develops from the surface of the pleura, pericardium, or peritoneum metaphysis  Wider part at the end of the shaft of a long bone, adjacent to the epiphyseal plate; located between the epiphysis and the diaphysis metastasis  Spread of disease to another organ or tissue in the body metastasize  To spread by metastasis microcephaly  Abnormal small head in relation to the body with associated underdevelopment of the brain micturate  Act of urinating midbrain  Major portion of the brainstem between the forebrain and hindbrain mineralocorticoids  Regulate salt and water balance by controlling sodium retention and potassium excretion by the kidneys mitral valve  Bicuspid valve situated between the left atrium and ventricle monoclonal immunoglobulin  Antibodies that are formed against a specific cell type monocytes  Large mononuclear leukocytes Monteggia fracture  Isolated fracture of the shaft of the ulna associated with anterior dislocation of the radius at the elbow morbidity  The rate that an illness or abnormality occurs Morgagni hernia  Protrusion of abdominal contents into the anterior and lateral aspects of the thoracic cavity morphologic  Pertaining to the form and structure of an organ mortality  The statistically expected death rate calculated by reviewing the population involved multilocular  Having many cells or compartments multiple myeloma  Bone marrow malignancy mural thrombosis  Thrombus originating in the vessel or cavity wall mutations  Alterations in the DNA structure that may become permanent hereditary changes mycoplasma  Colloquial usage for any of a genus of tiny microorganisms, smaller than bacteria but larger than viruses, that appear to be the causative agents of many diseases mycosis  Fungal infection myelin sheath  Insulated by a fatty covering myelocytic leukemia  Unregulated production of leukocytes myelomeningocele  Herniation of the spinal cord and meninges through the skin myocardial infarction (MI)  Infarction of the heart muscle (heart attack) myxedema  Puffy thickening of the skin with slowing down of physical and mental activity caused by failure of the thyroid gland

446

GLOSSARY

N nasal bone fractures  The most common fa-

cial fractures navicular  The most common fractures involving the carpal bones necrosis  Death of tissue necrotic  Dead or decayed neoplasia  Any new and abnormal growth, especially when the growth is uncontrolled and progressive neoplasm  Any new and abnormal growth, especially when the growth is uncontrolled and progressive nephrocalcinosis  Calcium deposits within the substance of the kidney neurogenic  Originating in the nervous system neuron  Basic nerve cell neutrophils  Polymorphonuclear granular leukocyte niacin  Vitamin B3 nidus  Focal point, especially of a stone or an inflammatory process noncommunicating (obstructive) hydrocephalus  Obstruction of cerebrospinal

fluid flow in the ventricular system causing enlarged ventricles normal-pressure hydrocephalus Defective resorption of cerebrospinal fluid or an overproduction of cerebrospinal fluid causing ventricular enlargement nosocomial  Incidences of infections being developed at the acute care facility nuclear medicine Using radiopharmaceuticals to produce ionizing radiation that is detected by a gamma camera to produce an image nutritional deficiency  In addition to inadequate intake, may be related to disorders of the liver, pancreas, and gastrointestinal tract that result in an inability of the body to digest and properly use proteins, carbohydrates, and lipids O oblique fracture  Runs a course of approxi-

mately 45 degrees to the long axis of the bone peptide tracer; a long-acting analog of the hormone somatostatin oligemia  Decreased blood volume oligodendrocytoma  Slow-growing glioma, usually arising in the cerebrum oligohydramnios  Very small volume of amniotic fluid oncology  The study of neoplasms open fracture  Overlying skin is disrupted open reduction  Surgical procedure utilizing direct or indirect manipulation of the fracture ossification  Bone formation osteoblastic  Forming bony tissue osteoblasts  Produce new bone around the outer circumference from the periosteum osteoclastic  Bone resorption osteoclasts  Enlarge the diameter of the medullary cavity by removing bone from the diaphysis walls osteogenic sarcoma  Malignant tumor composed of osteoblasts that produce osteoids and spicules of calcified bone octreotide  Radioactive

osteolytic  Destroying bone osteomalacia  Insufficient mineralization of

polyhydramnios  Excessive accumulation of

the adult skeleton osteomas  Tumor composed of bone tissue ovulation  Release of the ovum from the ovary

polypoid  Resembling a polyp pons  Part of the brainstem containing centers

P palpitations  Rapid or fluttering beating of the

heart, of which one is aware inflammatory process in which protein- and lipid-digesting enzymes become activated within the pancreas and begin to digest the organ itself papillary carcinoma  Slow-growing cystic thyroid carcinoma paradoxical  Seeming to contradict the known facts parathormone (PTH)  Secreted by the parathyroids and regulates the blood levels of calcium and phosphate parenchyma  Essential tissue of an organ patent ductus arteriosus  Abnormal connection between the pulmonary artery and aorta due to lack of the fetal ductus arteriosus pathognomonic  Especially distinctive or characteristic of a disease or pathologic condition pathologic fracture  Occurs when the bone weakens due to another process such as a tumor, infection, or metabolic disease pectus excavatum  Funnel chest: depressed sternum pedunculated  Having a stalk (pedicle) Pelken’s spur  Marginal spur formation pelvic kidney  Kidney located in the pelvis pericardium  Membrane surrounding the heart periosteum  Fibrous membrane covering the outer surface peripheral  Outside or away from the central portion of a structure peripheral nervous system  Motor and sensory nerves peristalsis  Wormlike movement by which the alimentary canal or other tubular organ propels its contents permeable  Membrane allowing fluids to pass through permeative  Diffusely spreading through or penetrating a substance, tissue, or organ, as by a disease process such as cancer pernicious anemia  Progressive megaloblastic anemia that results from lack of intrinsic factor that is required for absorption of the vitamin B12 petit mal  The mildest type of epilepsy, which occurs primarily in children petit mal seizure  Characterized by sudden, momentary loss of consciousness pia mater  Innermost meningeal covering pinna  Cartilaginous portion of the external ear pituitary adenomas  Tumor composed of glandular tissue of the pituitary gland platelets  Smallest blood cell and contains hemoglobin pneumococcus  Genus of gram-positive bacteria pneumoperitoneum  Presence of free gas in the peritoneal cavity pancreatitis  An

amniotic fluid

for some reflexes positron emission tomography (PET)  Us-

ing a radiopharmaceutical that emits a positron that the moving gamma camera detects to produce an image postmenstrual phase  Follows the menstruation phase in the menstrual cycle postpartum  After childbirth Pott’s disease  Tuberculosis of the spine primary cystadenocarcinoma  Cancer of the ovary often contains psammomatous bodies, depositions of calcium carbonate located in the fibrous stroma of the tumor that can be detected on plain abdominal radiographs primary hyperparathyroidism  Hyperactivity of the parathyroid glands resulting in excessive secretion of parathyroid hormone (PTH) and is usually caused by a discrete adenoma (80%) or carcinoma (2%) or by generalized hyperplasia (18%) of all glands primary hypoparathyroidism The most common radiographic finding on plain skull radiographs or CT of the skull is cerebral calcification, especially involving the basal ganglia, the dentate (tooth-shaped) nuclei of the cerebellum, and the choroid plexus caused by insufficient secretion of the glands primary stage  Initial phase of a disease process progesterone  Hormone secreted by the corpus luteum to help regulate menstrual cycle and fertilization prognosis  The expected patient outcome proliferate  To multiply rapidly, increase profusely prostate gland  Produces fluid that makes up the semen proximal convoluted tubule  Second part of the nephron, first part of the renal tubule psoriatic arthritis  Rheumatoid-like destructive process involving the peripheral joints in patients with psoriasis pulmonary mycosis  Fungal infection of the lung pulmonary valve  Three semilunar cusps between the right ventricle and the pulmonary trunk punctate  Marked with dots or tiny spots purpura  Spontaneous hemorrhages in the skin or mucous membrane pyloric stenosis  Also known as infantile hypertrophic pyloric stenosis (IHPS), occurs when the two muscular layers of the pylorus become hyperplastic and hypertrophic pyogenic  Bacteria that lead to the production of a thick, yellow fluid called pus pyosalpinx  Fallopian tube filled with pus R radiofrequency pulse (RF)  Refers to that por-

tion of the electromagnetic spectrum in which electromagnetic waves can be generated by alternating current—commonly in the 1- to 100-megahertz range—and their effect upon a body is potential heating of tissues in MRI

GLOSSARY radiopharmaceutical  A drug that is tagged to

small cell (oat cell) carcinomas  Specific type

emit ionizing radiation recessive  Genes that manifest themselves only when the person is homozygous for the trait reflex arc  Simple neurologic unit to carry impulses to the CNS and impulses to the PNS releasing hormones  Control the secretion of hormones by the anterior and posterior portions of the pituitary gland resection  Partial surgical removal of an organ or bone resorption  Bone destruction by osteoclasts retrovirus  Any of a family of ribonucleic acid (RNA) viruses containing the enzyme reverse transcriptase right-to-left shunting  Ventricle septal defect and overriding aorta causes unoxygenated blood into the left ventricle rudimentary  Imperfectly developed

of malignant bronchogenic epithelial neoplasm somatic nervous system  Supplies the striated skeletal muscles spermatogenesis  Formation of sperm spherocytosis  Anemia due to erythrocytes that have a circular rather than a biconcave shape, making them fragile and susceptible to rupture spina bifida occulta  Mild form in which there is a splitting of the bony neural canal but no clinical symptoms spin-echo (SE)  Most common pulse sequence used in MR using 90° radiofrequency pulses to excite the magnetization and one or more 180° pulses to refocus the spins to generate signal echoes spiral fracture  Encircles the shaft of a long bone spirochete  Spiral type of bacterium of the genus Spirochaeta spirometry  Measure of lung capacity using a spirometer spondylolisthesis  Spondylolysis with displacement of vertebral alignment spondylolysis  Cleft in the pars interarticularis situated between the superior and inferior articular process of the vertebra without displacement squamous carcinoma  Most common type of lung cancer stable  Resistant to change staghorn calculus  Renal calculi filling the entire renal pelvis of the kidney staging  Determination of the amount of spread of a neoplasm, necessary to select appropriate therapy and to predict the future course of a disease stasis  Stagnation of some fluid in the body (as of blood in veins); reduced peristalsis of the intestines resulting in the retention of feces stenosis  Narrowing stress, or fatigue, fracture  Fracture caused by repetitive stresses applied to the bone stroke  Cerebrovascular accident; denotes a sudden and dramatic focal neurologic deficit stroma  Supporting tissue of the matrix of an organ subarachnoid space Space beneath the arachnoid and above the pia mater that contains cerebrospinal fluid subchondral  Just beneath the articular margin subluxation  Incomplete or partial dislocation sulci  Shallow depressions on the surface of an organ supernumerary kidney  An extra kidney surfactant  Agent that lowers the surface tension symptoms  Subjective manifestations; the patient feels synapse  Point of contact between two neurons for impulses to flow syndrome  Indicates the presence of a combination of symptoms that commonly occur together and are related to a single cause systemic circulation  High-pressure system that carries blood to the organs and extremities systole  Phase in which the heart contracts

S saccular  Resembling a pouch-like sac saccular aneurysm  Bulging of only one side

of the arterial wall sarcoma  Highly malignant tumors arising

from connective tissues sclerosis  Conversion of a portion of bone into

an ivory-like, densely opaque mass; an abnormal hardening of body tissues or parts, especially of the walls of arteries seat belt fracture  Transverse fracture of a lumbar vertebra that is often associated with significant visceral injuries secondary hyperparathyroidism  Occurs more frequently than the primary form and is most often attributable to chronic renal failure secondary stage  Progression of the disease process into the phase that follows the initial stage secretory, or postovulatory, phase  Occurs between ovulation and the onset of the menses segmental fracture  Consists of a segment of the shaft isolated by proximal and distal lines of fracture seminal vesicles  Paired saclike gland that secretes a thick liquid that is rich in fructose for sperm motility sequestrum  Piece of dead bone that has become separated from the surrounding healthy bone serosa  Outer layer of a viscus (especially in the alimentary tract) serpiginous  Having a wavy border shock  Acute peripheral circulatory failure sickle cell anemia  Anemia characterized by crescentic red blood cells that contain abnormal hemoglobin molecules and are susceptible to rupture signs  Measurable manifestations of a disorder; objective manifestations silhouette (cardiac)  Outer border of the heart, seen against the radiolucent lungs simple bone cyst (unicameral)  True fluid-filled cyst with a wall of fibrous tissue single-photon emission computed tomography  Gamma camera moves around the

patient and detects the gamma rays produced by the radiopharmaceutical

447

T T1-weighted image  Equilibrium—high en-

ergy protons return to the low energy state T2-weighted image  Image relies on local de-

phasing of spins telangiectasia  Vascular lesion formed by

­dilatation of a group of small blood vessels teratoma  Neoplasm composed of various

kinds of embryonic tissue tertiary  Third in rank or order tertiary hyperparathyroidism  Refers to the

development of autonomous functioning parathyroid glands in patients who demonstrate progressive bone disease in the presence of biochemical and clinically controlled renal disease tertiary stage  Most serious stage of the disease in which radiographic abnormalities become apparent testicular dysgenesis  Characterized by small testes that fail to mature or produce sperm and testosterone testosterone  Stimulates the development and activity of the male accessory sex organs thalamus  Portion of the brain that receives and processes sensory information and relays it to the cerebral cortex thalassemia  Hemolytic anemia due to a defect in hemoglobin formation thiamine  Vitamin B1 thrombus  Blood clot in the vascular system thymoma  Tumor originating from the thymus gland thyroxine  Hormone influencing metabolic rate tortuous  Full of twists, turns, or curves torus (buckle) fracture  One cortex is intact with buckling or compaction of the opposite cortex toxoid  Chemically altered toxin trabeculae  Supporting or anchoring strands of connective tissue within body structures traction  Process of placing tension between two structures transitional vertebra  Vertebra with characteristics of another spinal region transverse fracture  Runs at a right angle to the long axis of a bone tricuspid valve Valve between the right atrium and right ventricle that has three ­ cusps trigone  Triangular area of the posterior bladder, between the openings for the ureters and urethra tripod fracture  Fractures of the zygomatic arch and the orbital floor or rim combined with separation of the zygomaticofrontal suture triradiate  Radiating in three directions trisomy  Presence of an additional (third) chromosome trophoblastic  Relating to the layer by which the fertilized ovum is attached to the uterine wall and from which the developing embryo receives its nourishment tuberculous arthritis  Chronic indolent infection with a slow progressive course by tuberculosis

448

GLOSSARY

U ulceration  Destruction of tissue creating an

opening within a structure ulcerogenic islet cell tumors (gastrinomas)  Tumor found in pancreas and duode-

num that is associated with peptic ulcers ultrasound  Images produced by high-frequency

sound waves emitted from the transducer that are echoed back to produce an image undifferentiated  Without form undisplaced fracture  The bone is without angulation or separation unilateral renal agenesis  Absence of a kidney unstable  As a result of a fracture, alignment is uncertain urate  Salt of uric acid uremia  Presence of excessive amounts of urea and nitrogen in the blood ureterocele  A cystic dilatation of the distal ureter near its insertion into the bladder V vaccine  Low dose of dead or deactivated bac-

teria or virus valvulae conniventes  Circular folds of the

small bowel vasculitis  Inflammation of a vessel

vas

deferens Muscular tube that passes through the inguinal canal as part of the spermatic cord connecting the epididymis and seminal vesicle to form the ejaculatory duct vasectomy  Severing of the vas deferens vegetations  Abnormal growth of tissue around a heart valve ventricular septal defect  Opening between the left and right ventricles allowing blood to flow back into the right ventricle instead of entering the systemic circulation vermis  Structure resembling a worm villi  Finger-like projections of the small bowel to increase the inner surface area viral meningitis  Inflammation of the meninges caused by virus virus  One of a group of minute infectious agents characterized by a lack of independent metabolism and by the ability to reproduce only within living host cells viscous  Thick, sticky viscus  Any large internal organ, especially in the abdomen vitamins  Organic compounds essential for normal physiologic and metabolic function volume-rendered imaging  Technique taking all the raw CT data density information and using them to simulate three-dimensional images

W water-soluble vitamins  Vitamins B and C,

which cannot be stored and therefore must be included in the daily diet Wimberger’s sign of scurvy  Epiphyseal ossification centers are demineralized and surrounded by dense, sharply demarcated rings of calcification Z Zenker’s diverticula  Outpouching that arises

from the posterior wall of the upper esophagus zygomatic arch fractures  Demonstrated on underexposed films taken in the basal (submentovertex) projection (“jug handle” view)

INDEX Note: Page numbers followed by “b”, “f” and “t” indicate boxes, figures and tables respectively.

A Abdomen contrast-enhanced MRA, 271f sonogram, 18f three-phase CT scanning protocol for, 23f ultrasound images, 17f Abdominal aorta, arterial phase demonstrating, 23f Abdominal aortic aneurysm, ultrasound/ CT axial scan, 267f Abdominal aortic stent, CTA, 268f ABO-incompatible blood, administration of, 11 Abscess, 4t Achalasia, 166 esophagus, distal part (rat-tail narrowing), 167f functional obstruction, 166 imaging appearance, 166 tortuous aorta, frontal chest radiograph, 166f treatment, 166 Achilles tendon, insertion, 112 bony erosion, 97f Achlorhydria, 174 Achondroplasia, 92 imaging appearance, 92 pelvis, view, 94f posterior scalloping, 94f treatment, 92 Acid-base balance, 217 Acidic corrosive agents, ingestion, 160–161 Acoustic barriers, 19 Acoustic neuroma, 299–300 CT scan, 304f imaging appearance, 299–300 MR T1-weighted axial/coronal images, 303f treatment, 300 Acquired immunodeficiency syndrome (AIDS), 12–13 gastrointestinal manifestations, 12 manifestations, MRI demonstration, 12–13 neurologic manifestations, 13f radiographic appearance, 12 treatment, 13 Acquired type, of tracheoesophageal fistula, 157–158 dentures, aspiration, 158f imaging appearance, 158 treatment of, 158 Acquired vascular disease, 256–274 findings, summary, 274t

Acromegaly, 364 extraskeletal manifestations, 365 heel pad, thickening, 365f lateral skull projection, 366f vertebral bodies, enlargement, 366f Active immunity, 11 Acute appendicitis avoidance of barium enema examination in, 185 clinical presentation, 185 clinical symptoms, 184 spot radiograph, 185f Acute arterial occlusion, streptokinase therapy for, 273, 273f Acute cholecystitis, 198–199 imaging appearance, 198–199 radionuclide hepatobiliary study, technetium-99m disofenin, 199f Acute coccidioidomycosis, symptoms (absence), 52 Acute diverticulitis, ultrasound appearance, 187 Acute embolic occlusion, left renal artery, 273f Acute epidural hematoma, CT scan, 311f Acute idiopathic thrombocytopenic purpura, 350–351 Acute inflammation, 3 Acute left middle cerebral artery infarct, 318f Acute leukemia, 342 bone destruction, cortical erosion, 344f neoplastic cells, proliferation, 344f Acute myocardial infarction, MRI, 258f Acute osteomyelitis, 339 proximal humerus, diffuse lytic destruction, 340f Acute pancreatitis, 206 CT scan, 206f imaging appearance, 206 plain abdominal radiographs, 206 symptoms, 206 transverse sonogram, 206f treatment, 208 ultrasound/CT imaging modalities, 206 Acute patellar tendinitis, 103f Acute renal failure, 243–245 excretory urogram, 245f excretory urography, 244 imaging appearance, 243–245 treatment, 245 ultrasonography, selection, 244–245 Acute renal vein thrombosis, right kidney (radiograph), 244f Acute staphylococcal arthritis, 100f

Acute subdural hematoma, 311f Acute ureteral colic, localized ileus, 181f Acute urinary tract obstruction, 233 Addison’s disease, 357 Adenocarcinoma, 8, 63 Adenomas, pituitary, 300 Adrenal adenoma, 356f Adrenal carcinoma, 358 anteromedial aspect, tissue tumor, 358f axial MR image, 360f imaging appearance, 358 treatment, 358 ultrasound image/CT scan, 358f Adrenal cortex benign/malignant tumors, 356 diseases of, 355–359 findings, summary, 359t Adrenal glands, 355–363 generalized enlargement, 355–356 metastases, 358–359, 360f imaging appearance, 358–359 treatment, 359 physiology of, 355 structure of, 355f Adrenal medulla, 355 diseases, 360–363 findings, summary, 364t epinephrine, secretion, 355 Adrenal virilism, 357 Adrenocortical insufficiency, CT scan, 358f Adrenocorticotropic hormone (ACTH), levels, decreased, 300 Adrenogenital syndrome, 357 adrenocortical tumor, 357f imaging appearance, 357 treatment, 357 Adult foot, osteogenesis imperfecta, 91f Adult respiratory distress syndrome (ARDS), 73 alveolar consolidation, ill-defined areas, 74f hypoxemia, 73 imaging appearance, 73 treatment, 73 Adult-type scoliosis, 147 Adynamic ileus, 180–181 gas/fluid retention, 181f imaging appearance, 180–181 intestinal motor activity, 180 treatment, 181 variants, 180–181 Aging degenerative changes of, axial MR image, 327f osteoporosis of, 109f

449

450

INDEX

Air embolism, 272 Alcoholic gastritis, 170 Aldosteronism, 356–357 Aldosteronoma, 357f Alkaline corrosive agents, ingestion, 160–161 Alkaptonuria, 429 Alveolar cell carcinoma (bronchiolar carcinoma), 65 Alveolar pneumonia, 45–46 imaging appearance, 46 right lobes, homogeneous consolidation, 46f Alzheimer’s disease, 327–328 FDG-PET metabolic brain images, 328f imaging appearance, 328 noncontrast CT scan, 328f presenile dementia, 327 treatment, 328 Amyotrophic lateral sclerosis (Lou Gehrig’s disease), 330 Anaphylactic reactions, 11 Anaplastic tumor, 8 Androgens (sex hormones), 355 Anechoic tissue, echo free, 17, 18f Anemia, 337–342 hemolytic, 338–341 iron deficiency, 337 megaloblastic, 341 myelophthisic, 341 Anencephaly, long-axis image, 415f Aneurysm, 266–267 abdominal aortic, ultrasound/CT axial scan, 267f aortic, MR image, 267f fusiform, 266, 266f saccular, 266 treatment, 267 walls, calcification, 266f Aneurysmal bone cysts, 122 tibia, cystic lesion, 122f Angina pectoris, oxygen insufficiency, 256 Angiography, comparison of contrast-­ enhanced CT coronary angiography and, 258f Angiomas, 8 Angulation (fractures), 132 Ankle, bimalleolar fracture, 141f Ankylosing spondylitis, 96–98 imaging appearance, 96–98 midcervical spine, oblique fracture, 97f sacroiliac joints, bilateral symmetric obliteration, 96f Annihilation, 29–30 Annular carcinoma (apple-core/ napkin-ring carcinoma), 192 Annulus fibrosis, tearing, 148f Anterior mediastinal mass chest projections, 80f CT scan, 82f right hilar adenopathy, 80f Anterior mediastinal/retrosternal nodes, involvement of, 344

Anterior mediastinum, lesions, 80 Anthracosis (coal worker’s pneumoconiosis), 61 diffuse reticular pattern, 62f imaging appearance, 61 treatment, 61 Anthrax, 47–48 imaging appearance, 47–48 treatment, 48 Antibodies, reaction, 11 Antidiuretic hormone (ADH), secretion, 216–217 Antigens, 11 immunologic responses, mechanisms, 11 Aorta coarctation, 254–255 imaging appearance, 255 plain chest radiograph, 255f sagittal MR image, 255f treatment, 255 dissection, 268–270 CT image, 269f diagnosis, aortography (usage), 270 imaging appearance, 269–270 MR image, 269f plain chest radiograph, 269f radiolucent intimal flap, aortogram demonstration, 270f treatment, 270 traumatic rupture, 267–268 chest radiograph, 268f imaging appearance, 267–268 mediastinum widening/nasogastric tube deviation, 268f treatment, 268 Aortic aneurysm, MR image, 267f Aortic arch (evaluation), echocardiography (usage), 255 Aortic insufficiency, 278 frontal chest radiograph, 279f Aortic knob, bulging, 255 Aortic orifice, overriding, 254 Aortic stenosis, 277–278 aortic valve, leaflets (calcification), 278f cardiac apex, frontal projection, 278f treatment, 278 Aortic valve, 248–249 Apical lordotic projection, 49f Aplastic anemia, 341 Appendicitis, 183–185 imaging appearance, 184–185 treatment, 185 ultrasound images, 185f Appendicolith, laminated calcification, 184f Appendix, cecum inferomedial aspect, 153 Apple-core carcinoma (annular carcinoma/napkin-ring carcinoma), 192 Appositional growth, 87 Aqueductal stenosis, T1-weighted sagittal MR image, 331f

Arachnodactyly, 428f Arachnoid membrane, 290 inflammation, 290–291 Arachnoid villi, 290 ARDS. see Adult respiratory distress syndrome (ARDS). Arteriovenous malformation axial MR image, 323f CT scan, 324f Artery, acute embolic occlusion, 272–273 Arthritis therapy, impact, 100–101 treatment, 100–101 Asbestosis, 60–61 CT scan, 61f imaging appearance, 60–61 PA image, 61f Ascending aorta, aneurysmal dilatation of, 384f Ascites (fluid accumulation), 202 plain radiograph, 203f Ascorbic acid (vitamin C), deficiency, 420 Aseptic necrosis, 430 Aspiration pneumonia, 47 bilateral, nonsegmental air-space consolidation, 47f imaging appearance, 47 treatment, 47 Asthma, 56–57 imaging appearance, 56–57 pulmonary infections, recurrence, 56f treatment, 57 Astrocytomas, 295–296 cystic astrocytoma, CT scan, 299f Asymptomatic patient, 2 Asymptomatic skeletal metastases, detection, 129 Atelectasis, 72–73 iatrogenic cause, 72 imaging appearance, 72–73 treatment, 73 Atherosclerosis, 270–271 chest, lateral projection, 270f Doppler ultrasound, usage, 270–271 imaging appearance, 270–271 superficial femoral arteries, bilateral atherosclerotic occlusion, 271f treatment, 271 Atlantoaxial joint, subluxation, 96f Atrial defects (identification), Doppler echocardiography (usage), 253 Atrial septal defect, 252 chest, frontal projection, 252f Eisenmenger’s syndrome in, 253f septal closure, absence, 254f Atrioventricular (AV) node, impulse passage, 250–251 Atrophic undescended testis, coronal MR image, 392f Atrophy, 6 Autoimmune hepatitis, ultrasound images, 201f

INDEX Autonomic nervous system, function, 287 Autosomal dominant disorders, 10 Autosomal recessive disorders, 10 Autosomes, 9–10 Avulsion fractures, 131–132

B Bacillus anthracis, 47 Bacteremia, 4t Bacterial gastritis (phlegmonous gastritis), 170 Bacterial meningitis, 290–291 Bacterial organisms, toxin production, 4 Bacterial osteomyelitis, 103–106 imaging appearance, 104–106 treatment, 106 Bacterial pneumonia, lung abscess, 48f Bacterial vertebral osteomyelitis, 106f Bamboo spine, 96f Barrett’s esophagus, 159–160 imaging appearance, 159–160 ulcerations, development, 160f upper thoracic esophagus, stricture, 161f Basal cisterns, subarachnoid enhancement, 291f Basal ganglia, 289 Basophil, 337 Battered-child syndrome, 137 imaging appearance, 137 left arm, frontal radiograph, 138f right arm, frontal radiograph, 138f treatment, 137 Benign bone tumors, 119–123 neoplasia, findings (summary), 123t treatment, 123 Benign breast disease, 409 Benign breast mass, screen-film mammogram, 408f Benign gastric ulcer contrast material, penetration, 172f en face projection, 172f hallmark of, 172 healing, 173 mucosal folds, radiation, 172 Benign prostatic hyperplasia, 387–388 bladder (base), smooth filling defect, 388f imaging appearance, 387–388 prostatic enlargement, T1-weighted MR image, 388f transrectal ultrasound, sagittal plane, 388f treatment, 388 Benign solitary pulmonary nodule (tuberculoma), 62f CT scan, 63f Benign thyroid adenomas, 371 Benign tumors, 7 Beriberi (thiamine deficiency), 420 diffuse pulmonary edema, 420f imaging appearance, 420

Berry aneurysm rupture, 324f subarachnoid hemorrhage, 324f Bicuspid valve (mitral valve), 248–249 Bifid renal pelvis, 221f Bilateral cervical ribs, 89f Bilateral orbital ecchymoses (raccoon eyes), 309 Bilateral renal vein thrombosis, 242–243 Bilateral subdural hematoma, coronal MR image, 312f Bilateral symmetric hilar lymph node enlargement, 57–58 Bilateral undescended testes, malignant neoplasms, 391f Bile, emulsifier, 153 Bilirubin, 338 Bimalleolar fracture, ankle, 141f Biparietal diameter (BPD), 414 cursor width, 414f Black lung, 61 Bladder calculi, plain radiograph, 232f carcinoma, 240–242 CT scan, 244f imaging appearance, 241–242 treatment, 242 tumor irregularity, 243f distention, CT (usage), 242 incontinence, 89 Bleeding disorders (platelet diseases), 349–352 findings, summary, 352t Blood coagulation (clotting), 349 electrolyte/acid-base balance, 217 oxygenation, 38 physiology of, 336 Blood oxygen level dependent (BOLD), 27 Blood vessels, terms for, summary of, 6t Blowout, 129 fracture cause, 314–315 tomogram, 314f metastases, 130f Body fluids, electrolyte/acid-base balance, 217 waste products, removal, 38 Bone metastases, 127–131 fluorodeoxyglucose-PET scan, 129f imaging appearance, 129–131 MR image, 131f treatment, 131 Bones abscess, osteomyelitis, 104 age, radiographic determination, 87 benign tumors, 129 congenital diseases, 89–92 cysts aneurysmal bone cysts, 122 simple bone cysts, 122 destruction (resorption), 87

451

Bones (Continued) formation (ossification), 87 fracture healing, 134f functions of, 88b hereditary diseases, 89–92 infarct, 119f ischemic necrosis, 116–119 imaging appearance, 117–119 T1-weighted MR image, 118f treatment, 119 islands, 122 femoral head, 123f multiple abnormalities, 385 neuroblastoma metastatic to, 362f quality changes (expectation), skeletal radiography (exposure factor), 2b radiographs, contrast requirement, 86b–87b sclerosis, 90f softening, osteomalacia, 110 Bony cortices, demineralization, 91f Border, in imaging, 16 Bougienage, 163 Bowel obstructions, CT scans, 180f Bowing fractures, 132 Bowman’s capsule, fluid filtration, 216–217 Boxer’s fractures, 138 fifth metacarpal, distal fragment (volar angulation), 140f Brain abscess, 292–293 imaging appearance, 292–293 T1-weighted MR image, 292f treatment, 293 divisions, 289f neurosurgical localization, 18–19 traumatic processes, 309–315 findings, summary, 316t Brainstem glioma, sagittal MR image, 297f Breast, 407f benign mass, screen-film mammogram, 408f carcinoma, unilateral sagittal T1-weighted fat-saturated postcontrast MR image, 410f disease, sonography, 409f implants, MRI, 411f lesions, 407–409 findings, summary, 413t removal, stereotaxic needle biopsy, 413f Breast cancer, 407–409 clustered calcifications, 408 CT scans, 411f full/magnified coned views, 408f imaging appearance, 407–409 malignant calcifications, 408f treatment, 409 Breast self-examination (BSE), 407 Brittle bones (osteogenesis imperfecta), 91

452

INDEX

Bronchial adenoma, 63 imaging appearance, 63 neoplasms, low-grade malignancy, 63 Bronchial mucosa, swelling, 54 Bronchial tree, esophagorespiratory fistula, 158f Bronchiectasis, 57 imaging appearance, 57 treatment, 57 Bronchioalveolar carcinoma, growth, 65 Bronchiolar carcinoma (alveolar cell carcinoma), appearances, 65 Bronchogenic carcinoma (malignant solitary pulmonary nodule), 63–65 airway obstruction, 63–64 cavitary right upper lobe mass, air-fluid level, 65f cavitation, 64–65 imaging appearance, 63–65 margins, definition (problems), 62f spread, 66f tomography, 65f Bronchopneumonia, 46 imaging appearance, 46 right base, consolidation, 46f Buckle fractures (torus fractures), 132 Bullae, appearance, 55 Bursitis, 101–102 elbow, posterior aspect (transverse scan), 101f first-line treatment, 101–102 imaging appearance, 101–102 treatment, 101–102 Butterfly fragment, 132

C C7 vertebral body, fracture, 143f Caffey’s disease (infantile cortical hyperostosis), 7f Calcific tendinitis, 102f Calcified pancreatic pseudocyst, 208f Calcified tuberculoma, 51f Calcified uterine fibroid, calcified mass, 401f Calor (heat), acute inflammation clinical sign, 4 Cancellous bone (spongy bone), 87 Cancerous lesion, treatment, 163 Cancers, 7 cause, 8 clinical symptoms of, 8 curable stage, 8–9 hematogenous spread of, 9 pain and, 8 Candida, 160 Candida esophagitis, 161f Carbon dioxide, level, 39 Carcinogens (causative factors), 8 Carcinomas, 8 Cardiac pacemaker, fracture, 42f Cardiac resting images, 32f Cardiothoracic ratio (C/T ratio), 261

Cardiovascular system, 248–285 function, 248 objectives, 248 physiology, 248–252 radiographer notes, 249b Carotid arteriosclerotic occlusive disease, ultrasound scan, 319f Carotid artery bifurcation, carotid arteriogram, 320f MRA, 320f Carotid artery injury, 313 Carpal navicular bone, fractures (nonunion), 135f Cartilage, hypertrophy, 365 Cavitary right upper lobe mass, 65f Cecal volvulus, 193–194 barium enema examination, 195f imaging appearance, 194 Cecum, dilatation, 193f Cell growth, alterations, 6–7 terms, summary, 6t Centers for Disease Control and Prevention (CDC), Standard Precautions, 11 Central nervous system components, 287 degenerative diseases, 327–330 findings, summary, 330t diseases, findings, summary, 334t infections, 290–295 findings, summary, 294t tumors of, 295–309 findings, summary, 308t–309t imaging appearance, 295 treatment, 295 vascular disease, 317–322 findings, summary, 323t Central venous catheters, 40–41 breakage, 41 location, 41f embolization, 41 insertion, problems, 40 Central venous pressure (CVP) catheters, internal device (findings), 42t measurement, 40 Cerebellar atrophy, 329 sagittal MR image, 329f Cerebellum, 289, 289f Cerebral arteriography, usage, 295 Cerebral contusion, 312–313 CT scan, 312f imaging appearance, 312–313 treatment, 313 Cerebral cortex, responsibility, 288–289 Cerebrospinal fluid (CSF), 290 formation, 290 Cerebrovascular disease, 317 Cerebrum, 288, 289f Cervical rib, 89 Cervical spine, injury, 89 Cervical spine separation, 143f

Cervix, carcinoma, 404–406 bladder invasion, CT scan, 405f CT scan, 405f imaging appearance, 404–406 sagittal T1-weighted MR image, 405f sagittal T2-weighted MR image, 405f sonogram, 405f treatment, 406 Chest, frontal projection, atrial septal defect, 252f Chest radiography kVp optimum, 2b patient positioning, 37b performing, 37b Chewing (mastication), 153 Chiari II malformation, 89 Childhood, rickets (system disease), 110 Children, pneumoperitoneum, 211 Cholecystitis, treatment for, 199 Cholelithiasis (gallstones), 197–198 Chondromas, 8 Chondrosarcoma, 124–125 calcification, 125f cartilaginous origin, 124 imaging appearance, 124–125 Chordoma, 306–307 clival, sagittal MR image, 307f CT scan, 306f imaging appearance, 306–307 plain skull radiograph, 306f treatment, 307 Chorion, 395–396 Choroid plexus papilloma, T1-weighted MR image, 332f Choroid plexuses, plasma filtration, 290 Chromophobe adenomas, 300 Chromosomal aberrations, 426–428 Chronic atrophic gastritis (nonerosive gastritis), 170 Chronic bronchiectasis bronchogram, 57f interstitial markings, coarsening, 57f Chronic bronchitis, 54 imaging appearance, 54 right lower lung, coned view, 55f treatment, 54 Chronic Crohn’s colitis, 190f Chronic duodenal ulcer disease, cloverleaf deformity, 172f Chronic glomerulonephritis, nephrotomogram, 224f Chronic idiopathic thrombocytopenic purpura, 352f Chronic left subdural hematoma, CT scan, 312f Chronic leukemia, 342 indium-111 whole-body scan, 345f splenomegaly, 345f Chronic obstructive pulmonary disease (COPD), 54–57 Chronic osteomyelitis, 105f

INDEX Chronic pancreatitis, 206–208 diffuse pancreatic calcifications, 207f imaging appearance, 207–208 treatment, 208 ultrasound examination, 207 ultrasound image, 207f Chronic pelvic inflammatory disease, transverse sonogram, 397f Chronic pyelonephritis, 225f Chronic renal failure, 245–246 imaging appearance, 245–246 treatment, 246 ultrasound image, 246f Chronic right middle cerebral artery infarct, low-attenuation region, 318f Chronic sinusitis, mucosal thickening, 332f Chronic ulcerative colitis (lead-pipe colon), 189f Chyme, 153 Circulatory system, relative attenuation, 3b Clay shoveler’s fractures, 144 frontal/lateral projections, 145f Clinical breast examination (CBE), 407 Clival chordoma, sagittal MR image, 307f Closed fractures, 131 Clubfoot, 89 prenatal ultrasound, 416f Coagulation factors, 349 Coarctation, aorta, 254–255 Coccidioidomycosis, 52–53 Coccidioides immitis, 52 imaging appearance, 52–53 posteroanterior/lateral views, 53f pulmonary consolidations, 52 treatment, 53 Codman’s triangle, periosteal elevation, 125f Coeur en sabot appearance, 254 Cold thyroid nodules, 368 Collateral circulation (progressive development), aortic blood flow obstruction and, 254–255 Collecting tubules, urine passage, 217 Colles’ fracture, 137 wrist, frontal/lateral projections, 139f Collimator, 28 Colon, 183–197 carcinoma, 188–189 cause, 192 development, 189f Crohn’s disease, 189 diverticular disease, complication, 186 findings, summary, 196t–197t obstruction, 182f volvulus, 193–195 Colon cancer, 191–193 CT virtual colonoscopy, 192 18F-fluorodeoxyglucose (FDG-PET), 193 imaging appearance, 191–193 transrectal ultrasound, 192 treatment, 193 Colonic diverticula, 185–186

Colonic ileus, 181 large bowel, distention, 181f Colonic obstruction, 193 Color-flow Doppler studies, 18 Comminuted fractures, 132 Communicating hydrocephalus, 331 Community acquired disease, 2 Compact bone, 87 Compensatory hypertrophy, 219 acquired condition, 219 hypoplastic kidney, 219f Complete fracture, 131 Completed stroke, 317 Complex thyroid mass, ultrasound images, 372f Compound fractures (open fractures), 131 Compression fractures, 132 Compton scattering, 28 Computed axial tomography, imaging modality, 15–16 Computed tomography (CT), 20 angiography, 23f esophagography, 157 myelogram, 22f number (Hounsfield number), 20 scout image, 20f single-scan protocol, change, 21 spiral scanning (helical scanning), 21 summary of, 22t three-dimensional surface-rendered images, 24f Computed tomography angiography, 23f Computerized technology, imaging prevalence, 16 Coned x-ray beam, usage, 21 Congenital bone diseases, findings (summary), 93t–94t Congenital diseases, 43–44, 218–222 findings, summary, 222t number/size, anomalies of, 218–219 rotation/position/fusion, anomalies of, 219–220 treatment of, 221 Congenital heart disease, 252–255 findings, summary, 256t Congenital hip dysplasia (dislocation), 92 imaging appearance, 92 treatment, 92 ultrasound imaging (ultrasonography), 92 Congenital syphilis, 383 metaphyses, transverse bands (density decreased), 385f Congenital tracheoesophageal fistulas, 156 imaging appearance, 156–157 treatment of, 157 type I, 156 type II, 156 type III, 157, 157f type IV (H fistula), 157, 157f

453

Congestive heart failure, 260–261 imaging appearance, 260–261 result, 256–257 treatment, 262–263 Connective tissue, 219–220 Consciousness, levels (decrease), 309 Constipation, 153 Contrast-enhanced CT coronary angiography, angiography (comparison), 258f Contrast extravasation, 229f Convulsive disorders findings, summary, 326t imaging appearance, 326–327 treatment, 327 Coronary angiography, 259f–260f Coronary artery disease, 256–259 imaging appearance, 257–259 intravascular ultrasound (IVUS), 258 percutaneous transluminal coronary angioplasty (PTCA), balloon catheter (usage), 259 radionuclide thallium perfusion scanning, usage, 257 single-photon emission computed tomography (SPECT), 257, 257f treatment, 258–259 Coronary sinus, pacemaker tip, 42f Corpus callosum, 289 Corpus luteum, growth, 394–395 Corrosive agents, ingestion of, 160–161 imaging appearance, 161 treatment of, 161 Corrosive gastritis, 170 Cortex, 288 Craniopharyngioma, 303–304 CT scan, 305f imaging appearance, 303–304 plain skull radiograph, 305f sagittal MR image, 305f treatment, 304 Craniotomy, history, 309 Cretinism, skull (lateral projection), 370f Crohn’s colitis, 189–191 benign, stricture, 190f colon cancer, development, 190 CT demonstration, 189–190 diffuse aphthous ulcers, 190f findings, summary, 190t imaging appearance, 189–190 progression, 189 transverse colon, intramural fistula, 190f treatment, 190–191 Crohn’s disease (regional enteritis), 176–177 clinical spectrum, 176 cobblestone appearance, 176f fistula formation, 176–177 imaging appearance, 176–177 skip lesions, 177f

454

INDEX

Crohn’s disease (Continued) terminal ileum/sigmoid colon, fistulization, 178f treatment, 177 ultrasound, 177f Crossed ectopia, 219 Croup, 44 imaging appearance, 44 trachea, tapered narrowing, 45f treatment, 44 Crown-to-rump length, 414 measurement, cursor delineation, 414f Cryptorchidism (undescended testis), 390–391 CT. see Computed tomography (CT). Cushing’s syndrome, 355–356 adrenal adenoma, 356f functioning cortical adenoma, 356f imaging appearance, 355–356 treatment, 356 CVP. see Central venous pressure (CVP). Cystadenocarcinoma, endovaginal sonogram, 399f Cystadenomas, 8 longitudinal/transverse sonograms, 399f Cystic astrocytoma, CT scan, 299f Cystic fibrosis (mucoviscidosis), 43 cysts, superimposition, 43f imaging appearance, 43 meconium ileus, bowel distention, 43f recombinant human deoxyribonuclease (DNase) inhalation, 43 treatment, 43 Cystine stones, plain image/excretory urogram, 230f Cystinuria, 430 Cystitis, 227, 228f imaging appearance, 227 treatment, 227 Cysts, 234–242, 397–406 findings, summary, 242t Cytomegalovirus, 8 Cytotoxic reaction, 11

D Dandy-Walker cyst, 330–331, 331f Deep venous thrombosis, 281 contrast venogram, 282f detection, modalities, 281 Doppler image, 282f imaging appearance, 281 treatment, 281 Degenerative diseases, 327–330 Alzheimer’s disease, 327–328 normal aging, 327 Degenerative disk disease, 146f Degenerative follicular adenoma, radioactive iodine scan, 373f Degenerative joint disease (osteoarthritis), 98 Deglutition (swallowing), complexity, 153 Delayed reaction, 11

Demarcation, in imaging, 16, 16t Density, in imaging, 16, 16t Deoxygenated venous blood, return to heart, 250 Depressed fractures, 132 stellate shape, 310 Depressed nasal fracture, 314f Dermoid cyst (teratoma), 400 imaging appearance, 400 multiple well-formed teeth, 400f sagittal sonogram, 401f transverse sonogram, 401f treatment, 400 Diabetes, complication, 378–379 Diabetes insipidus, 367 Diabetes mellitus, 378–381 calcification, 379f findings, summary, 380t imaging appearance, 379–381 neuropathic joint, 379f treatment, 380–381 vas deferens, bilateral calcification, 379f Diabetic gangrene, 380f Diabetic neuropathy, 380 Diagnosis, of disease, 2 Diagnostic imaging modalities, 15–35 Diagnostic mammogram, 16–17 Diaphragm disorders of, 82–83 findings (summary), 83t eventration, 83 imaging appearance, 83 treatment, 83 leaves, diffuse elevation, 83f Diaphragm elevation causes of, 83 imaging appearance, 83 Diaphragmatic paralysis, 82 imaging appearance, 82 treatment, 82 Diaphysis, 87 Diarrhea, 153 Diarrheogenic islet cell tumors, 209 Diastatic fracture, 309–310 Diastole (relaxation phase), 250–251 Diencephalon, 289–290, 289f Diffuse aphthous ulcers, 190f Diffuse lung disease, 54–61 findings, summary, 59t Diffuse lymphomatous infiltration, 346 Diffuse osteoblastic metastases, 390f Diffuse osteoporosis, 356 Diffuse pulmonary disease, development, 58 Diffuse pulmonary edema, demonstration, 263f Diffusion imaging, 25–26 Digestion, occurrence, 153 Digestive organs, location, 154f Digestive system, physiology of, 153–156 Digital mammography, advantages, 16–17 Diploic space, widening, 338

Diploic vessel, dilatation, 299 Direct fusion equipment, 31–33 Diseases, 2–9 miscellaneous, 419–431 terms, summary, 2t Disk herniation, L5-S1 level (CT scan), 147f Dislocations, 141–144 congenital hip dysplasia, 92 fractures, 137–140 spine, 141–144 Disorders, miscellaneous, summary of findings for, 425t Displacement (fractures), 132 Disuse osteoporosis, 108f Diverticula, occurrence, 185–186 Diverticulitis, 186–187 contrast material, thin projection, 186f CT scan, 187f fibrotic healing, spasm, 187 imaging appearance, 186–187 sigmoid, 187f treatment, 187 Diverticulosis, 185–186 imaging appearance, 186 sawtoothed configuration, 186f treatment, 187 DNA structure, mutations, 10 Dolor (pain), acute inflammation clinical sign, 4 Dominant genes, 10 Down syndrome, 426–427 imaging appearance, 426–427 pelvis, examples, 426f treatment, 427 Dual-energy x-ray absorptiometry (DEXA) bone densitometry, usage, 108 bone mineral density (BMD) scan, 109f Duchenne’s muscular dystrophy (DMD), 425 Duodenal ulcer, 171 imaging appearance, 171 ulcer niche, appearance, 171f Duplication (duplex kidney), 220–221 Dura mater, 290 extensions, 290 Dwarfism, 92 Dysarthria, 317 Dysphagia (swallowing difficulty), cause, 161–162 Dysplasia, 7

E Ecchymosis, 5–6 Echo free, 17 Echo time (TE), 24 Ectopic kidney, 219 Ectopic pacemaker, 251–252 Ectopic parathyroid adenoma, CT scan, 376f Ectopic pheochromocytoma, soft tissue mass, 362f

INDEX Ectopic pregnancy, 416 adnexa, live embryo (endovaginal sonography), 416f imaging appearance, 416 treatment, 416 Ectopic ureteroceles appearance, 221 intravenous urogram/cystogram, 223f Edema, 4–5 terms, summary, 5t Eisenmenger’s syndrome (pulmonary hypertension), 253 Elbow fat pad sign, 140f fractures, detection, 138–139 posterior aspect, transverse scan, 101f subchondral cysts, 351f tuberculous arthritis, 100f Electrode fractures, 42 Electrolyte balance, maintenance, 217 Embolism, 271–274 Embolus, 272 Emphysema, 55–56 bullae, 55 chest projections, 55f dirty chest appearance, 56 imaging appearance, 55–56 treatment, 56 vascular change, 55 Emphysematous blebs, 56f Emphysematous cholecystitis, 199 imaging appearance, 199 lumen/gallbladder, gas, 200f Emphysematous cystitis, 229f Emphysematous pyelonephritis, 225, 225f imaging appearance, 225 treatment, 225 Empyema, 79–80 imaging appearance, 79–80 large soft tissue mass, 79f treatment, 79–80 Emulsifier, 153 Encephalitis, 291 Enchondral bone formation, decrease, 92 Enchondromas, 8f, 119–120, 120f imaging appearance, 119–120 Endocrine system, 354–382 physiology of, 354 radiographer notes, 354b Endometrial carcinoma, 402–403 bladder invasion, 403f endovaginal sonogram, 403f imaging appearance, 402–403 sagittal T2-weighted MR image, 403f treatment, 403 Endometrioma, endovaginal sonogram, 404f Endometriosis, 403–404 endometrial implants, 404f imaging appearance, 403–404 treatment, 404 urinary tract, involvement, 404

Endometritis, ultrasound image, 397f Endosteum, 87 Endotracheal tube, 40 internal devices, findings (summary), 42t position, 40f, 73f Enteric-enteric fistula, development, 404–406 Enzyme deficiency, 9 Eosinophils, 337 Ependymomas, 296 Epidemiology, 9 Epididymis, sperm maturation, 386 Epididymitis, 391–392 imaging appearance, 392 longitudinal ultrasound image, 393f radionuclide scan, 393f treatment, 392 Epidural empyema, 293 imaging appearance, 293 right frontal region, epidural fluid collection, 293f treatment, 294 Epidural hematoma, 311 Epiglottitis, 44–45 Haemophilus influenzae, 44–45 imaging appearance, 45, 45f treatment, 45 Epilepsy, 326–327 FDG-PET brain images, 327f findings, summary, 326t imaging appearance, 326–327 treatment, 327 Epinephrine (adrenaline), secretion, 355 Epiphrenic diverticula, 163, 164f Epiphyseal cartilage, 87 Epiphyses, 87 Erosive gastritis, causative agent, 170 Erythrocytes (red blood cells), 336, 337f Erythropoietin, kidney production, 218 Esophageal cancer, 161–163 imaging appearance, 162–163 treatment of, 163 Esophageal diverticula, 163 Esophageal varices, 163–165 complication, 165 filling defects, 165f imaging appearance, 164–165 treatment of, 165 Esophagitis, 158–160 treatment, 160 Esophagorespiratory fistula, 158f Esophagram, lesion infiltration, 163f Esophagus, 156–169 carcinoma, 162f CT staging, 163f early, 162f distal part, rat-tail narrowing, 167f distal section, functional obstruction (achalasia), 166 esophagorespiratory fistula, 158f findings, summary, 168t–169t

455

Esophagus (Continued) fistulization, 157 fistulous communication, 157 lower cervical portion, fish bone, 167f meat impaction, 167f midthoracic portion, traction diverticulum, 164f nonopaque foreign bodies, 167 perforation, 168–169 contrast material, extravasation, 169f Estrogen, secretion, 394 Etiology, 2 Ewing’s sarcoma, 125–126 diffuse permeative destruction, 126f imaging appearance, 126 External bony callus, formation of, 134f External carotid artery angiogram, lateral projection, 314f External sphincter, voluntary contraction, 217–218 Extramedullary hematopoiesis, 339, 339f Extravascular fluid, accumulation, 5 Extrinsic asthma, 56

F Facial fractures, 313–315 imaging appearance, 314–315 treatment, 315 Facial skeleton, mandible (exposure), 315 Fallopian tubes, 395–396 unilateral/bilateral gross dilatation, 398f Fat CT number, 20 suppression, 26–27 Fat-soluble vitamins, 419 Fatigue fractures (stress fractures), 136–137 Feeding arteries, arteriography, 299 Feet interphalangeal joints, bony ankylosis, 97–98 mutilating arthritis, 98f Female breast, 407f Female infertility, 417–418 Female reproductive system, 394–396, 396f diseases, findings (summary), 406t physiology of, 394–396 Femoral head aseptic necrosis, 340f bone island, 123f ischemic necrosis, 118f Femur distal ends of, marrow infiltration in, 430f fracture, 136f mid shaft projections, osteoid osteoma, 121f Fetal age measurement, BPD, 414 Fetal femur, length measurement, cursors in, 414f Fetus BPD in, 414f cranial architecture in, 18f

456

INDEX

Fibromuscular dysplasia, 264 string-of-beads pattern, 264f Fibrous dysplasia, 116, 118t humerus, expansile lesion, 117f imaging appearance, 116 medullary cavities, ground-glass appearance, 117f treatment, 116 Fifth metacarpal, neck fracture, 140f Fifth metatarsal base, Jones fracture, 141f Fingers osteoarthritis, 99f proximal interphalangeal joint of, effusion and periarticular swelling of, 112f First metatarsophalangeal joint rat bite erosions, 113f soft tissue swelling, 105f Fissures, 288 Fluid-filled structures, echoes, 17 18F-fluorodeoxyglucose (18F-FDG), decreased uptake of, 31f Fluorodeoxyglucose-PET scan, bone metastases, 129f Focal neurologic signs, 309 Folic acid, deficiency, 341 Follicle-stimulating hormone (FSH), 364 Follicular carcinoma, 371–372 Forearm, fractures, 139–140 Foreign bodies, 166–168 Fractures, 131–137 angulation, 132 C7 vertebral body, 143f casts, 133 classification, 132f delayed union, 135 dislocation, 137–140 displacement, 132 elbow, detection, 138–139 external fixation, 133 lower leg, 133f external reduction (closed reduction), 133 findings, summary, 142t healing, 134–135 tibia, 135f hematoma, formation, 134f imaging appearance, 132–134 internal fixation, 133 scaphoid, 133f malunion, 135, 135f nonunion, 135 carpal navicular bone, 135f complication, 138 odontoid process, 143–144 open reduction, 133 internal fixation, usage, 133f reduction, 133 site, upper body (bone scan), 138f spine, 141–144 stress images, 134–135 treatment, 133–134 types of, 131–134 union, dense callus formation, 134f

Frontal sinus, osteoma, 121f Full-field digital mammography (FFDM), 16–17 Full spine images, acquisition, 147 Function, loss of, as acute inflammation clinical sign, 4 Functional MRI (fMRI), 27 Functioning parathyroid adenoma, preoperative localization, 375 Fused image, creation, 16 Fusiform aneurysm, 266, 266f Fusiform soft tissue mass, production, 106 Fusion imaging, 31–35 PET/CT of the body, 34f summary of, 33t

G Gadolinium (intravenous contrast agent) enhancement, 27f usage, 25 Gait disturbances, 89 Galeazzi fracture, 139–140 Gallbladder, 156, 156f, 197–200 calculi, 198f findings, summary, 200t hypoechoic, 18f ultrasound images, 17f Gallstones (cholelithiasis), 197–198 diagnosis, oral cholecystography (OCG) technique, 197–198 fissuring, Mercedes-Benz sign, 198f imaging appearance, 197–198 oral cholecystogram, 198f radiopaque contrast material, malabsorption, 198 ultrasound image, 199f Gamma camera, 28 Ganglion cells, damage in, 5 Gangrene, 5 Gastric atrophy, 341 Gastric banding, in obesity, 423 Gastric carcinoma CT staging, 176f imaging appearance, 174–176 linitis plastica pattern, 174f polypoid mass, 174 ulceration, presence, 174f Gastric ulcer, 171–173 evaluation, endoscopy (role), 173 healing, 173f imaging appearance, 172–173 radiating folds, 173f Gastrinomas, 209 Gastritis, 170 imaging appearance, 170 rugal folds, thickening, 170f superficial gastric erosions, presence, 174f treatment, 170 Gastroesophageal reflux disease (GERD), 158–159 Gastrointestinal system, 152–215 radiographer notes, 153b

Gastroplasty, in obesity, 423 Gaucher’s disease, 430–431 femurs, distal ends (marrow infiltration), 430f imaging appearance, 430 treatment, 430–431 Genders, infectious diseases, 383–386 Generalized osteoporosis, causes, 109 Genetic amino acid disorders, 428–431 summary of findings for, 431t GERD. see Gastroesophageal reflux disease (GERD). Germinomas, 305 Ghon lesion, 49 Giant cell tumors (osteoclastoma), 120 distal femoral metaphysis, lesion, 120f imaging appearance, 120 Giant emphysematous bulla, 56f Gibbous deformity, 106 Gigantism, 364 Glioblastoma multiforme, T1-weighted axial/coronal MR images, 296f Glioblastomas, 295–296 Glioma, 295–299 brainstem glioma, sagittal MR image, 297f imaging appearance, 296–299 infiltrating glioma, T2-weighted MR image, 298f treatment, 299 Glomerulonephritis, 224 chronic glomerulonephritis, nephrotomogram, 224f excretory urographic findings, 224 imaging appearance, 224 treatment, 224 Glomerulus, urine formation, 216–217 Glucocorticoids, 355 Glucose, 378 Glycogen, 155–156 Glycogen storage diseases, 430 generalized globular cardiac enlargement, with left ventricular prominence, 430f Glycosuria, 378 Goiter, 370–371 imaging appearance, 370–371 thyroid gland, enlargement, 371f treatment, 371 ultrasound, 371 Gonadal dysgenesis (Turner’s syndrome), 427 Gonadotropins, levels, decreased, 300 Gonococcal urethral stricture, retrograde urethrogram, 386f Gonorrhea, 385–386 Gout, 111–112 calcium, deposition, 113f imaging appearance, 112 joint effusion, severity, 112f periarticular swelling, 112f tophi deposits, effusion, 112f treatment, 112

INDEX Grading, 9 Grand mal epilepsy, 326 Granulation tissue, 4, 4t Graves’ disease, 368–369 Greenstick fractures, 132 Growth hormone, 364 levels, decreased, 300 Gynecomastia, 409 Gyri, 288

H Haemophilus influenzae, in meningitis, 290–291 Haemophilus influenzae type B (HiB), vaccine, inception, 44–45 Hampton’s hump, 69 Hands calcification in moderate-size vessels of, in diabetes mellitus, 379f dislocation/joint destruction, posteroanterior image, 101f frontal and oblique projections of, 424f interphalangeal joints, bony ankylosis, 97–98 in Turner’s syndrome, frontal projection, 427f Hangman’s fracture, 144 neural arch fracture/C2-C3 subluxation, 145f Hashimoto’s thyroiditis, 368 Haversian systems, 87 Head trauma, radiographic imaging purpose in, 309 Heart chambers, 248–249 conduction system, 249f deoxygenated venous blood, return, 250 diastole (relaxation phase), 250–251 enlarged, 252f PET scan, 30f right atrium of, ultrasound images, 17f SPECT images, 30f systole (contraction phase), 250–251 vascular anatomy, 249f Heart valves damage, rheumatic fever, 275 insufficiency, 275 malfunction, 275 narrowing (stenosis), 275 structure, 250f vegetations, 275 Heberden’s nodes, thickening, 98 Heel pad, thickening of, 365f Helical scanning (CT technology), 21 Helicobacter pylori infection, 170 Hematogenous metastases, 66f Hematogenous spread, 9 Hematoma, 5–6 Hematopoietic system, 336–353 radiographer notes, 336b Hemiparesis, 317 Hemiplegia, 317

Hemoglobin, 336–337 breakdown, 338 Hemolytic anemia, 338–341 extraskeletal abnormality, 339 imaging appearance, 338–339 treatment, 339–341 Hemophilia, 350 elbow, subchondral cysts, 351f imaging appearance, 350 intercondylar notch, widening, 352f treatment, 350 Hemorrhage, 5–6 Hemorrhoids, 195–197 imaging appearance, 196–197 rectal filling defects, 196f treatment, 196–197 Hemotympanum, fluid discharge, 309 Heparin, for thrombosis, 273 Hepatic arteries, 204f Hepatic carcinoma metastases, In-111 octreotide scan, 29f Hepatic metastases, 205 CT scan, 205f imaging appearance, 205 treatment, 205 Hepatitis, 201 Hepatitis A virus (HAV), 201 Hepatitis B virus (HBV), 201, 201f Hepatitis C virus (HBC), 201 Hepatitis E virus, 201 Hepatocellular carcinoma, 203–204 CT scan, 204f imaging appearance, 203–204 treatment, 204 Hereditary bone diseases, findings (summary), 93t–94t Hereditary diseases, 9–10, 43–44, 218–222, 426–431 findings, summary, 222t, 428t number/size, anomalies, 218–219 rotation/position/fusion, anomalies, 219–220 terms, summary, 11t treatment of, 221 Hereditary disorders, findings (summary), 44t Herniation, intervertebral disks, 144–146 imaging appearance, 145–146 treatment, 146 Herpesvirus, 160 Heterozygous trait, 10 Hiatal hernia, 165–166 air-fluid level, lateral chest radiograph, 166f imaging appearance, 165–166 lower quadrant pain, CT scan, 165f sac, ulcer, 159f treatment, 166 High blood pressure (hypertension), 263 definition, 263 prolongation, 264

457

High-output cardiac failure, development, 369 Hilar lymph node calcification, popcorn radiographic appearance, 52 Hilum, unilateral enlargement, 64 Hip calcific debris, 384f dislocations, 142f dysplasia, 95f osteoarthritis, 99f Hippocampal sclerosis (mesial temporal sclerosis), 326 Histoplasmoma, 52 central calcification, 52f Histoplasmosis, 52 diffuse calcifications, 52f Homocystinuria, 428–429 imaging appearance, 429 spine, osteoporosis, 429f treatment, 429 Homozygous trait, 10 Horizontal partial-thickness tear, 103f Hormones, 354 chemicals, power, 355 hyperactive production, 354 hypoactive production, 354 Horseshoe kidney, 219–220 nephrogram/calyceal filling, 221f Hot thyroid nodules, 368 Human immunodeficiency virus (HIV), 12 Humerus expansile lesion of, 117f osteolytic metastasis to, 130f Huntington’s disease, 328–329 CT scan, 329f imaging appearance, 328–329 treatment, 328–329 Hyaline membrane disease (idiopathic respiratory distress syndrome), 44 imaging appearance, 44, 44f lungs, progressive underaeration, 44 treatment, 44 Hydatidiform mole, longitudinal sonogram, 417f Hydrocephalus, 330–332 aqueduct, obstruction, 331f communicating, 331 foramen of Monro, obstruction, 330f fourth ventricle outlet, obstruction, 331f imaging appearance, 331–332 noncommunicating (obstructive), 330–331 normal-pressure, 331 treatment, 332 Hydronephrosis distinguishing Wilms’ tumor from, ultrasound in, 240 excretory urogram, 235f longitudinal ultrasound images, 235f pelvicalyceal system, dilatation, 234f physiologic form, 234

458

INDEX

Hydrosalpinx, 396 fallopian tubes, unilateral/bilateral gross dilatation, 398f Hydroureter, 231 Hyperechoic, echo intensity, 17, 18f Hyperglycemia, 378 Hypernephroma (renal cell carcinoma), 237–238 Hyperparathyroidism, 374–377 brown tumors, production, 375f distal clavicle, erosion, 374f imaging appearance, 374–377 lumbar spine, lateral projection, 375f primary hyperparathyroidism, 374 salt-and-pepper skull, 375f secondary hyperparathyroidism, 374 subperiosteal bone resorption, 374f tertiary hyperparathyroidism, 374 treatment, 377 tumoral calcification, 376f Hyperpituitarism, 364–366 imaging appearance, 364–366 treatment, 366 Hyperplasia, 7 Hypertension (high blood pressure), 263–265 imaging appearance, 263–265 renovascular, 264f secondary hypertension, 263 treatment, 264–265 Hypertensive heart disease, 265–266 ascending aorta, generalized tortuosity/ elongation, 266f chest, lateral projection, 265f imaging appearance, 265–266 treatment, 266 Hyperthyroidism, 368–369 imaging appearance, 369 radioactive iodine scans, 370f treatment, 369 Hypertrophic pyloric stenosis, longitudinal sonogram, 171f Hypertrophic spurring, 146f Hypertrophy, 7 Hypervitaminosis, 421–422 imaging appearance, 421–422 shoulder joints, calcification, 422f treatment, 422 Hypoadrenalism, 357 Hypoechoic, echo intensity, 17, 18f Hypoglycemic shock (insulin shock), 379 Hypoparathyroidism, 377–378 imaging appearance, 377–378 primary hypoparathyroidism, 377–378 skull, frontal projection, 377f treatment, 378 Hypopituitarism, 366 Hypoplastic kidney, 219 Hypothalamus, 289–290 Hypothyroidism, 369–370 Hypoxemia, ARDS, 73 Hysterectomy, involvement, 406 Hysterosalpingogram, 397f

I Iatrogenic disease, 2 Iatrogenic pneumoperitoneum, 212 Idiopathic atrophy, 357 Idiopathic disease, 2 Idiopathic respiratory distress syndrome (IRDS), 44 Ileocecal valve, intussusception, 182 Imaging integrated, 31–33 perfusion, 26–27 Imaging descriptors, summary of, 16t Imaging features, 16 Immune, term (usage), 11 Immune response, suppression, 2b Immunity disorders, 11 terms, summary, 12t Incomplete fracture, 131 Incontinence, 217–218 Infancy, rickets (system disease), 110 Infantile cortical hyperostosis (Caffey’s disease), 7f Infantile hypertrophic pyloric stenosis (IHPS), occurrence, 170 Infantile polycystic kidney disease, excretory urogram, 238f Infants, mediastinal emphysema, 75f Infarct, 5 Infarction, 5 Infectious arthritis, 98–100 imaging appearance, 99–100 Infectious disease exposure, 11 Infectious disorders, 95–106, 107t Infectious gastritis, diagnosis, 170 Infectious hepatitis. see Hepatitis A virus (HAV). Infectious mononucleosis, 349 chest, frontal/lateral projections, 350f imaging appearance, 349 treatment, 349 Infective endocarditis, 278–280 echocardiogram, 279f imaging appearance, 278–280 treatment, 280 Infiltrating cancer, progression, 162 Infiltrating glioma, T2-weighted MR image, 298f Inflammation, 3–4, 4t Inflammatory disorders, 95–106, 107t, 224–227 findings, summary, 228t Inflammatory process, summary of terms for, 4t Inflammatory response, events in, 4b Injuries, healing, 4 Insulin shock (hypoglycemic shock), 379 Insulinoma, 209 Integration, in imaging, 16, 16t Internal bony callus, formation of, 134f Internal carotid artery, ulceration, 320f Interphalangeal joints, bony ankylosis, 97–98

Interstitial pneumonia, 46–47 diffuse peribronchial infiltrate, 47f imaging appearance, 46 treatment, 47 Intervertebral disks central bulging, CT scan, 147f herniation, 144–146 imaging appearance, 145–146 MR image, 148f treatment, 146 space, narrowing, 146f Intraarticular components, treatment, 103 Intrabronchial foreign bodies, 74 imaging appearance, 74 nail, presence, 74f treatment, 74 Intracerebral brainstem hematoma, 322f Intracerebral hematoma, 313 imaging appearance, 313 lateral ventricles, acute bleeding, 313f noncontrast CT scan, 321f treatment, 313 Intracranial hemorrhage, 317 Intramembranous ossification, 87 Intramural fistula, 190f Intraparenchymal hemorrhage, 320–321 Intrathoracic kidney, 219 image, 220f Intravenous contrast agent (gadolinium), usage, 25 Intrinsic asthma, 56 Intrinsic rhythm, of pacemaker cells in SA node, 250–251 Intussusception, 181–182 colon, obstruction, 182f doughnut-shaped lesion, ultrasound image, 183f imaging appearance, 182 reduction, rectal insufflation, 182 treatment, 182 Iodinated contrast material, intravenous injection, 20 Ionizing radiation, 15–16 IRDS. see Idiopathic respiratory distress syndrome (IRDS). Iron deficiency anemia, 337 Irritable bowel syndrome, 191 Ischemia, 5 Ischemic colitis, 191 imaging appearance, 191 soft tissue polypoid densities, 191f treatment, 191 Ischemic heart disease, frontal projection of chest, 258f Ischemic necrosis, bone, 116–119, 118t Isoechoic, echogenicity, 17 Ivory vertebra, 389–390 lymphoma, 347f Ivory vertebral body, 130 diffuse sclerosis, 130f

INDEX

J Jaundice (development), cirrhosis, 202 Jefferson fractures, 143 frontal projection, CT scan, 144f Joint fragmentation, 384f Joint hemorrhages, repetition, 350 Joint space destruction, 100f Jones fracture, 140 fifth metatarsal, base, 141f Juvenile-onset diabetes, 378 Juxta-articular osteoporosis, 99–100 Juxtaglomerular apparatus, 218

K Kaposi’s sarcoma, 12 alimentary tract dissemination, 12 small bowel study, 12f Kidney stones, 228 formation, 229–231 imaging appearance, 228–231 preventive measures, 231 treatment, 231 Kidneys complete fusion of, 219–220 excretory phase of, 23f function, deterioration, 243 hypoplastic, with compensatory hypertrophy, 219f importance, 218 internal structure, 218f intrathoracic, image, 219, 220f left, malrotation, 220f renal cysts, unifocal masses, 234 right-sided pelvic, 220f solitary, excretory urogram/aortogram, 219f urinary system component, 216 venous occlusion, 243 Klinefelter’s syndrome, 427 Knees menisci, tears, 103 multiple lytic lesions, brown tumors, 375f osteoarthritis, 99f Paget’s disease, 115f sagittal MR image, 103f Kwashiorkor (protein-calorie malnutrition), 422 Kyphotic angulation, 106

L L4 vertebral body, diffuse sclerosis of, 130f L5-S1 level, disk herniation, CT scan, 147f Large bowel, distention, 181f Large bowel obstruction, 193 annular carcinoma, 195f cecum, dilatation, 193f gas pattern, upper/lower abdominal radiographs, 194f imaging appearance, 193 treatment, 195 Large intestine, divisions of, 155f

Laryngeal edema, 11 Le Fort fractures, severity, 315 Le Fort II fracture, 317f Lead lines, 116f Lead-pipe colon (chronic ulcerative colitis), 189f Lead poisoning, 114–115, 118t imaging appearance, 115 treatment, 115 Left arm, battered-child syndrome (frontal radiograph), 138f Left atrial calcification, mitral stenosis, 276f Left kidney malrotation, 220f parenchyma, multiple deposits, 231f sagittal ultrasound image, 237f Left main coronary artery, posteroanterior cranial projection, 259f Left posterior rib fracture, CT scan, 78f Left renal artery, acute embolic occlusion, 273f Left renal pelvis, nephrostomy tube placement in, 230f Left renal vein invasion, renal cell carcinoma, 240f Left-sided heart failure cardiac enlargement, radiographic appearance, 260–261 diffuse perihilar alveolar densities, demonstration, 261f Left sylvian fissure, subarachnoid enhancement, 291f Left-to-right shunts, 252–254 Left ureter, contrast extravasation, 229f Leukemia, 342–344 Leukocytes (white blood cells), 336, 337f migration, 3–4 Linear skull fracture, 309–310 Lingular collapse, 74f Lipomas, 8 Liver, 201–205 cells, metabolism role, 155–156 cirrhosis, 202–203 fatty infiltration, CT scan, 202f imaging appearance, 202–203 treatment, 202–203 findings, summary, 205t marginated infrahepatic mass in, T1-weighted coronal MR image, 243f responsibility, 153–155 three-phase CT scanning, 204f transverse image, 25f Localized ileus, 180–181 Location, in imaging, 16, 16t Loculated pleural fluid (phantom tumors), frontal chest radiograph, 263f Long bone, 88f aneurysmal bone cyst, presence, 122 Paget’s disease, destructive phase, 113 Longitudinal spinal ligaments (poker spine), ossification, 96

459

Loop of Henle, 217 Lou Gehrig’s disease (Amyotrophic lateral sclerosis), 330 Low-grade brain tumor, PET cerebral study (three-dimensional reconstruction), 297f Lower abdomen, CT scan, 20f Lower abdominal aorta, calcification in the walls of aneurysms of, 266f Lower cervical portion, fish bone, 167f Lower leg demineralized bones of, 426f external fixation, 133f Lower lumbar spine lateral view, 149f plain lateral radiograph, 148–149 Lower respiratory system, inflammatory disorders, 45–54 findings, summary, 48t Lower tibial shaft, expansile lesion, 351f Lumbar disk CT scan, 146f herniation MR image, 147f myelogram, 146f Lumbar spine frontal projection of, 430f lateral projection of, 375f vertebral fusion, 97f Lumen finger-like projections, 241 gas in, 200f Luminal obstruction, carcinoma, 162 Lung abscess, 48–49 bacterial pneumonia, 48f imaging appearance, 48–49 multiloculated capsule, CT scan, 48f treatment, 48–49 Lungs air passage, blockage, 43 apices, 49f diffuse alveolar pattern, 262f diffuse bilateral symmetric infiltration, 262f diffuse calcifications in, 52f disorders, 72–76 findings (summary), 76t high-resolution CT scan, 21f illustration, 39f interstitial spaces of, transudation of fluid into, 261–262 metastases to, 371 vital gas exchange, 39 Luteinizing hormone (LH), 364 Lye, ingestion (corrosive stricture), 162f Lymphadenopathy, CT scan, 193f Lymphangitic metastases, bronchovascular markings (coarsening), 68f Lymphatic leukemia, 342 Lymphatic spread, 9 Lymphocytes, representation, 337 Lymphography, 346–348

460

INDEX

Lymphoma, 344–348 chest image, 345f CT scan, 348f diffuse reticular/reticulonodular changes, 345f imaging appearance, 344–348 ivory vertebra, 347f manifestation, 346f nodal uptake, gallium scanning, 348 right kidney, lymphomatous mass replacement, 347f skeletal involvement, 347f staging, 346–348 stomach, 346f supraclavicular adenopathy, history, 348f treatment, 348

M Magnetic resonance angiography (MRA), 25 image, 27f intravenous contrast agent (gadolinium), 25 Magnetic resonance imaging (MRI), 12–13, 24–28 advantages, 24–25 brain image, 26f diffusion imaging, 25–26 disadvantage, 25 fat suppression, 26–27 functional MRI (fMRI), 27 importance, 24 patient claustrophobia, 25 perfusion imaging, 26–27 physics, 24 pulse sequence, scanning parameters, 24 radio frequency (RF) pulse, 24 receiver coil, 24 relaxation, 24 sagittal lumbar spine image, 26f summary of, 27t T1-weighted images, 24 T2-weighted images, 24 upper abdomen image, 25f Magnetic resonance spectroscopy (MRS), 25 Malabsorption, sprue, 184f Malabsorption disorder, 182 Male fertility, 387 Male reproductive system, 386–387, 387f diseases, findings, summary, 394t physiology, 386–387 Malignant bone tumors, 124–127 neoplasia, findings (summary), 127t–128t treatment, 127 Malignant gastric ulcer, transition (abruptness), 173f Malignant neoplasms, 7 Malignant solitary pulmonary nodule (bronchogenic carcinoma), 62f CT scan, 63f Malignant teratoma, transverse testicular scan, 395f

Malignant tumor, grading, 9 Mallory-Weiss syndrome, 168 Mammography, 16–17, 17t magnification-spot compression, 410f Mandibular fractures, 315 panoramic examination, 317f Marfan’s syndrome, 427–428 arachnodactyly, 428f arteriogram, 428f imaging appearance, 427 treatment, 428 Marrow hyperplasia, 342 neoplastic cells, proliferation, 343 Master gland. see Pituitary gland. Mastication, digestion, 153 Mastoid process, ecchymosis, 309 Maximum intensity projections (MIPs), CT postprocessing, 21 Mechanical small bowel obstruction, 178 Meconium ileus, bowel distention, 43f Mediastinal emphysema (pneumomediastinum), 75 imaging appearance, 75 infants, 75f lateral displacement, 75f treatment, 75–76 Mediastinal masses, 80–82 configuration, 80 findings, summary, 81t plain chest radiographs, 80 treatment, 80–82 Medulla, 289, 289f Medullary carcinoma, 372 Medullary cavity (marrow), 87 Medulloblastomas, 296 Megaloblastic anemia, 341 chronic atrophic gastritis, 341f imaging appearance, 341 treatment, 341 Melanoma, 424–425 Membranous bone formation, autosomal dominant condition, 92 Menarche, 394 Meningeal vessel, dilatation, 299 Meninges, 290, 290f Meningioma, 299 CT scan, 301f imaging appearance, 299 MRI, 300f parietal meningioma, plain skull image, 301f spinal meningioma, anteroposterior/ lateral myelogram, 302f treatment, 299 Meningitis, 290–291 bacterial meningitis, 290–291 imaging appearance, 291 subarachnoid enhancement, 291f treatment, 291 viral meningitis, 290–291 Meningocele, 89

Meningomyelocele, 90f Meniscal tear, 103f Menopause, 396 Menorrhagia, 337 Menstrual cycle, 395–396 Menstruation menstrual phase, 396 proliferative phase (postmenstrual phase), 396 secretory phase (postovulatory phase), 396 Mental deterioration, 309 Mercedes-Benz sign, fissuring, 198f Metabolic bone disease, 108–115, 115t Metabolism, maintenance, 217 Metacarpal sign, 427 Metaphysis, 87 Metastases, brain axial T2-weighted/FLAIR MR image, 307f CT scan, 307f–308f Metastatic carcinoma, 307–309 Metastatic melanoma, small bowel (filling defects), 425f Metastatic testicular seminoma, CT scan, 395f Metastatic thyroid carcinoma, 66f Microcephaly, 429 Micturate, 217–218 Midbrain, 289, 289f Middle mediastinal mass, chest projections, 81f Miliary tuberculosis, 50 nodules, presence, 50f Mineralocorticoids, salt/water balance, 355 Minimum intensity projections (MinIPs), CT postprocessing, 21 Mitral insufficiency, 276–277 chest, frontal/lateral projections, 277f Mitral stenosis, 275–276 chest, frontal/lateral projections, 276f echocardiogram, 277f imaging appearance, 276 left atrial calcification, 276f treatment, 277 Mitral valve (bicuspid valve), 248–249 prosthetic replacement, 275f Monocytes, 337 Monteggia fractures, 139–140 anterioposterior/lateral projection, 141f Morbidity, 9 Mortality, 9 MRA. see Magnetic resonance angiography (MRA). MRI. see Magnetic resonance imaging (MRI). MRS. see Magnetic resonance spectroscopy (MRS). Mucormycosis homogeneous mass, fungus ball, 380f infection, 380 roof of right orbit, destruction of, 333f

INDEX Mucoviscidosis (cystic fibrosis), 43 Mucus, production (excess), 54 Multiloculated capsule, CT scan, 48f Multinodular goiter radioactive iodine scan, 371f ultrasound image, 371f Multiplanar body imaging, PET scan with, 30f Multiple myeloma, 126–127 bone formation, absence, 127 diffuse infiltration, 127f imaging appearance, 126–127, 126f malignancy, dissemination, 126 osteolytic lesions, 126f PET oncologic survey findings, 128f Multiple pregnancies, endovaginal sonogram, 415f Multiple sclerosis, 324–325 axial T2-weighted MR image, 325f findings, summary, 326t imaging appearance, 324–325 treatment, 325 Munchausen syndrome by proxy, 137 Muscular dystrophy, 425 imaging appearance, 425–426 lower leg, demineralized bones of, 426f treatment, 426 Mutations, 10 Mycobacterium tuberculosis, 49 Myelin sheath, 287 Myelocytic leukemia, 342 Myelomeningocele, 89 Myelophthisic anemia, 341–342 Myocardial infarction, 256–257 Myocardial stress/rest perfusion single-photon emission computed tomography scan, 257f Myocardium (perforation), intravenous electrode, 42 Myomas, 8

N Napkin-ring carcinoma (annular carcinoma/apple-core carcinoma), 192 Nasal bone fractures, 314 Navicular fractures (scaphoid fractures), 137–138 avascular necrosis, 140f detection, absence, 139f nonunion, complication, 138 Neck anteroposterior perspective, 320f of fifth metacarpal, fracture at, with volar angulation of distal fragment, 140f lateral projection of, 372f Necrotic debris, removal, 4 Necrotic process, 226 Necrotic renal cell carcinoma, CT scan, 240f Negative feedback mechanism, 355 Neoplasia, 7–9 categories, 7

Neoplasms, 61–68 Neoplastic cells, proliferation, 343, 344f Neoplastic transformation, induced by DNA and RNA viruses, 8 Nephroblastoma (Wilms’ tumor), 240 imaging appearance, 240 treatment, 240 Nephrocalcinosis, 229 multiple deposits, 231f Nephrogenic diabetes insipidus, 367 Nephrostomy tube placement, 230f Nervous system, 286–335 physiology, 287 radiographer notes, 287b radiographic contrast material, administration, 287b radiographs, exposure factors, 287b Neural arch fracture, C2-C3 subluxation, 145f Neuroblastoma, 360–363 bone scan, 363f demonstration, nephrotomogram, 363f excretory urography, 360 imaging appearance, 361–363 metastatic to bone, 362f paravertebral stripes, bilateral widening, 363f treatment, 363 Neurologic patients, PET usage in, 31 Neuron, structure, 288f Neutrophils (polymorphonuclear leukocytes), 337 Newborn, hemolytic anemia (erythroblastosis fetalis), 338 Niacin deficiency (pellagra), 420 Non-Hodgkin’s lymphoma, CT scan, 349f Non-small cell carcinoma, multiplanar PET lung scan, 67f Noncommunicating (obstructive) hydrocephalus, 330–331 Noncontrast helical CT scanning, usage, 231 Noncontrast renal MRA, appearance, 264f Nonerosive gastritis (chronic atrophic gastritis), 170 Noninvasive imaging modality, 17 Nonopaque urate crystals, deposition, 112 Nonpituitary tumors, ACTH production, 356 Norepinephrine, secretion, 355 Normal aging, 327 axial MR image, 327f CT scan, 327f imaging appearance, 327 Normal-pressure hydrocephalus, 331 Nosocomial disease, 2 Nuclear magnetic resonance. see Magnetic resonance imaging (MRI). Nuclear medicine, 28 bone scan, 28f gamma camera, 28 radiopharmaceutical ingestion, 28 summary of, 29t

461

Nutritional deficiency, 419 Nutritional diseases, 419–423 findings, summary, 423t radiographer notes, 420b

O Oat cell carcinomas (small cell carcinomas), 63 Obesity, 422–423 imaging appearance, 422–423 retrogastric space, enlargement, 422f treatment, 423 Oblique fractures, 131–132 Obstructing ureteral calculus, 231f Obstructive (noncommunicating) hydrocephalus, 330–331 Occluded internal carotid artery, intravenous DSA, 320f Ochronosis, 429 lumbar spine, frontal projection, 430f Odontoid process, fractures, 143–144 open-mouth frontal projection, 144f Olecranon bursa, transverse scan, 101f Olecranon fossa, posterior fat pad (appearance), 138–139 Oligodendrocytomas, 296 Oligohydramnios, 414–415 Omental cake CT appearance, 398 metastases, 400f Oncology, 7 Open fractures (compound fractures), 131 Oral cholecystogram, 198f Orbital floor fracture, coronal CT scan, 315f Ossification (bone formation), 87 Osteitis deformans (Paget’s disease), 112–114 Osteoarthritis (degenerative joint disease), 98 imaging appearance, 98 joint space narrowing, 98 Osteoblastic metastases, 130f Osteoblasts, 87 Osteochondromas, 119–122 imaging appearance, 119 long axis, tumor (presence), 119f Osteoclasts, 87 Osteogenesis imperfecta (brittle bones), 91 anteroposterior/lateral projections, 93f imaging appearance, 91, 92f treatment, 91 Osteogenic sarcoma, 124–127 CT scan, 124f destructive lesion, 125f imaging appearance, 124 MRI, 124f Osteoid osteomas, 120–122 femur, mid shaft projections, 121f imaging appearance, 121–122 Osteolytic metastases, 129

462

INDEX

Osteomalacia, 109–110, 420–421 imaging appearance, 110 spongy bone, trabeculation (increase), 111f treatment, 111 Osteomas, 120 frontal sinus, 121f imaging appearance, 120 Osteomyelitis, 104, 104f changes, 104 radionuclide bone scan, 104f skull, 294–295 Osteopetrosis, 90–91 bones, sclerosis, 90f imaging appearance, 90–91 treatment, 91 Osteoporosis, 108–109 aging, 109f dual-energy x-ray absorptiometry (DEXA) bone densitometry, usage, 108 imaging appearance, 109 spine, DEXA BMD scan, 109f treatment, 109 Osteoporotic bone, mineral salts (loss), 108 Ottonello method, 86b–87b Ovarian carcinoma, recurrence (PET scan), 400f Ovarian cysts, 397–400 imaging appearance, 398–400 omental cake, CT appearance, 398 T2-weighted axial MR image, 399f treatment, 398–400 ultrasound image, 398f Ovarian tumors, 397–400 Ovaries cyclic changes, 395 cystadenocarcinoma, psammomatous calcifications, 399f primary cystadenocarcinoma, 398 Overriding aorta, spin-echo MRI demonstration, 254 Ovulation, 394 Oxytocin, production, 364

P Pacing failure, electrode failures, 42 Paget’s disease (osteitis deformans), 112–114 clinical complications, 113–114 imaging appearance, 113–114 knee, cortical thickening (appearance), 115f skull, nuclear medicine bone scan, 114f treatment, 114 Pancreas, 156, 206–210 cancer, 209 cure, 210 detection, 209 imaging appearance, 209–210 treatment, 210

Pancreas (Continued) carcinoma, noncontrast CT scan, 209f control, 156 findings, summary, 210t head, carcinoma, 209–210 transhepatic cholangiogram, 210f surgical resection (total pancreatectomy), 210 tissue, cytologic examination, 209 Whipple procedure, 210 Pancreatic adenocarcinoma, 209f Pancreatic calcifications, 207 Pancreatic pseudocyst, 208–209 calcified, 208f CT scan, 208f imaging appearance, 208–209 loculation, 208 pseudocysts, visibility, 208 treatment, 208–209 ultrasound examination, 208 ultrasound image, longitudinal sonogram, 208f Pansinusitis coronal CT scan, 333f mucormycosis, 333f Papanicolaou smear examination, 404 Papillary carcinoma, 371 Papillary destruction, early stage of, 226f Papillary necrosis, 226–227 generalized saccular/club-shaped configuration, 227f imaging appearance, 226 treatment, 226–227 Papilloma, 8 Parathormone (parathyroid hormone), 374 Parathyroid adenoma, technetium-99m sestamibi (injection), 376f Parathyroid glands, 374–378 diseases, 374–378 findings, summary, 378t physiology, 374 thyroid and, 368f Paravertebral tissues, ossification, 96 Parietal meningioma, plain skull image, 301f Parkinson’s disease, 329 Passive immunity, 11 Patent ductus arteriosus, 252–253 cardiomegaly, frontal chest radiograph, 253f Pathologic conditions, radiography, 2 Pathologic fractures, 132, 135–136, 136f CT/MRI, usage, 136 imaging appearance, 136 treatment, 136 Pathology, introduction to, 1–14 Pectus excavatum, lateral chest radiograph, 429f Pelken spur, 420 Pellagra (niacin deficiency), 420

Pelvic inflammatory disease, 385–386, 396–397 chronic, transverse sonogram, 397f imaging appearance, 396–397 suspicion, 386 treatment, 397 Pelvic kidney, 219 collecting system, 220f Pelvicalyceal system dilatation, 234f distortion/displacement, 241f Pelvis bladder calculi, plain radiograph, 232f contrast-enhanced MRA, 271f osteoblastic metastases, 130f Paget’s disease, sclerosis/cortical thickening, 114f Peptic ulcer disease, 171–174 complications, 171 treatment, 174 Percutaneous transluminal coronary angioplasty (PTCA), 260f Perfusion, in imaging, 16, 16t Periarticular demineralization, 108f Pericardial effusion, 280–281 cardiac silhouette, globular enlargement, 280f demonstration angiocardiography/intravenous carbon dioxide injection/ pericardial tap, usage, 280 CT scan, usage, 280f echocardiogram, 281f findings, summary, 280t imaging appearance, 280–281 MRI, transverse/sagittal images, 281f treatment, 281 Pericardium, 252 Periosteum, 87 Peripheral bronchial adenoma, nonspecific solitary pulmonary nodule, 65f Peripheral lung nodule, CT-guided FNAB, 65f Peripheral nervous system (PNS), 287 Peripherally inserted central catheter (PICC) line placement, 41f long-term venous access device, 41 Peristalsis (smooth muscle contractions), 153 Peristaltic contractions, sexual stimulation, 386–387 Peritoneal cavity, fluid accumulation (ascites), 202 Permeable membrane, 4t Pernicious anemia, 341 Personal protective equipment (PPE), usage, 11 Petit mal epilepsy, 326 Phagocytosis, 3–4 Phantom tumors (loculated pleural fluid), frontal chest radiograph, 263f

INDEX Phenylketonuria, 429 Pheochromocytoma, 360 axial MR image, 362f ectopic, 362f imaging appearance, 360 longitudinal/transverse, ultrasound images, 361f pear-shaped mass, 361f treatment, 360 Phlegmonous emphysematous gastritis, distal stomach (ulceration), 170f Phlegmonous gastritis (bacterial gastritis), 170 Photoelectric effect, 28 Physiologic map, nuclear medicine production, 28 Pia mater, 290 acute inflammation (meningitis), 290–291 Pica, ingestion, 116f Pineal germinoma, sagittal T1-weighted MR image, 305f Pineal teratoma, nonenhanced CT scan, 306f Pineal tumor, 305–306 Pituitary adenoma, 300 coronal CT scan, 304f imaging appearance, 301–303 sagittal/coronal T1-weighted contrast-enhanced MR image, 304f sella turcica (ballooning), 366f treatment, 303 Pituitary gland, 364–367 anterior lobe, hormones (secretion), 364 diseases, 364–367 findings, summary, 367t hormones, 365f physiology, 364 posterior lobe, hormones (production), 364 Pituitary tumor detection/defining, MRI, 301–302 diagnosis of, 365–366 Platelets (thrombocytes), 336, 337f diseases (bleeding disorders), 349–352 findings, summary, 352t Platelike atelectasis, 73f Pleura double-walled membrane, 39 illustration, 39f involvement, 345–346 Pleural disorders, 76–82 findings, summary, 79t Pleural effusion, 77–79, 78f chest, frontal projection, 79f chest radiograph appearance, 78 imaging appearance, 77–79 left posterior rib fracture, CT scan, 78f pleural thickening/fibrosis, 77–78 right lateral decubitus chest radiograph, 78f sharp angle blunting, 78f treatment, 79

Pleural space, CVP catheter placement, 41f Pneumoconiosis, 59–61 findings, summary, 61t Pneumocystis jirovecii pneumonia, 8 diffuse bilateral airspace, 13f Pneumomediastinum (mediastinal emphysema), 75 Pneumonia, 45–47 air bronchogram sign, 46f single lobe infiltrate, density increase (CT scan), 47f Pneumoperitoneum, 210–212 cause, 211–212 double-wall sign, 212f falciform ligament sign, 212f findings, summary, 212t gas accumulation, chest radiograph, 211f imaging appearance, 211–212 semierect projection, intraperitoneal gas, 211f treatment, 212 Pneumothorax, 76–77 frontal chest image, 77f imaging appearance, 76–77 treatment, 77 Poker spine (longitudinal spinal ligaments), ossification, 96 Polycystic kidney disease, 236–237 CT scan, 238f imaging appearance, 236–237 infantile polycystic kidney disease, excretory urogram, 238f left kidney sagittal ultrasound image, 237f multiple cysts (detection), CT scans (usage), 237 nephrogram phase, 237f treatment, 237 ultrasound demonstration, 236–237 Polycystic ovarian syndrome (PCOS), 397–398 Polycythemia, 342 Polycythemia vera (primary polycythemia), 342 Polydactyly, right foot (image), 10f Polydipsia, 367 liquid, drinking (excess), 378 Polyhydramnios, 414–415 amniotic fluid, accumulation (excess), 415f Polymorphonuclear leukocytes (neutrophils), 337 Polyp, 8 Polypoid mass, localization, 162 Polyuria, 367 urination, excess, 378 Pons, 289, 289f Porcelain gallbladder, 199–200 imaging appearance, 200 mural calcification, 200f treatment, 200 Portal veins, branches of, in MRI, 25f

463

Positron emission tomography, 29–31 annihilation, 29–30 brain image, 33f chemotherapy, effectiveness of, 31f heart image, 32f imaging, signal detection, 30–31 multiplanar body imaging, 30f myocardial viability, demonstrating, 32f radionuclides, 30 summary of imaging for, 31t usefulness, 31 Post-traumatic carotid-cavernous fistula, 314f Posterior mediastinal mass chest projections, 81f CT scan, 82f Posterior urethral valves, 222 treatment, 222 voiding cystourethrogram, 224f Pott’s disease, 106 Pott’s fracture, malleoli involvement, 140 Pregnancy, 414–416 ectopic, 395–396 findings, summary, 417t Primary hyperparathyroidism, 374 Primary hypoparathyroidism, 377–378 Primary liver cell carcinoma, occurrence, 203 Primary polycythemia (polycythemia vera), 342 hypoventilation, severity, 342f imaging appearance, 342 treatment, 342 Primary tuberculosis, 49–50 imaging appearance, 49–50 right hilar lymph nodes, enlargement, 50f right upper lobe, consolidation, 49f unilateral right tuberculous pleural effusion, 50f Probiotics, 182 Progesterone, secretion, 394–395 Prognosis, 2 Progressive fibrosis, histoplasmosis and, 52 Prolactin, 364 Prostate gland, 386 cancer, transrectal ultrasound image, 389f carcinoma, 388–389 axial MR image, 389f imaging appearance, 388 mass, elevation, 389f staging, 389–390 enlargement, excretory urography, 387–388 metastatic carcinoma CT scan, 390f T1-weighted spin-echo MR image, 390f Prosthetic aortic/mitral valves, 275f Protein-calorie malnutrition (kwashiorkor), 422

464

INDEX

Protrusio acetabuli, 111f Proximal convoluted tubule, water/ nutrients reabsorption, 216–217 Proximal femur, osteoblastic metastases, 130f Proximal humerus, diffuse lytic destruction, 340f, 384f Proximal ulna, displaced fracture, 141f Psammomatous calcifications, ovary cystadenocarcinoma, 399f Pseudocysts plain radiographs, 208 spontaneous resolution, 208–209 Pseudohypoparathyroidism, 378 Pseudokidney, 182 Pseudopseudohypoparathyroidism, 378 Psoriatic arthritis, 96–98 asymmetric bone destruction/ subluxation/ankylosis, 98f imaging appearance, 97–98 mutilating arthritis, 98f Pulmonary arteries, embolic occlusion (physiologic consequences), 68 Pulmonary arteriogram, 71f Pulmonary arteriovenous fistula, 72 imaging appearance, 72 right lung, radiographic image, 73f treatment, 72 Pulmonary capillary wedge (PCW) pressure, measurement, 41 Pulmonary edema, 261–263 butterfly pattern, 262f diffuse pulmonary edema, demonstration, 263f imaging appearance, 261–262 interstitial, 262f treatment, 262–263 Pulmonary embolism, 68–71 chest projections, 69f CT scan, 5f imaging appearance, 68–71 left main pulmonary artery, filling defect (CT scan), 71f plain chest radiograph, 69f pulmonary arteriogram, 71f radionuclide perfusion lung scan, 70f right pulmonary artery, filling defect, 71f treatment, 69–71 ventilation-perfusion ratio (V/Q) scan, screening effectiveness, 69 Pulmonary hypertension (Eisenmenger’s syndrome), 253 Pulmonary infections, recurrence, 56f Pulmonary metastases, 65–68 imaging appearance, 66–68 PET images, 64f solitary nodule, growth, 67f treatment, 68 Pulmonary mycosis, 52–53 findings, summary, 53t fungal infection, 52 Pulmonary neoplasms, findings (summary), 68t

Pulmonary neoplastic diseases, treatment of, 65 Pulmonary parenchyma, involvement, 345–346 Pulmonary stenosis, 254 Pulmonary stenosis (right ventricular outflow), spin-echo MRI demonstration, 254 Pulmonary trunk, enlargement, 252f Pulmonary valve, location, 248–249 Pulmonary vascular diseases, findings (summary), 72t Pulse sequence, 24 Purpura (thrombocytopenia), 350–352 Pus, pyogenic bacteria, 4 Pyelonephritis, 224–225 chronic pyelonephritis, 225f CT, usage, 225 imaging appearance, 225 treatment, 225 Pyloric stenosis, 170 Pyogenic bacteria, 4t presence, 4 Pyogenic brain abscess, CT scan, 292f Pyogenic organisms (pus-forming organisms), joint entry, 98–99 Pyosalpinx, 396

R Raccoon eyes (bilateral orbital ecchymoses), 309 Radio frequency (RF) pulse, 24 Radioactive iodine scan hyperfunctioning (hot) nodules, 369f nonfunctioning (cold) nodules, 369f normal, 368f Radioactive iodine scanning, 367–368 Radionuclide bone scan MRI, comparison with, 117 screening, 129f sensitivity, 117 triple-phase technique, usage, 137 Radionuclide cholescintigram, results, 199 Radionuclide subtraction imaging, 377f Radiopharmaceuticals, 28 usage, increase, 131 Rat bite erosions, examples, 113f Reactivation tuberculosis (secondary tuberculosis), 50–51 Reactive sclerosis, 146f Recessive genes, 10 Recombinant human deoxyribonuclease (DNase), inhalation, 43 Rectal carcinoma, 192f CT scan, 192f Red blood cells (erythrocytes), 336, 337f bulging, 339 diseases, 337–342 findings, summary, 343t Reduced penetrance, 10 Reflex arc, 287

Reflux (gastroesophageal reflux disease), 158–159 Reflux esophagitis development, 159 long esophageal stricture, 160f ulcer, penetration, 159f Regional enteritis (Crohn’s disease), 176–177 Reiter’s syndrome, 96–98 bony erosion, 97f imaging appearance, 96–97 metatarsophalangeal joint, erosive changes, 97f Relaxation, 24 Releasing hormones, secretion, 289–290 Renal abnormalities, 339 Renal carcinoma, 237–240 imaging appearance, 238–240 treatment, 240 Renal cell carcinoma (hypernephroma), 237–238 distortion/displacement, 238f left renal vein invasion, CT scan, 240f nephrotomogram, 239f sagittal T1-weighted MR image, 241f ultrasound image, 239f Renal congenital anomalies, 221 Renal cyst, 234–236 anechoic lesion, 235f appearance, nonenhancing left renal mass, 236f imaging appearance, 234–236 nephrotomogram, 235f puncture, contrast material (instillation), 236f treatment, 236 ultrasound, 235–236 unifocal masses, 234 Renal disease, complication, 380 Renal disorders, findings (summary), 246t Renal dysfunction, occurrence, 112 Renal failure acute, 243–245 chronic, 245–246 Renal parenchyma (isthmus), 219–220 Renal pelvis anomalies, 220–221 staghorn calculi, 230f ureters, relationship, 222f Renal vein thrombosis, 242–243 acute renal vein thrombosis, right kidney (radiograph), 244f imaging appearance, 242–243 occurrence, 242 renal venogram, 245f treatment, 243 Renovascular hypertension, 264f fibromuscular dysplasia, 264 string-of-beads pattern, 264f PTA for, 265f Renovascular lesion, presence of, 264 Repetition time (TR), 24

INDEX Reproductive system, 383–418 infectious diseases, findings (summary), 385t radiographer notes, 384b Resorption (bone destruction), 87 Respiration cellular process, 420 control, 39 Respiratory syncytial virus (RSV), 53 bilateral pulmonary infiltrates, 54f imaging appearance, 53 treatment, 53 Respiratory system, 36–84 endotracheal tube, 40 internal devices, 40–42 physiology of, 38 radiographer notes, 37b relative attenuation, 3b role of, 38 structure plan of, 38f Respiratory tract, fistulization, 157 Rh-positive newborn, hemolytic anemia of, 11 Rheumatic heart disease, 275 Rheumatoid arthritis, 95–96 atlantoaxial joint, subluxation, 96f hand, posteroanterior image, 101f imaging appearance, 95–96 ligamentous involvement, 96 mutilation, 95f periarticular osteoporosis, 95f radiographic evidence, 95 Rheumatoid nodules, soft tissue masses, 96 Rheumatoid variants, 96–98 Rickets (vitamin D deficiency), 110–111, 420–421 imaging appearance, 110–111 treatment, 111 wrist, metaphyseal ends (cupping/ fraying), 111f Right arm, battered-child syndrome (frontal radiograph), 138f Right atrioventricular valve (tricuspid valve), 248–249 Right external iliac artery stenosis, PTA, 272f Right foot, metatarsals/digits (polydactyly), 10f Right hemidiaphragm eventration, 83f paralysis, 82f Right hip, dysplasia, 95f Right internal jugular vein, CVP catheter in, 40f Right kidney, lymphomatous mass replacement, 347f Right lower lung, coned view, 55f Right middle cerebral artery infarct, diffusion-weighted MR image, 319f Right middle lobe, collapse, 74f Right sentinel lymph node, SPECT/CT fusion imaging, 412f

Right-sided heart failure, 261 chest, front/lateral projections, 261f Right-sided pelvic kidney, bone scan, 220f Right-to-left shunting, 254 Right ventricular hypertrophy, spin-echo MRI demonstration, 254 Ring-enhancing lesions, computed tomography, 13f Rotator cuff tears, 102–103 MR image, 102f shoulder arthrography, 102f Rubor (redness), acute inflammation clinical sign, 4 Rugal folds, thickening, 170f Ruptured berry aneurysm, 324f Ruptured silicone breast implants, mammogram, 410f

S Saccular aneurysm, 266 Sacroiliac joints, bilateral symmetric obliteration, 96f Sagittal lumbar spine, MRI of, 26f Salmonella infection, 339 Salt-and-pepper skull, 375f Salt maintenance, electrolyte/acid-base balance, 217 Sarcoidosis, 57–59, 58f chest projections, 58f diffuse coarse interstitial pattern, 58f end-stage disease, 59f high-resolution CT (HRCT), 57–58 imaging appearance, 57–59 treatment, 59 Sarcomas, 8 Scaphoid fractures (navicular fractures), 137–138 internal fixation, 133f Scintigraphic image, 28 Sclerosis, 384f Scoliosis, 147 anteroposterior spine image, curvature measurements, 148f imaging appearance, 147 treatment, 147 Scotty dog sign, diagram, 149f Screening radionuclide bone scan, 129f Scurvy (vitamin C deficiency), 420 frontal projections, 421f imaging appearance, 420 white line, 421f Wimberger’s sign, 420 Seat belt fracture, 144 CT scan, 146f Secondary hyperparathyroidism, 374 Secondary polycythemia, 342 Secondary tuberculosis (reactivation tuberculosis), 50–51 bilateral fibrocalcific changes, 51f imaging appearance, 51 Seeding, 9 Segmental fractures, 132

465

Seizure disorder, hippocampal sclerosis, 326f Sella turcica ballooning, 366f enlargement, plain skull radiographs, 302 imaging, tomography/CT, 356 Seminal vesicle, 386 Seminoma, hypoechoic intratesticular mass, 393f Septic embolism, 71–72 imaging appearance, 71–72 treatment, 72 Septic pulmonary emboli, cavitary lesions, 72f Serum hepatitis. see Hepatitis B virus (HBV). Severe acute respiratory syndrome (SARS), 53–54 imaging appearance, 54 treatment, 54 Sex hormones (androgens), 355 Sex-linked disorders, 10 Shaded surface rendering, CT postprocessing, 21 Shaken-baby syndrome, 137 Shaking palsy (Parkinson’s disease), 329 Shape, in imaging, 16, 16t Shoulder arthrography, 102f dislocation, 140 anterior/posterior dislocation, 142f Sickle cell anemia, 338 acute osteomyelitis, 340f biconcave indentations, 340f complication, acute osteomyelitis, 339 femoral head, aseptic necrosis, 340f intervertebral disks, expansile pressure, 339 red blood cells, bulging, 339 Sigmoid colon, annular carcinoma, 192f Sigmoid diverticulitis, 187f Sigmoid volvulus, 194–195 imaging appearance, 195 luminal tapering, 196f Signs, characteristics, 2 Silicone breast implants, ruptured (mammogram), 410f Silicosis, 59–60 chest tomogram, 60f imaging appearance, 60 miliary nodules, calcification, 60f progressive massive fibrosis, 60f Simple bone cysts, 122 imaging appearance, 122 proximal humerus, oval configuration, 122f Single-photon emission computed tomography, 28–29 brain images, 29f disadvantage, 28–29 heart image, 30f Sinoatrial (SA) node, impulse passage, 250–251

466

INDEX

Sinusitis, 332–334 acute, mucosal thickening, 332f chronic, mucosal thickening, 332f imaging appearance, 332–334 treatment, 334 Sixth-generation scanners, slice performance, 21 Size, in imaging, 16, 16t Skeletal lymphoma, right shoulder radiograph/T1-weighted axial MR image, 347f Skeletal metastases, detection, 129 Skeletal system, 85–151 bone radiographs, contrast requirement, 86b–87b middle kVp ranges, usage, 86b–87b pathologic conditions, 86b–87b physiology of, 87 radiographer notes, 86b–87b syphilitic involvement, 384 tomography, requirement, 86b–87b x-ray attenuation, 3b Skull, 294–295 depression, 309 hair-on-end appearance, 338f ossification, 91 osteomyelitis, 294–295 blastomycosis, 295f imaging appearance, 294–295 treatment, 294–295 Paget’s disease, 114f traumatic processes, 309–315 findings, summary, 316t Skull fracture, 309–311 CT bone-window image, 310f imaging appearance, 309–311 lateral projection, 310f treatment, 311 Small bowel, 176–182 diffuse dilatation, 184f findings, summary, 183t folds, thickening (irregularity), 184f Small bowel obstruction, 177–180 CT diagnosis, 180f CT scans, 180f dilated loops, 179f gas-filled bowel, dilated loops, 179f imaging appearance, 177–180 impacted bezoar, barium upper gastrointestinal series, 179f site, 178 supine/upright projections, 178f treatment, 180 Small cell carcinomas (oat cell carcinomas), 63 Smooth muscle contractions (peristalsis), 153 Soft tissue calcification, 375 relative attenuation, 3b Soft tissue polypoid densities, 191f Solitary kidney, excretory urogram/ aortogram, 219f

Solitary metastases, 66–68 examination, 67f Solitary pulmonary nodule, 61–63 CT scan, 62–63 imaging appearance, 61–63 Somatic nervous system, function, 287 Specialized imaging techniques, 15–35 radiographer notes, 16b Sperm, formation (spermatogenesis), 386 Spherocytosis, 338 Spiculated lesion, 410f Spina bifida, 89–90 imaging appearance, 89–90 occulta, 89f treatment, 89–90 Spinal cord, location, 290 Spinal disorders, findings, summary, 149t Spinal meningioma anteroposterior/lateral myelogram, 302f demonstration, 299 Spine DEXA BMD scan, 109f dislocations, 141–144 stable/unstable injury, 141–142 fractures, 141–144 stable/unstable injury, 141–142 frontal projection, 143 Spiral fractures, 131–132 Spiral scanning (CT technology), 21 Spleen, 212–214 enlargement, 212–213 imaging appearance, 212–213 lymphoma, 213f rupture, 213–214 imaging appearance, 213–214 Splenectomy, for spherocytosis, 339 Splenic disorders findings, summary, 214t treatment, 213–214 Splenomegaly, CT scan, 213f Spondylolisthesis, 148–149 imaging appearance, 148–149 lower lumbar spine, lateral view, 149f treatment, 149 Spondylolysis, 148–149 diagnosis, 149 imaging appearance, 148–149 lumbar spine, oblique projection, 149f Scotty dog sign, diagram, 149f treatment, 149 Spontaneous pneumothorax, 76f Squamous carcinoma, 65 Squamous cell carcinoma, 8 Staghorn calculi, spiral CT scan, 230f Staging, 9 Standard Precautions (CDC), 11 Staphylococcal osteomyelitis, 105f Steatorrhea, 182 Stenosis, luminal tapering, 196f Stereotaxic needle biopsy, 413f Stomach, 155f, 170–176 cancer, 174–176 imaging appearance, 174–176

Stomach (Continued) treatment, 175–176 fat planes, obliteration, 175 findings, summary, 175t lymphoma, 346f Stress fractures (fatigue fractures), 136–137 imaging appearance, 136–137 radionuclide bone scan, triple-phase technique, usage, 137 third metatarsal, 136f tibial, 137f treatment, 137 Stroke syndrome, 317–319 imaging appearance, 317–319 treatment, 319 Structure, in imaging, 16, 16t Subarachnoid hemorrhage, 313, 321–322 Subarachnoid (SA) space enhancement, axial projection, 22f fluid circulation, 290 nonionic contrast agent, injection, 22f Subclavian region, central catheter (usage), 40 Subcutaneous emphysema, 75 frontal chest radiograph, 76f imaging appearance, 75 treatment, 75–76 Subdural empyema, 293 imaging appearance, 293 T2-weighted MR image, 293f treatment, 294 Subdural hematoma, 311–312 imaging appearance, 311–312 Submucosal bleeding, 350 Subperiosteal hemorrhage, occurrence, 420 Subsecond scanning, 21 Sudden infant death syndrome, 137 Sulci, 288 Superficial gastric erosions, 173–174 gastritis, presence, 174f Supernumerary kidney, 219 Supraspinatus tendon, low signal intensity, 102f Surfactant, components, 44 Suspected non-accidental trauma (SNAT), 137 Swallowing deglutition, complexity, 153 difficulty (dysphagia), 161–162 Swan-Ganz catheters, 41 complication, 41 internal devices, findings (summary), 42t position, 41 Symptoms, characteristics, 2 Synapse, 287 Syndrome, 2 indication, 426 Synovial membrane, inflammation of, 95 Syphilis, 383–385 congenital syphilis, 383 imaging appearance, 383–385 neuropathic joint disease, 384f primary stage, 383

INDEX Syphilis (Continued) secondary stage, 383 tertiary stage, 383 treatment, 385 Syphilitic aortitis, 384f Syphilitic lesions, 384–385 Syphilitic osteomyelitis, 384f Systemic arterial system, 251f Systemic circulation, 250 Systemic lupus erythematosus, 423–424 bilateral pleural effusions, 424f hand, frontal/oblique projections, 424f imaging appearance, 423–424 treatment, 424 Systemic manifestations, acute inflammation and, 4 Systole (contraction phase), 250–251

T T1-weighted images, 24 T2-weighted images, 24 TB. see Tuberculosis (TB). Technetium-99m-labeled bone scintigraphy, 28f Tension pneumothorax, 77f Teratomas, 305 dermoid cysts, 400 Terminal ileum/sigmoid colon, fistulization, 178f Tertiary hyperparathyroidism, 374 Testicular dysgenesis, 427 Testicular seminoma, T2-weighted MR image, 395f Testicular torsion, 391–392 arterial perfusion, diminished, 393f Doppler ultrasound image, 392f imaging appearance, 392 scrotal ultrasound, 392f treatment, 392 Testicular tumors, 393–394 imaging appearance, 393–394 treatment of, 394 types of, 393 Testosterone, 386 Tetralogy of Fallot, 254 imaging appearance, 254 plain chest radiograph, 254f treatment, 254 Thalamus, 289–290 Thalassemia, 338 extramedullary hematopoiesis, 339f lateral projection (skull), hair-on-end appearance, 338f medullary spaces, widening, 338f Thiamine deficiency (beriberi), 420 Third metatarsal, stress fracture, 136f Thoracentesis, procedure, 79 Thoracic vertebroplasty, demonstration, 110f Three-phase CT scanning protocol, 23f Thrombectomy catheter (AngioJet catheter), usage, 273 Thrombocytes (platelets), 336, 337f

Thrombosis, 271–274 Thrombus (intravascular clot development), 271 Thumbprinting, in ischemic colitis, 191 Thyroid adenoma, neck (lateral projection), 372f Thyroid carcinomas, 371–373 imaging appearance, 372–373 radioactive iodine scan, 372f Thyroid gland, 367–373 diseases, 367–373 findings, summary, 373t and parathyroid, 368f physiology, 367 Thyroid goiter, ultrasound image, 370f Thyroid tumors, treatment, 373 Thyroidectomy, 373 Thyrotropic hormone, levels, decreased, 300 Thyroxine, 367 Tibia aneurysmal bone cyst, 122f healed fracture in, 135f Tissue death (necrosis), 5 Tortuous aorta, frontal chest radiograph, 166f Torus fractures (buckle fractures), 132 Total pancreatectomy (surgical resection), 210 Toxic megacolon, ulcerative colitis, 188f Toxic multinodular goiter, 370–371 Toxoid, 11 Trabeculae, 87 Tracheobronchial tree, fistulous communications, 157 Tracheoesophageal fistula, 156–158 acquired type, 157–158 congenital type, 156–157 types of, findings for, 158t Traction diverticula, 163 esophagus, midthoracic portion, 164f Transducer, recording, 17 Transient ischemic attacks, 319–320 Transitional vertebrae, 89f Transmission-based precautions, 11 Transurethral resection (TUR), 388 Transvenous cardiac pacemakers, 42 internal devices, findings (summary), 42t Transverse colon, intramural fistula, 190f Transverse fractures, 131–132 Traumatic splenic rupture, CT scan, 213f Treponema pallidum, 383 Tricuspid valve (right atrioventricular valve), 248–249 Trigone, 217–218 Triiodothyronine (T3), 367 Tripod fracture, 315 orbital rim, interruption, 315f Trisomy disorders (trisomy 21), 426 Trophoblastic disease, 416 Tuberculoma, 51–52 benign solitary pulmonary nodule, 62f imaging appearance, 51 treatment, 51–52

467

Tuberculosis (TB), 49–52, 225–226 bladder, involvement, 226 findings, summary, 51t imaging appearance, 226 large cavities, air-fluid levels, 50f Mycobacterium tuberculosis, 49 papillary destruction, early stage, 226f treatment, 226 ureter, involvement, 226 ureteral tuberculosis, 227f Tuberculous arthritis imaging appearance, 99–100 joint space destruction, 100f Tuberculous autonephrectomy, plain image, 226f Tuberculous osteomyelitis, 106 imaging appearance, 106 midthoracic vertebrae, vertebral collapse/anterior wedging, 108f treatment, 106 Tubo-ovarian abscess, ultrasound image, 397f Tumors, 7, 234–242, 397–406. see also specific tumor extensiveness, staging, 9 findings, summary, 242t swelling, acute inflammation clinical sign, 4 Turner’s syndrome, 427 hand, frontal projection, 427f imaging appearance, 427 treatment, 427

U Ulcer hiatal hernia sac, 159f treatment of, 174 Ulcerative colitis, 187–189 disease, progression, 188f double-contrast studies, 188 findings, summary, 190t imaging appearance, 187–189 rectosigmoid, involvement, 188f toxic megacolon, 188f treatment, 190–191 Ulcerogenic islet cell tumors (gastrinomas), 209 Ultrasound, 17–20 abdominal, 18 imaging knowledge requirement, 19 modality, 17 role, expansion, 19 limitation, acoustic barriers, 19 needle localization, 19f safety, advantage, 18 summary of, 20t Ultrasound-guided localization, 19f Unconsciousness, 309 Undescended testis (cryptorchidism), 390–391 atrophic undescended testis, coronal MR image, 392f

468

INDEX

Undescended testis (Continued) bilateral undescended testes, malignant neoplasms, 391f imaging appearance, 390–391 treatment, 391 ultrasound image, transverse plane, 391f Undifferentiated tumor, 8 Undisplaced fractures, 132 Unilateral pulmonary edema, diffuse alveolar pattern, 262f Unilateral renal agenesis, 218–219 Unilateral renal vein thrombosis, 242–243 Unilateral right tuberculous pleural effusion, 50f Unilateral ureterocele, filled with contrast material, 223f Upper abdomen MRI of, 25f plain image of, 362f Upper bladder, CT scan of, 244f Upper body, fracture sites (bone scan), 138f Upper pelvis, CT scan of, 185f Upper respiratory system, inflammatory disorders, 44–45 findings (summary), 45t Upper thoracic esophagus, stricture, 161f Urate crystals, deposition (continuation), 112 Uremia, 245 Ureter anomalies, 220–221 distal portion, kidney stone (nonopaque filling defect), 232f left ureter, contrast extravasation, 229f renal pelvis, relationship, 222f Ureteral calculus obstructing, 231f stone, 232f Ureteral tuberculosis, 227f Ureterocele, 221–222 bilateral, contrast material, 223f ectopic, excretory urogram/cystogram, 223f imaging appearance, 222 treatment, 222 unilateral, contrast material, 223f Urinary bladder inflammation, 227 structure/location, 218f Urinary calculi, 228–231 imaging appearance, 228–231 treatment, 231 Urinary obstructions, findings (summary), 234t Urinary system, 216–247 organs, location, 217f physiology of, 216–218 radiographer notes, 217b scout image, 217b Urinary tract, congenital/hereditary anomalies, 221

Urinary tract obstruction, 231–234 excretory urogram, 233f imaging appearance, 231–234 treatment, 234 Uterine agenesis, ultrasound images, 417f Uterine fibroids, 400–402 excretory urogram, 401f imaging appearance, 401–402 longitudinal sonogram, 402f submucosal, endovaginal ultrasound, 402f T2-weighted MR sagittal image, 402f treatment, 402

V Vaccine, bacteria/viruses (presence), 11 Valvular disease, 275–280 findings, summary, 279t Variable expressivity, 10 Varicose veins, 281–284 blood, stasis, 283 imaging appearance, 283–284 lower extremity venogram, 282f soft tissues, calcifications, 283f treatment, 283–284 Vas deferens, 386 Vascular anatomy, 249f Vascular diseases, 68–72 Vascular studies, 18 Vascular system, in MRA, 25 Vasectomy, 386 Vasopressin (ADH), production, 364 Vegetations, 275 Venous disease, 281–284 findings, summary, 283t Ventricles, midline shift, 6f Ventricular defects (identification), Doppler echocardiography (usage), 253 Ventricular septal defect, 252 heart enlargement, 252f septal closure, absence, 254f spin-echo MRI demonstration, 254 Ventricular system, generalized enlargement of, 328f Ventriculomegaly, cranial axial ultrasound, 415f Vermis, 289 Vertebral anomalies, 89 imaging appearance, 89 treatment, 89 Vertebral bodies enlargement of, 366f fracture, 145f softening, 111 Vertebral fusion, 97f Vertebral marrow, caseous necrosis, 106 Vesicoureteral reflux/infection, 220–221 Villi, digestion, 153 Viral meningitis, 290–291 Virtual reality (VR), CT postprocessing, 21 Virtual reality (VR) reconstructions, 21 Viruses, findings (summary), 54t Visceral peritoneum, penetration, 9

Visual impulses, transmission, 288–289 Vitamin A deficiency, 421 Vitamin B deficiencies, dietary modifications, 421 Vitamin B12 deficiency, 341 Vitamin C (ascorbic acid) deficiency (scurvy), 420 Vitamin D deficiency (rickets), 420–421 Vitamin deficiencies, 419–421 treatment, 421 Vitamin K deficiency, 421 Vitamins, 419 Voiding cystourethrogram, 224f Volume-rendered imaging, 21 Volvulus, 193 treatment, 195

W Wagging jaw, 86b–87b Warfarin (Coumadin), for thrombosis, 273 Water-soluble vitamins, 419 Whipple procedure, 210 White blood cells (leukocytes), 336, 337f diseases, 342–349 findings, summary, 349t Wilms’ tumor (nephroblastoma), 240 CT scan, 242f hydronephrosis (contrast), ultrasound (usage), 240 right kidney pelvicalyceal system, distortion/ displacement, 241f ultrasound, 241f T1-weighted coronal MR image, 243f Wimberger’s sign of scurvy, 420 Window level, 20 Window width, 20 Work-related lung disease, 59–60 Wrist calcification in, in diabetes mellitus, 379f Colles’ fracture, frontal/lateral projections, 139f musculoskeletal architecture, ultrasound image, 19f

X X-linked inheritance pattern (muscular dystrophy), 425 X-rays, relative attenuation, 3b circulatory system, 3b decreased, 3b increased, 3b respiratory system, 3b skeletal system, 3b soft tissue, 3b

Z Zenker’s diverticula, 163 saccular outpouching, 164f Zygomatic arch fractures, 315 submentovertex projection, 315f Zygomatic arch vulnerability, 315

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