What Radiology Residents Need to Know: Chest Radiology [1st ed. 2020] 978-3-030-16825-4, 978-3-030-16826-1

This book is an introduction to chest radiology, specifically designed for the needs of first-year residents. On the fir

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What Radiology Residents Need to Know: Chest Radiology  [1st ed. 2020]
 978-3-030-16825-4, 978-3-030-16826-1

Table of contents :
Front Matter ....Pages i-xviii
Introduction (Ronald L. Eisenberg)....Pages 1-6
Fissures, Lines, and Stripes (Ronald L. Eisenberg)....Pages 7-16
Patterns of Lung Disease (Ronald L. Eisenberg)....Pages 17-23
Tubes, Lines, and Catheters and Their Complications (Ronald L. Eisenberg)....Pages 25-42
Volume Loss (Ronald L. Eisenberg)....Pages 43-53
Pneumonia (Ronald L. Eisenberg)....Pages 55-81
Pleural Effusion (Ronald L. Eisenberg)....Pages 83-91
Pulmonary Edema (Ronald L. Eisenberg)....Pages 93-103
Pulmonary Vascular Diseases (Ronald L. Eisenberg)....Pages 105-116
Solitary Pulmonary Nodule (SPN)/Pulmonary Neoplasms (Ronald L. Eisenberg)....Pages 117-146
Pleural Neoplasms (Ronald L. Eisenberg)....Pages 147-152
Emphysema (Ronald L. Eisenberg)....Pages 153-159
Pulmonary Fibrosis (Ronald L. Eisenberg)....Pages 161-171
Inhalational Diseases (Ronald L. Eisenberg)....Pages 173-182
Miscellaneous Diffuse Pulmonary Diseases (Ronald L. Eisenberg)....Pages 183-202
Mediastinal Masses (Ronald L. Eisenberg)....Pages 203-227
Trachea and Bronchi (Ronald L. Eisenberg)....Pages 229-245
Aorta (Ronald L. Eisenberg)....Pages 247-255
Cardiac-Pericardial Disease (Ronald L. Eisenberg)....Pages 257-269
Diaphragm (Ronald L. Eisenberg)....Pages 271-277
Esophagus (Ronald L. Eisenberg)....Pages 279-284
Abnormal Air (Ronald L. Eisenberg)....Pages 285-295
Abnormalities Outside the Thorax (Ronald L. Eisenberg)....Pages 297-312
Back Matter ....Pages 313-316

Citation preview

What Radiology Residents Need to Know: Chest Radiology Ronald L. Eisenberg

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What Radiology Residents Need to Know: Chest Radiology

Ronald L. Eisenberg

What Radiology Residents Need to Know: Chest Radiology

Ronald L. Eisenberg, MD, JD Department of Radiology Beth Israel Deaconess Medical Center Boston, MA USA

ISBN 978-3-030-16825-4    ISBN 978-3-030-16826-1 (eBook) https://doi.org/10.1007/978-3-030-16826-1 © Springer Nature Switzerland AG 2020 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, express or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Switzerland AG. The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

To Zina, Avlana, and Cherina

Preface

Each first-year rotation is a scary experience for new radiology residents. A contributing factor is the lack of a textbook specifically geared to their needs. When asked by several residents what they should read during their first chest rotation, I realized that I had no good answer. Current available series have far too much material for a generation that does not like to read books and wants to receive information in a shorter and simpler format. Although some residents read at night about topics they encountered in cases interpreted during the day, this is ineffective, since first-year residents need to know something about the many conditions that they never will see during a four-week rotation. My solution was to develop What Radiology Residents Need to Know: Chest Radiology, a new approach to meet the needs of residents during their first rotation on thoracic imaging. It is divided into 23 sections covering all of chest radiology, as well as an introduction to cardiovascular conditions involving the thorax. Using an easy-to-read bullet format, the book includes all the necessary material for a first-­ year resident. In addition, it provides valuable tips on how to approach and interpret chest radiographs and CT examinations based on decades of practical experience and teaching residents at the work station. All books suffer from a limitation on the number of images due to space requirements and cost. To address this problem, a critical component of What Radiology Residents Need to Know: Chest Radiology is the accompanying e-platform. This contains new images amounting to twice the number in the printed version to fully illustrate points made in the text. Boston, MA, USA

Ronald L. Eisenberg

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Acknowledgments

Special thanks for image editing go to Michael Larson, Department of Radiology Media Specialist at Beth Israel Deaconess Medical Center, for adding arrows and cropping the large number of illustrations in the print and electronic formats, as well as ensuring that all images have been transformed into a resolution level suitable for printing. I also want to thank the faculty of our chest section and the residents rotating through it for their tireless efforts in identifying many of the excellent examples used in this book.

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Contents

1 Introduction ��������������������������������������������������������������������������   1 Search Pattern������������������������������������������������������������������������    1 Comparison with Old Studies/Reports: Better or Worse������    2 The Value of Symmetry��������������������������������������������������������    2 All Abnormalities Can Look the Same ��������������������������������    2 Special Areas for Focus��������������������������������������������������������    4 Dictations as Conversations��������������������������������������������������    5 2 Fissures, Lines, and Stripes��������������������������������������������������   7 Fissures����������������������������������������������������������������������������������    7 Anterior Junction Line����������������������������������������������������������    8 Posterior Junction Line����������������������������������������������������������    9 Hilum Overlay Sign��������������������������������������������������������������    9 Right Paratracheal Stripe������������������������������������������������������    9 Aorticopulmonary (AP) Window������������������������������������������   11 Paraspinal Lines ������������������������������������������������������������������   11 Right Paraspinal Line��������������������������������������������������������   13 Left Paraspinal Line ����������������������������������������������������������   14 Retrosternal Stripe ����������������������������������������������������������������   14 Posterior Tracheal Stripe ������������������������������������������������������   14 Azygoesophageal Line and Recess ��������������������������������������   15 References ����������������������������������������������������������������������������   16 3 Patterns of Lung Disease������������������������������������������������������  17 Other Classic Patterns and Signs������������������������������������������   19 Ground-Glass Opacity ������������������������������������������������������   19 Tree-in-Bud Pattern ����������������������������������������������������������   20

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Mosaic Attenuation Pattern ����������������������������������������������   21 Silhouette Sign ������������������������������������������������������������������   22 Spine (Vertebral Fade-Off) Sign ��������������������������������������   22 References ����������������������������������������������������������������������������   23 4 Tubes, Lines, and Catheters and Their Complications������  25 Endotracheal (ET) Tube��������������������������������������������������������   25 Tracheostomy Tube ��������������������������������������������������������������   27 Peripherally Inserted Central Catheters (PICC lines) ����������   28 Port-a-Cath and Other Tunneled Catheters ��������������������������   32 Swan-Ganz Catheters������������������������������������������������������������   32 Intra-Aortic Balloon Pump (IABP) ��������������������������������������   34 Nasogastric/Orogastric Tube ������������������������������������������������   35 Dobhoff (Feeding) Tube��������������������������������������������������������   36 Cardiac Devices��������������������������������������������������������������������   38 Chest Tube����������������������������������������������������������������������������   40 Reference������������������������������������������������������������������������������   42 5 Volume Loss ��������������������������������������������������������������������������  43 Subsegmental/Discoid/Platelike Atelectasis�������������������������   43 Relaxation (Compressive) Atelectasis����������������������������������   44 Obstructive Atelectasis����������������������������������������������������������   45 Round Atelectasis ����������������������������������������������������������������   45 Lobar Collapse����������������������������������������������������������������������   46 Right Upper Lobe ������������������������������������������������������������   46 Golden S Sign ������������������������������������������������������������������   47 Right Middle Lobe ������������������������������������������������������������   48 Lingula ������������������������������������������������������������������������������   48 Lower Lobe ����������������������������������������������������������������������   49 Left Upper Lobe ����������������������������������������������������������������   50 Total Lung ������������������������������������������������������������������������   51 References ����������������������������������������������������������������������������   53 6 Pneumonia�����������������������������������������������������������������������������  55 Caveats����������������������������������������������������������������������������������   55 Types of Pneumonia��������������������������������������������������������������   56 Community-Acquired Pneumonia (CAP)��������������������������   56 Hospital-Acquired Pneumonia (HAP) ������������������������������   57 Ventilator-Acquired Pneumonia (VAP) ����������������������������   57 Imaging Patterns��������������������������������������������������������������������   57 Lobar Pneumonia ��������������������������������������������������������������   57 Lobular Pneumonia (Bronchopneumonia) ������������������������   58

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Interstitial Pneumonia��������������������������������������������������������   59 Round Pneumonia ������������������������������������������������������������   59 Aspiration Pneumonia��������������������������������������������������������   60 Follow-up of Pneumonia����������������������������������������������������   62 Complications of Pneumonia������������������������������������������������   62 Pneumatocele ��������������������������������������������������������������������   62 Lung Abscess ��������������������������������������������������������������������   63 Empyema ��������������������������������������������������������������������������   64 Empyema Necessitans ������������������������������������������������������   66 Special Types of Bacterial Pneumonia����������������������������������   66 Klebsiella ��������������������������������������������������������������������������   66 Septic Emboli ��������������������������������������������������������������������   67 Loeffler’s Syndrome����������������������������������������������������������   68 Chronic Eosinophilic Pneumonia ������������������������������������   69 Fungal Pneumonia����������������������������������������������������������������   70 Aspergillosis����������������������������������������������������������������������   70 Other Fungal Diseases ������������������������������������������������������   72 Pneumocystis Jirovecii (formerly Carinii) Pneumonia ����   72 Viral Pneumonia��������������������������������������������������������������������   74 Infectious Mononucleosis (Epstein-Barr virus) ����������������   74 Varicella (Chickenpox) Pneumonia ����������������������������������   74 Tree-in-Bud Pattern in Other Viral Pneumonias����������������   75 Tuberculosis��������������������������������������������������������������������������   75 References ����������������������������������������������������������������������������   81 7 Pleural Effusion ��������������������������������������������������������������������  83 Caveats����������������������������������������������������������������������������������   83 Imaging ��������������������������������������������������������������������������������   85 Subpulmonic Effusion ����������������������������������������������������������   88 Loculated Effusion ��������������������������������������������������������������   89 Fissural Pseudotumor ����������������������������������������������������������   90 Hemothorax ��������������������������������������������������������������������������   90 Chylothorax ��������������������������������������������������������������������������   91 References ����������������������������������������������������������������������������   91 8 Pulmonary Edema����������������������������������������������������������������  93 Imaging����������������������������������������������������������������������������������   94 Neurogenic Pulmonary Edema����������������������������������������������   97 Pulmonary Hemorrhage��������������������������������������������������������  101 Adult Respiratory Distress Syndrome (ARDS)��������������������  101 References ����������������������������������������������������������������������������  103

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9 Pulmonary Vascular Diseases���������������������������������������������� 105 Pulmonary Embolism������������������������������������������������������������  105 Non-thrombotic Pulmonary Emboli��������������������������������������  110 Chronic Pulmonary Thromboembolism��������������������������������  111 Pulmonary Arterial Hypertension������������������������������������������  112 Pulmonary Veno-occlusive Disease��������������������������������������  115 References ����������������������������������������������������������������������������  115 10 Solitary Pulmonary Nodule (SPN)/Pulmonary Neoplasms������������������������������������������������������������������������������ 117 Imaging Criteria for Benignancy������������������������������������������  118 Mimics of Nodules ��������������������������������������������������������������  123 Follow-Up of Nodules (Fleischner Criteria) ������������������������  124 Benign Nodule(s)������������������������������������������������������������������  124 Granuloma��������������������������������������������������������������������������  124 Hamartoma������������������������������������������������������������������������  125 Pulmonary Arteriovenous Fistula (AVM)��������������������������  125 Rheumatoid Necrobiotic Nodule ��������������������������������������  125 ANCA-Associated Granulomatous Vasculitis ������������������  126 Lung Cancer��������������������������������������������������������������������������  126 Adenocarcinoma����������������������������������������������������������������  127 Adenocarcinoma in Situ����������������������������������������������������  127 Squamous Cell Carcinoma������������������������������������������������  130 Small Cell Lung Carcinoma (SCLC)��������������������������������  132 Large Cell Carcinoma��������������������������������������������������������  133 Carcinoid Tumor����������������������������������������������������������������  133 Pancoast (Superior Sulcus) Tumor������������������������������������  135 Metastases to the Lungs��������������������������������������������������������  136 Hematogenous Spread ������������������������������������������������������  136 Lymphangitic Spread ��������������������������������������������������������  139 Direct Spread ��������������������������������������������������������������������  141 Lymphoma ������������������������������������������������������������������������  142 Kaposi’s Sarcoma��������������������������������������������������������������  144 Sequestration ������������������������������������������������������������������������  145 References ����������������������������������������������������������������������������  146 11 Pleural Neoplasms ���������������������������������������������������������������� 147 Mesothelioma������������������������������������������������������������������������  147 Metastases ����������������������������������������������������������������������������  149 Fibrous Tumor of the Pleura��������������������������������������������������  150

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Pleural Lipoma����������������������������������������������������������������������  151 References ����������������������������������������������������������������������������  152 12 Emphysema���������������������������������������������������������������������������� 153 Centrilobular Emphysema ����������������������������������������������������  153 Panlobular (Panacinar) Emphysema ������������������������������������  154 Paraseptal Emphysema ��������������������������������������������������������  155 Bullous Disease ��������������������������������������������������������������������  157 Alpha-1 Antitrypsin Deficiency��������������������������������������������  158 Congenital Lobar Emphysema����������������������������������������������  159 References ����������������������������������������������������������������������������  159 13 Pulmonary Fibrosis �������������������������������������������������������������� 161 Chronic����������������������������������������������������������������������������������  161 Usual Interstitial Pneumonia (UIP)������������������������������������  161 Nonspecific Interstitial Pneumonia (NSIP)������������������������  163 Acute and Subacute��������������������������������������������������������������  164 Cryptogenic Organizing Pneumonia (COP)����������������������  164 Acute Interstitial Pneumonia (AIP) ����������������������������������  166 Smoking-Related������������������������������������������������������������������  167 Respiratory Bronchiolitis-Interstitial Lung   Disease (RB-ILD)����������������������������������������������������������  167 Desquamative Interstitial Pneumonia (DIP)����������������������  168 Pulmonary Langerhans Cell Histiocytosis (PLCH)����������  169 References ����������������������������������������������������������������������������  171 14 Inhalational Diseases������������������������������������������������������������ 173 Pneumoconioses��������������������������������������������������������������������  173 Silicosis ��������������������������������������������������������������������������������  174 Asbestosis������������������������������������������������������������������������������  176 Hypersensitivity Pneumonitis�����������������������������������������������  177 Allergic Bronchopulmonary Aspergillosis (ABPA)��������������  180 Crack Lung����������������������������������������������������������������������������  182 References ����������������������������������������������������������������������������  182 15 Miscellaneous Diffuse Pulmonary Diseases������������������������ 183 Sarcoidosis����������������������������������������������������������������������������  183 Lymphangioleiomyomatosis (LAM)������������������������������������  188 Pulmonary Alveolar Proteinosis��������������������������������������������  190 ANCA-Associated Granulomatous Vasculitis����������������������  191 Scleroderma��������������������������������������������������������������������������  193

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Cystic Fibrosis����������������������������������������������������������������������  194 Drug Toxicity������������������������������������������������������������������������  195 Radiation-Induced Lung Disease������������������������������������������  197 Lymphoid Interstitial Pneumonia (LIP)��������������������������������  199 Amyloidosis��������������������������������������������������������������������������  200 References ����������������������������������������������������������������������������  202 16 Mediastinal Masses �������������������������������������������������������������� 203 Anterior Mediastinum ����������������������������������������������������������  203 Middle Mediastinum ������������������������������������������������������������  203 Posterior Mediastinum����������������������������������������������������������  204 ITMIG Classification of Mediastinal Compartments������������  205 Prevascular (Anterior)��������������������������������������������������������  206 Visceral (Middle) ��������������������������������������������������������������  206 Paravertebral (Posterior)����������������������������������������������������  206 Anterior Mediastinal Masses (Superior Mediastinum) ��������  207 Thymoma ��������������������������������������������������������������������������  207 Thymoma Versus Thymic Carcinoma��������������������������������  209 Thymic Hyperplasia����������������������������������������������������������  210 Thymic Cyst����������������������������������������������������������������������  210 Teratoma ��������������������������������������������������������������������������  211 Thyroid Mass ��������������������������������������������������������������������  213 Lymphoma Lipoma ����������������������������������������������������������  214 Hemorrhage ����������������������������������������������������������������������  215 Aneurysm of the Ascending Aorta or Sinus of Valsalva ������������������������������������������������������  216 Anterior Mediastinal Masses (Lower Mediastinum)������������  216 Pericardial Cyst������������������������������������������������������������������  216 Epicar­dial Fat Pad ������������������������������������������������������������  217 Morgagni Hernia ��������������������������������������������������������������  217 Middle Mediastinal Masses��������������������������������������������������  218 Lymphadenopathy ������������������������������������������������������������  218 Enlarged Pulmonary Artery ����������������������������������������������  219 Bronchogenic Cyst ������������������������������������������������������������  219 Posterior Mediastinal Masses������������������������������������������������  220 Hiatal Hernia ��������������������������������������������������������������������  220 Bochdalek Hernia ��������������������������������������������������������������  220 Foregut Duplication Cyst (Esophageal Duplication, Neurenteric, or Bronchogenic Cyst)������������������������������  221 Esophageal Dilatation ������������������������������������������������������  221

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Esophageal Neoplasm (Benign or Malignant)������������������  222 Esophageal Varices������������������������������������������������������������  223 Neurogenic Tumor ������������������������������������������������������������  223 Spinal Neoplasm or Infection��������������������������������������������  223 Meningocele ����������������������������������������������������������������������  224 Extramedullary Hematopoiesis ����������������������������������������  224 Descending Thoracic Aortic Aneurysm ����������������������������  225 Diffuse Mediastinal Processes����������������������������������������������  226 Mediastinal Lipomatosis ��������������������������������������������������  226 Acute Mediastinitis ����������������������������������������������������������  226 Fibrosing Mediastinitis ����������������������������������������������������  226 References ����������������������������������������������������������������������������  227 17 Trachea and Bronchi������������������������������������������������������������ 229 Tracheobronchomegaly ��������������������������������������������������������  229 Relapsing Polychondritis������������������������������������������������������  230 Tracheomalacia ��������������������������������������������������������������������  231 Saber-Sheath Trachea������������������������������������������������������������  232 Post-intubation Stenosis��������������������������������������������������������  232 Other Causes of Tracheal Stenosis and Wall  Thickening������������������������������������������������������������������������  235 Bronchiectasis ����������������������������������������������������������������������  235 Mucoid Impaction ����������������������������������������������������������������  241 Broncholithiasis��������������������������������������������������������������������  242 Bronchopleural Fistula (BPF) ����������������������������������������������  243 Foreign Body ������������������������������������������������������������������������  244 Trauma����������������������������������������������������������������������������������  245 References ����������������������������������������������������������������������������  245 18 Aorta�������������������������������������������������������������������������������������� 247 Acute Aortic Injury����������������������������������������������������������������  247 Aortic Dissection������������������������������������������������������������������  250 Aortic Aneurysm ������������������������������������������������������������������  252 Pseudoaneurysm of the Aorta������������������������������������������������  254 Coarctation of the Aorta��������������������������������������������������������  254 Reference������������������������������������������������������������������������������  255 19 Cardiac-Pericardial Disease ������������������������������������������������ 257 Mitral Annulus Calcification ������������������������������������������������  262 Myocardial Infarction: Complications����������������������������������  262 High-Output Failure��������������������������������������������������������������  264

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Pericardial Disease����������������������������������������������������������������  265 Pericardial Effusion��������������������������������������������������������������  265 Constrictive Pericarditis��������������������������������������������������������  268 Pericardial Calcification��������������������������������������������������������  268 References ����������������������������������������������������������������������������  269 20 Diaphragm ���������������������������������������������������������������������������� 271 Eventration ��������������������������������������������������������������������������  273 Phrenic Nerve Paralysis ��������������������������������������������������������  274 Traumatic Rupture of Hemidiaphragm ��������������������������������  275 Diaphragmatic Herniation ����������������������������������������������������  276 Juxtaphrenic Peak ����������������������������������������������������������������  277 References ����������������������������������������������������������������������������  277 21 Esophagus������������������������������������������������������������������������������ 279 Achalasia ������������������������������������������������������������������������������  279 Boerhaave Syndrome������������������������������������������������������������  281 Foreign Body������������������������������������������������������������������������  282 References ����������������������������������������������������������������������������  284 22 Abnormal Air������������������������������������������������������������������������ 285 Pneumothorax������������������������������������������������������������������������  285 Mimics of Pneumothorax������������������������������������������������������  288 Tension Pneumothorax����������������������������������������������������������  290 Pulmonary Interstitial Emphysema ��������������������������������������  291 Pneumomediastinum ������������������������������������������������������������  291 Pneumopericardium��������������������������������������������������������������  293 Subcutaneous Emphysema����������������������������������������������������  294 References ����������������������������������������������������������������������������  295 23 Abnormalities Outside the Thorax�������������������������������������� 297 Mass Impressing/Displacing the Lower Cervical Trachea��������������������������������������������������������������������  297 Cervical Rib��������������������������������������������������������������������������  298 Gastrointestinal Abnormalities����������������������������������������������  299 Pneumoperitoneum����������������������������������������������������������������  300 Injuries to the Bones of the Thorax ��������������������������������������  304 Miscellaneous ����������������������������������������������������������������������  309 References ����������������������������������������������������������������������������  312 Index���������������������������������������������������������������������������������������������� 313

1

Introduction

For many first-year residents, the chest is their most challenging rotation. The major reason is that interpretations of chest radiographs are often subjective. One attending may read a radiograph as entirely normal, while another may detect a subtle consolidation or mild elevation of pulmonary venous pressure. Also, technical factors may play an important role. Many inpatient studies are portable AP images, which are more difficult to interpret than the standard upright PA and lateral views. Differences in the degree of inspiration and obliquity of the patient can make it difficult to compare the current study with previous examinations.

Search Pattern It is essential to develop a rigorous search pattern to ensure that you do not miss anything on chest radiographs (and CT). At some point, you need to evaluate the size and shape of the heart and mediastinum, the pulmonary markings, and the lungs; check for pleural effusion and pneumothorax; and make certain that the monitoring and support devices (various tubes and catheters) are in the proper position.

Electronic Supplementary Material  The online version of this chapter (https:// doi.org/10.1007/978-3-030-16826-1_1) contains supplementary material, which is available to authorized users. © Springer Nature Switzerland AG 2020 R. L. Eisenberg, What Radiology Residents Need to Know: Chest Radiology, https://doi.org/10.1007/978-3-030-16826-1_1

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1 Introduction

2

Some experienced readers prefer to first examine everything outside the chest (bones, soft tissues, trachea, upper abdomen) because of the danger of satisfaction of search. Once you have found an abnormality in the heart or lungs, there is less chance that you will remember to also look at the other structures visible on chest radiographs. A popular system utilized by our residents is to begin with “ABCD” – airways, bones, cardiomediastinal silhouette, and diaphragm.

Comparison with Old Studies/Reports: Better or Worse Failure to examine one (or more) prior studies and the dictated report is a cardinal sin. Much of chest radiology, especially in ICU patients undergoing frequent portable studies, revolves around the determination of whether there has been any interval change. Indeed, when viewing a new image, it is important to answer the following question: better, worse, or no change. This decision will influence how you shape your eventual report.

The Value of Symmetry The markings in the right and left lung should be symmetric. Therefore, part of your search pattern should be to artificially divide the chest from top to bottom into a series of horizontal rectangular areas and compare the appearance of the right and left lungs. Any asymmetric increase in opacification on one side should raise the suspicion of an abnormality (Figs. 1.1 and 1.2; see Fig. e1.1). (All electronic images (Figs. e1.1–e1.4) can be found on this chapter’s website on SpringerLink: [https://doi.org/10.1007/ 978-3-030-16826-1_1])

All Abnormalities Can Look the Same An important limitation of chest radiography is that most disorders produce an abnormal area of opacification that is similar for a wide variety of underlying causes. The specific appearance, combined with the clinical history and location within the lung, may be sufficient to make a precise diagnosis. However, at times it may be impossible

All Abnormalities Can Look the Same

3

Fig. 1.1  Value of asymmetry. The large mass in the right apex (arrow) is somewhat obscured by overlying bony structures in this region. However, it is clearly asymmetric with the opposite side. (Courtesy of Gillian Lieberman, MD, Boston)

a

b

Fig. 1.2  Value of asymmetry and old studies. Subtle pneumonia. (a) Increased opacification with air bronchograms in the left perihilar region when compared with the opposite side (arrow), consistent with developing pneumonia. (b) On the normal study obtained 3 weeks previously, this area was completely clear, and there has been a definite change

to distinguish among various diagnostic possibilities. The classic example is the ICU patient with increased opacification at the left base and obscuration of the hemidiaphragm. This could represent volume loss in the lower lobe, pleural effusion, aspiration, or pneumonia – and in most cases there is a combination of two or more of these

4

1 Introduction

possibilities. In the appropriate clinical setting, there also could be an underlying primary or metastatic malignancy that adds to the area of opacification. If necessary clinically, CT can distinguish among these various possibilities (see Figs. e1.2 and e1.3).

Special Areas for Focus Apices – overlapping ribs and clavicle and cartilage calcification in the first rib can hide areas of consolidation and especially neoplasms, only showing mild asymmetry. Also, it may be difficult to determine whether a round opacification in the apex represents a lung nodule or merely a bone island in a rib. In both of these cases, consider an apical lordotic view. This effectively lifts up the bony structures, so that the lung parenchyma can be seen much better. An opacification that persists is in the lung and can be characterized better on this view (Fig. 1.3). Hila – the overlapping tangle of normal arteries and veins makes it difficult to detect small abnormalities in this region, especially in patients with vascular congestion.

a

b

Fig. 1.3  Value of apical lordotic projection. (a) Initial radiograph demonstrates asymmetric increased opacification in the right apical region. (b) Apical lordotic view clearly shows that parenchymal nodule in the right upper lung (arrow)

Dictations as Conversations

5

Dictations as Conversations Consider your report as a conversation between you and the referring clinician. An effective approach is to describe the findings and indicate what you think is the most likely diagnosis. Explain if there are technical factors limiting your conclusion. For example, apparent clearing of bilateral layering effusions could merely represent a more upright position of the patient (Fig. e1.4). Never hesitate to offer alternative diagnoses that the referring clinician may not have considered. For example, diffuse bilateral opacifications would be consistent with pulmonary edema if the patient has cardiomegaly and bilateral pleural effusions (Fig. 1.4). However, you could mention that, in the appropriate clinical setting, a similar pattern could represent widespread infection, pulmonary hemorrhage, or ARDS. If some finding just does not fit – such as a pulmonary edema pattern in a stroke patient with a normal-sized heart – raise an alternate possibility (in this case, neurogenic rather than cardiac pulmonary edema).

Fig. 1.4  Pulmonary edema. Characteristic diffuse bilateral pulmonary opacifications (batwing pattern). However, in the appropriate clinical setting, other possibilities could be suggested as alternative diagnoses

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1 Introduction

As long as you are not using structured reporting for chest radiographs, remember English 101 and write a coherent narrative, relating your findings in a logical fashion in flowing sentences. You may have to include a host of impertinent negatives during your first rotation on chest. However, as you progress, think back to internship. Did you want the radiology report to be a long dissertation or just provide the answer to your clinical question? Remember that an endless rambling report is not a sign of erudition, and this practice will pose a major problem when you finally take call.

2

Fissures, Lines, and Stripes

Fissures (Fig. 2.1) • Lines composed of layers of visceral and parietal pleura that separate the lobes of the lungs • Major fissures – run obliquely from superior to inferior and extend from the fifth thoracic vertebra to the diaphragm, separating the lower lobe (posteriorly) from the anterior and middle lobe/lingula • Minor (horizontal) fissure – runs anteriorly and laterally from the right hilum to the lateral chest wall, separating the anterior segment of the right upper lobe (above) from the right middle lobe • Accessory fissures ○○ Azygos fissure – normal anatomic variant, in which a deep pleural fissure into the apical segment of the right upper lobe during embryologic development is caused by a laterally displaced azygos vein, which takes a curvilinear path from the upper aspect of the right lung to end in a teardrop shadow just above the right hilum ○○ Superior accessory fissure – separates the superior segment from the lower basal segments of the lower lobe, more commonly on the right, and runs in a horizontal plane posterior to the minor fissure Electronic Supplementary Material  The online version of this chapter (https:// doi.org/10.1007/978-3-030-16826-1_2) contains supplementary material, which is available to authorized users. © Springer Nature Switzerland AG 2020 R. L. Eisenberg, What Radiology Residents Need to Know: Chest Radiology, https://doi.org/10.1007/978-3-030-16826-1_2

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8

2  Fissures, Lines, and Stripes

a

b

c

d

Fig. 2.1  Normal fissures. (a) Minor fissure (arrow). Note the markedly enlarged heart without vascular congestion, a discordance consistent with the diagnosis of cardiomyopathy. (b) Minor fissure (black arrow) and portions of the major fissures (white arrows). (c, d) Azygos fissure (arrow)

○○ Inferior accessory fissure – separates the medial basal segment from the rest of the lower lobe, extending superiorly and slightly medially from the inner third of the hemidiaphragm ○○ Left minor fissure – separates the lingula from the superior segment of the left upper lobe

Anterior Junction Line (See Figs. e2.1 and e2.2) (All electronic images (Figs. e2.1–e2.14) can be found on this chapter’s website on SpringerLink: [https://doi.org/10.1007/​978-3-030-16826-1_2]) • Formed by apposition of the visceral and parietal pleura of the anteromedial aspects of the lungs with a small amount of intervening mediastinal fat

Right Paratracheal Stripe

9

• Appears on up to 50% of radiographs as an oblique line crossing the superior two-thirds of the sternum from upper right to lower left • Obliteration of the line ○○ Because of its location in the anterior mediastinum, obliteration or abnormal convexity of the line suggests underlying anterior mediastinal disease (thyroid mass, lymphadenopathy, neoplasm, thymic mass, lipomatosis, volume loss, or hyperinflation of the adjacent lung)

Posterior Junction Line (See Figs. e2.3 and e2.4) • Formed by the apposition of the visceral and parietal pleura of the posteromedial portion of the lungs, posterior to the esophagus and anterior to the third through fifth thoracic vertebrae • Appears as a straight or mildly leftward convex line, typically projecting through the trachea • The posterior junction line demonstrates more cranial extension than the anterior junction line and, unlike its counterpart, is seen above the clavicles

Hilum Overlay Sign (Fig. 2.2; See Figs. e2.5 and e2.6) • To distinguish true cardiomegaly from a large anterior mediastinal mass mimicking cardiac enlargement • Normally, the main pulmonary artery is always lateral to the cardiac shadow or just within its outer edge • An anterior mediastinal mass often overlaps a main pulmonary artery, which is then clearly visible within the margins of the mass (which extends >1 cm beyond the pulmonary artery margin)

Right Paratracheal Stripe (Figs. 2.3 and 2.4; See Fig. e2.7) • Formed when the visceral and parietal pleura of the right upper lobe come in contact with the right lateral border of the trachea and the intervening mediastinal fat • Air within the right lung and trachea outlines these entities to form the right paratracheal stripe, which has a maximum normal thickness of 4 mm

10

2  Fissures, Lines, and Stripes

Fig. 2.2  Hilum overlay sign. The right hilar mass overlaps the main pulmonary artery, unlike the normal appearance on the left. (Heilman/Wikimedia)

a

b

Fig. 2.3 (a, b) Normal right paratracheal stripe (arrow) [1]

• It begins superiorly at the level of the clavicles and extends inferiorly to the right tracheobronchial angle at the level of the azygos arch • The right paratracheal stripe is the most commonly seen mediastinal line or stripe, visualized in up to 97% of posteroanterior chest radiographs as it courses through the right brachiocephalic vein and SVC

Paraspinal Lines

11

Fig. 2.4  Abnormal right paratracheal stripe. Paramediastinal opacification (arrow) obliterating the right paratracheal stripe represents mediastinal hemorrhage related to the insertion of the right subclavian catheter

• Widening or obliteration of the right paravertebral stripe is an indication of mediastinal bleeding in trauma and of lymphadenopathy in sarcoidosis and lymphoma • The similar left paratracheal stripe is less frequently evident, extending from the reflection of the left subclavian artery to the aortic arch

 orticopulmonary (AP) Window (Figs. 2.5 and 2.6; A See Fig. e2.8) • Shallow concave interface between the aorta and pulmonary artery. • Convexity of the AP window interface indicates a mediastinal abnormality, most frequently lymphadenopathy or a saccular thoracic aortic aneurysm

Paraspinal Lines (Figs. 2.7 and 2.8; See Fig. e2.9) • Formed by the lungs and pleura coming into tangential contact with the posterior mediastinal fat, paraspinal muscles, and adjacent soft tissues on each side

12

a

2  Fissures, Lines, and Stripes

b

Fig. 2.5  Normal AP window. (a) Shallow concave interface (∗) between the aorta and the pulmonary artery. (b) CT image shows the normal AP window (∗). The concave interface seen in (a) actually represents the lateral border (arrow) of the AP window formed by the left lung and pleura contacting the aortic arch and extending to the pulmonary artery [1]

a

b

Fig. 2.6  Abnormal AP window (bronchogenic carcinoma). (a) In addition to the abnormal bulge in the AP window (arrow), there is thickening of the right paratracheal stripe (∗), left lower lobe consolidation, and left pleural effusion. (b) CT image shows a significant soft-tissue mass within the AP window and subcarinal space, compatible with metastatic lymphadenopathy. Lymphadenopathy in the paratracheal region accounted for the thickened right paratracheal stripe [1]

Paraspinal Lines

13

Fig. 2.7  Normal right and left paraspinal lines (arrows) [1]

a

b

Fig. 2.8  Abnormal paraspinal lines (abscess). (a) Mass (arrow) effacing the left paraspinal line. The lateral wall of the descending aorta is seen as a separate entity (arrowhead). (b) CT image confirms the presence of an abscess (arrow) that effaces the paraspinal lines. The air-soft tissue interface between the lung and aorta remains intact on the left (arrowhead), thereby preserving the normal radiographic appearance of the lateral aortic wall [2]

RIGHT PARASPINAL LINE • Seen on about 25% of PA radiographs, it appears straight and typically extends from the 8th to 12th thoracic vertebral levels • Lateral displacement may reflect osteophytes, prominent mediastinal fat, or such posterior mediastinal disorders as hematoma, mass, and extramedullary hematopoiesis

14

2  Fissures, Lines, and Stripes

LEFT PARASPINAL LINE • Seen on about 40% of PA radiographs, it extends vertically from the aortic arch to the diaphragm, typically lying medial to the lateral wall of the descending thoracic aorta • Lateral displacement may reflect osteophytes, prominent mediastinal fat, tortuosity of the descending thoracic aorta, or such posterior mediastinal abnormalities as hematoma, mass, extramedullary hematopoiesis, and esophageal varices

Retrosternal Stripe (See Figs. e2.10 and e2.11) • Formed by the interface between the anterior lungs and the retrosternal soft tissues (fat, internal mammary vessels) • Normally measures 20 mm Hg, and radiographic clearing of pulmonary edema typically lags behind the clinical status of the patient. Other causes of a similar pulmonary edema pattern include: • Fluid overload (hypervolemia, hypoproteinemia) – common cause, particularly during the postoperative period and in elderly patients, in whom there is rapid clearing with appropriate treatment • Overtransfusion or incompatible blood transfusion Electronic Supplementary Material  The online version of this chapter (https://doi.org/10.1007/978-3-030-16826-1_8) contains supplementary material, which is available to authorized users. © Springer Nature Switzerland AG 2020 R. L. Eisenberg, What Radiology Residents Need to Know: Chest Radiology, https://doi.org/10.1007/978-3-030-16826-1_8

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• Renal failure/uremia  – complex mechanism (left ventricular failure, decreased oncotic pressure, hypervolemia, increased capillary permeability) Another cause of this pattern is neurogenic and other types of noncardiogenic pulmonary edema, in which there is no enlargement of the cardiac silhouette unless there is unrelated heart disease (see below).

Imaging • Interstitial edema – earliest stage ○○ Loss of the normal sharp definition of pulmonary vascular markings (especially in the lower lungs) (Fig. 8.1) ○○ Redistribution of blood flow to the upper lungs (cephalization) (Fig. 8.2) ○○ Perihilar haze ○○ Peribronchial cuffing (see Fig. e8.1b) (All electronic images (Figs. e8.1–e8.17) can be found on this chapter’s website on SpringerLink: [https://doi.org/10.1007/​ 978-3-030-16826-1_8]) ○○ Thickening of the interlobular septa, which appear as fine, short, linear horizontal opacities extending to the pleura (Kerley B lines) and may develop when the wedge pressure is >13 mm Hg (see Fig. e8.1)

Fig. 8.1  Interstitial pulmonary edema. Loss of the normal sharp definition of pulmonary vascular markings and a perihilar haze. At the bases, note the thin horizontal lines of increased opacity (Kerley B lines) that represent fluid in the interlobular septa [1]

Imaging

95

Fig. 8.2  Redistribution of pulmonary blood flow. Apical vascular redistribution, as indicated by the diameters of upper lobe vessels (arrows) equal to those of lower lobe vessels (open arrows). Note the moderate enlargement of the heart [2]

a

b

Fig. 8.3  Batwing appearance of alveolar edema. (a) Frontal radiograph and (b) CT image demonstrate diffuse alveolar filling through both lungs. Note the characteristic sparing of the outermost portions of the lungs

○○ Enlargement of the azygos vein may be seen in overhydration edema (see Fig. e8.2) • Alveolar edema (Fig. 8.3; see Figs. e8.3 and e8.4) ○○ Typical appearance of bilateral air-space opacifications (butterfly or batwing pattern), which are most prominent in the central perihilar regions and develop when the wedge pressure is >25 mm Hg ○○ Generally spares the outermost portions of the lungs

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Fig. 8.4  Unilateral pulmonary edema. Diffuse alveolar pattern is limited to the dependent left lung in a homeless patient who developed pulmonary edema while sleeping on a park bench lying on his left side [1]

• Asymmetric pulmonary edema usually most prominently affects the right lung • Unilateral appearance is most frequently related to dependency of the affected side (Fig. 8.4; see Figs. e8.5 and e8.6) • In acute mitral insufficiency secondary to papillary muscle rupture or other cause, pulmonary edema primarily involves the right upper lung (see Fig. e8.7) • Patchy asymmetric pattern may develop in patients with pre-existing lung disease, especially emphysema, because only areas with intact pulmonary vessels are affected (see Fig. e8.8) • Recurrent episodes of interstitial and alveolar edema and hemorrhage in patients with chronic left heart failure may result in the development of a coarse, often poorly defined reticular pattern that predominantly involves the middle and lower lung zones (may be impossible to distinguish from COPD in older patients and often represents both conditions coexisting in the same patient) (see Fig. e8.9) • Radiographic resolution of pulmonary edema usually occurs hours or days after symptoms improve and wedge pressure measurements have returned to normal (especially in patients with left-sided heart failure), because of the time lag before the large amount of extracellular fluid is reabsorbed

Neurogenic Pulmonary Edema

97

Fig. 8.5  CT of interstitial edema. In a patient with postoperative fluid overload and a pulmonary capillary wedge pressure of 20 mm Hg, there are interlobar septal lines predominating in the anterior portion of the left lung, along with some peribronchial cuffing (arrow). Both lungs display diffuse ground-glass areas of increased attenuation with a gravitational anteroposterior gradient [3]

• Serial widening of the vascular pedicle (width of the superior mediastinum measured from the right lateral border of the SVC at the point where it crosses the right main bronchus to the left lateral margin of the left subclavian artery as it arises from the aortic arch) • CT ○○ Smooth thickening of interlobular septa, which appear as lines in the lung periphery running perpendicular to the pleura (Kerley B lines) (Fig. 8.5) ○○ Ground-glass, low-grade lung opacification or frank air-space consolidation with a central distribution (see Fig. e8.10)

Neurogenic Pulmonary Edema • Important cause of non-cardiogenic pulmonary edema that is reported to develop in up to 30% of patients after head trauma, seizures, or stroke (Fig. 8.6) • Related to increased intracranial pressure, neurogenic pulmonary edema typically disappears within several days of surgical relief

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Fig. 8.6  Non-cardiogenic pulmonary edema. Pulmonary vascular congestion with a normal cardiac silhouette following a stroke

Differences between the two major types of edema • Cardiac ○○ Low-protein transudate due to increased hydrostatic pressure generated across the capillary membrane ○○ Initially accumulates in the connective tissues surrounding the blood vessels and secondary pulmonary lobules • Noncardiac ○○ Protein-rich exudate that accumulates in the extravascular space as a consequence of increased microvascular permeability ○○ Because of inherent disruption of the alveolocapillary membrane in this condition, water may not flow into the loose connective tissue, instead directly flooding the alveolar space ○○ Clearance of the protein-rich exudate is slower than with a nonproteinaceous transudate Other causes of non-cardiogenic pulmonary edema • Inhalation of toxic gases (e.g., hydrocarbons, chlorine, sulfur dioxide, nitrogen dioxide in silo-filler’s disease) (see Fig. e8.11) • Near-drowning (Fig. 8.7)

Neurogenic Pulmonary Edema

99

Fig. 8.7  Near-drowning. Diffuse pulmonary edema pattern [1]

a

b

Fig. 8.8  Re-expansion edema after thoracentesis. (a) Initial radiograph shows a massive left malignant effusion. (b) Repeat examination 2 hours after the rapid removal of 2500 mL of fluid shows re-expansion pulmonary edema on the left (arrows). The segment of left lung not compressed by effusion remains free of edema. Over the next 6 days, the edema resolved spontaneously [1]

• Rapid re-expansion of lungs – unilateral pulmonary edema pattern that follows the rapid removal of large amounts of air or fluid from the pleural space (Fig. 8.8; see Fig. e8.12) • Chronic renal failure (see Fig. e8.13)

100

8  Pulmonary Edema

• Non-traumatic pulmonary hemorrhage (bleeding diatheses, idiopathic pulmonary hemosiderosis, Goodpasture’s syndrome, polyarteritis nodosa, ANCA-­associated granulomatous vasculitis) • Narcotic abuse (heroin, methadone, cocaine) (Fig.  8.9; see Figs. e8.14 and e8.15) • ARDS (sepsis, oxygen toxicity, disseminated intravascular coagulation, cardiopulmonary bypass)

Fig. 8.9  Cocaine abuse. Extensive bilateral heterogeneous central and parahilar opacities, representing cardiogenic pulmonary edema in a woman who presented with shortness of breath and chest pain after smoking crack cocaine [1]

Imaging – chest radiographs can distinguish between cardiac and non-­ cardiogenic (permeability) edema in about 80% of patients (Table 8.1) Table 8.1  Cardiac and noncardiac edema

Major signs Kerley lines Pleural effusions Cardiomegaly Opacities in lung

Cardiac

Noncardiac

Present Present Present Diffuse

Less common Less common Less common Patchy and peripheral

Minor signs Air bronchograms Rare Perihilar haze Present Peribronchial cuffing Present

Often present Infrequent Unusual

Adult Respiratory Distress Syndrome (ARDS)

101

Pulmonary Hemorrhage • Alveolar process that is extremely difficult to differentiate radiographically from pulmonary edema and pneumonia (see Fig. e8.16)

Adult Respiratory Distress Syndrome (ARDS) • Severe, unexpected acute respiratory distress (usually requiring mechanical ventilation) that develops in a patient with no major underlying lung disease • Diffuse alveolar damage from increased pulmonary capillary permeability, which develops in response to numerous types of lung injury and results in leakage of proteinaceous fluid into the alveoli • This process eventually results in alveolar disruption and hemorrhage, a reduction in surfactant, and alveolar collapse • Causes include: ○○ Diffuse severe pulmonary infection (bacterial or viral) ○○ Prolonged or profound shock ○○ Inhalation of toxins and irritants ○○ Oxygen toxicity ○○ Systemic reaction to a broad spectrum of non-pulmonary processes • Diagnosis is based on clinical grounds  – acute onset of bilateral lung opacities, no clinical signs of congestive failure (pulmonary artery wedge pressure ≤ 18 mm Hg), PaO2/FIO2 ≤ 300 mm Hg. • High mortality rate of up to 60% Imaging (Figs. 8.10 and 8.11; see Fig. e8.17) • Bilateral pulmonary edema pattern that is typically delayed 12 hours or more after the clinical onset of respiratory failure (unlike cardiogenic pulmonary edema, in which the chest radiograph is often abnormal before or concurrent with the onset of symptoms) • Cardiac silhouette is not enlarged (unless there is underlying heart disease), and there is infrequently any associated pleural effusion • Lung opacities evolve rapidly (maximum during the first 3 days) and may progress to areas of consolidation

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8  Pulmonary Edema

Fig. 8.10  ARDS. Diffuse bilateral pulmonary edema pattern with normal cardiac silhouette. No evidence of appreciable pleural effusion

Fig. 8.11  ARDS. Diffuse bilateral alveolar process involving all lobes with no cardiomegaly or pleural effusion. (Courtesy of Jeffrey Klein, MD, Burlington, CT)

References

103

• Radiographic findings may be less severe than expected by the clinical degree of hypoxemia • CT – diffuse ground-glass opacities (but a more patchy distribution with some portions of normal-appearing lung) • In those who survive ARDS, there is clearing of the ground-glass opacifications and consolidations but frequently a residual prominence of interstitial markings with traction bronchiectasis, architectural distortion, and functional disability • Need for prolonged mechanical ventilation and decreased lung compliance frequently leads to the development of barotrauma (pneumothorax, pneumomediastinum, pulmonary interstitial emphysema, pneumatoceles)

References 1. Eisenberg RL.  Clinical Imaging: An Atlas of Differential Diagnosis. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins; 2010. 2. Nemec SF, Bankier AA, Eisenberg RL. Lower lobe-predominant diseases of the lung. AJR. 2013;200:712–28. 3. Gluecker T, Capasso P, Schnyder P, et al. Clinical and radiological features of pulmonary edema. Radiographics. 1999;19:1507–31. 4. Gotway MB, Marder SR, Hanks DK, et al. Thoracic complications of illicit drug use: an organ system approach. Radiographics. 2002;22:S119–35. 5. Rossi SE, Erasmus JJ, McAdams HP, et al. Pulmonary drug toxicity: radiologic and pathologic manifestations. Radiographics. 2000;20:1245–59.

9

Pulmonary Vascular Diseases

Pulmonary Embolism • Third most common form of acute cardiovascular disease (after myocardial infarction and stroke) • Nonspecific presenting signs and symptoms (tachypnea, dyspnea, hemoptysis, pleuritic chest pain) often make it difficult to diagnose pulmonary embolism • Major risk factors: ○○ Prolonged bed rest ○○ Hypercoaguable state (protein C or S, antithrombin III deficiency, anticoagulants) ○○ Recent surgical procedure ○○ Recent myocardial infarction or chronic congestive heart failure ○○ Venous thrombosis in the deep veins of the lower extremities or pelvis ○○ Indwelling venous catheter ○○ Malignancy and chemotherapy • Negative D-dimer assay essentially excludes deep venous thrombosis and pulmonary embolus • Pulmonary infarction develops in ≤15% of patients with pulmonary emboli

Electronic Supplementary Material The online version of this chapter (https://doi.org/10.1007/978-3-030-16826-1_9) contains supplementary material, which is available to authorized users. © Springer Nature Switzerland AG 2020 R. L. Eisenberg, What Radiology Residents Need to Know: Chest Radiology, https://doi.org/10.1007/978-3-030-16826-1_9

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Imaging • Radiographs ○○ Usually normal (may be nonspecific opacity, pleural effusion, atelectasis, or elevation of the hemidiaphragm indistinguishable from other pulmonary or pleural processes) ○○ Primarily performed to exclude other disorders that could mimic a pulmonary embolism (pneumonia, rib fracture, pneumothorax) ○○ Classic peripheral, pleural-based, wedge-shaped opacity (Hampton hump) is seen in a minority of cases with pulmonary infarction (Fig. 9.1) ○○ Uncommon findings of: • Focal oligemia (Westermark sign) (Fig. 9.2; see Fig. e9.1) (All electronic images (Figs. e9.1–e9.15) can be found on this chapter’s website on SpringerLink: [https://doi. org/10.1007/978-3-030-16826-1_9]) • Enlargement of the ipsilateral pulmonary artery (Fleischner sign) (Fig. 9.3) associated with rapid tapering of the occluded pulmonary artery distally (knuckle sign) ○○ Essential for accurate interpretation of radionuclide ventilationperfusion (V/Q) lung scan

a

b

Fig. 9.1  Hampton hump sign of pulmonary embolism/infarction. (a, b) Wedge-shaped, pleural-based areas of increased opacification/attenuation (arrows) in two different patients. (a) From [1]; (b) from [2]

Pulmonary Embolism

a

107

b

Fig. 9.2  Westermark sign of pulmonary embolism. (a) Hyperlucency of the left lung. (b) CTPA demonstrates a large pulmonary embolism filling the left pulmonary artery (arrow)

a

b

Fig. 9.3  Fleischner sign of pulmonary embolism. (a) Enlargement of the ipsilateral pulmonary artery (arrow), associated with rapid tapering of the occluded pulmonary artery distally. (b) CT image confirms the clot-filled pulmonary artery (arrow). (Courtesy of Jeffrey Klein, MD, Burlington, CT)

• CT pulmonary angiogram (CTPA) (Fig. 9.4; see Figs. e9.2–e9.7) ○○ Has replaced V/Q lung scanning in most institutions as the preferred imaging modality for detecting and excluding pulmonary emboli ○○ Shows a pulmonary embolus as a central filling defect surrounded by contrast within the pulmonary artery or as an abrupt cutoff (complete obstruction) of a pulmonary artery branch

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Fig. 9.4  Acute pulmonary embolus. Large filling defects in the right main (white arrow) and left interlobar (black arrow) pulmonary arteries [3]

Fig. 9.5  Acute pulmonary embolism. Eccentric partial filling defect, which is surrounded by contrast material and forms acute angles with the arterial wall (arrows) [3]

○○ If eccentric, the filling defect forms an acute angle with the pulmonary artery wall (Fig. 9.5) ○○ Saddle embolism is the infrequent development a large pulmonary embolism that straddles the main pulmonary arterial trunk at its bifurcation (Fig. 9.6) ○○ Pulmonary infarcts appear as peripheral ground-glass opacifications or consolidations that often have a wedge-shaped configuration (see Fig. e9.6) ○○ May demonstrate other diseases that could mimic pulmonary embolism

Pulmonary Embolism

109

Fig. 9.6  Saddle embolus. The pulmonary embolism straddles the main pulmonary arterial trunk at its bifurcation. (Glitzy queen00 / English Wikipedia)

○○ Part of the three-pronged study in which patients presenting with chest pain are also assessed for coronary artery disease and aortic dissection • Radionuclide ventilation-perfusion (V/Q) lung scan (see Fig. e9.7) ○○ Normal perfusion study excludes significant embolization, and no further examinations are needed ○○ Two or more segmental or larger perfusion defects with normal ventilation in these areas (V/Q mismatch) are highly likely for pulmonary embolism ○○ Relatively large number of indeterminate examinations, especially in patients with chronic obstructive pulmonary disease or parenchymal abnormalities seen on chest radiographs Management • Clinical significance of small emboli is unclear (if there is no impairment of cardiopulmonary reserve, these small clots may be left untreated without adverse effect) • Immediate anticoagulation therapy (heparin) for patients with suspected DVT or pulmonary embolism reduces mortality rates from 30% to 25 mm Hg at rest, >30 mm Hg during exercise) • General causes ○○ Increased pulmonary blood flow (left-to-right shunt) ○○ Narrowing of pulmonary vessels (chronic pulmonary embolism) ○○ Increased resistance to pulmonary venous drainage (mitral valve disease) • Major types ○○ Primary • Uncommon subtype of sustained elevation of pulmonary artery pressure in which no underlying cause is identified • Typically affects young females (20–45 years) ○○ Secondary • Diffuse lung disease (obstructive emphysema, interstitial fibrosis) • Diffuse pulmonary arterial disease (thromboembolism, arteritis) • Chronic heart disease (mitral valve disease, left ventricular failure)

Pulmonary Arterial Hypertension

113

• Chronic hypoxia (chest deformity, neuromuscular disease, Pickwickian obesity, dwelling at high altitude) • High-output heart disease (anemia, thyrotoxicosis, peripheral AVMs, Paget’s disease, polycythemia vera, pregnancy) Imaging • Radiographs ○○ Prominent enlargement of the central pulmonary arteries with rapid peripheral tapering (Fig. 9.9) ○○ Right ventricular enlargement ○○ Hilum convergence sign – convergence of pulmonary vessels to join a dilated pulmonary artery (to distinguish the hilar changes of pulmonary artery hypertension from a bulky hilar mass or adenopathy)

a

b

Fig. 9.9  Pulmonary artery hypertension. (a, b) Slight cardiomegaly and a great increase in the size of the pulmonary trunk. The right and left pulmonary arteries are huge (arrows), but the peripheral pulmonary vasculature is relatively sparse. Note the hilum convergence sign on the right. Long-standing pulmonary hypertension has produced degenerative intimal changes in the pulmonary arteries, which have become densely calcified. The patient had an atrial septal defect and Eisenmenger’s physiology (reversed left-to-right shunt) [1]

114

a

9  Pulmonary Vascular Diseases

b

Fig. 9.10  Prominence of pulmonary outflow tract (arrow). (a) Normal appearance in a young woman. (b). Pulmonary valvular stenosis [1]. Note that in both cases the heart size and pulmonary vascularity remain within normal limits

○○ Note that isolated prominence of the pulmonary outflow tract (with normal pulmonary vessels and no associated cardiac abnormality) is a common appearance in adolescents and adults younger than 30  years of age (especially in women) (Fig. 9.10a); however, if there is an appropriate murmur, further studies must be performed to exclude pulmonic stenosis (Fig. 9.10b) • CT (see Figs. e9.13 and e9.14) ○○ Much more accurate for detecting pulmonary artery enlargement when the diameter of the main pulmonary artery is greater than that of the ascending aorta or ≥3 cm ○○ Pulmonary artery calcifications are virtually pathognomonic ○○ Demonstrates right ventricular enlargement and bulging of the interventricular septum ○○ Mosaic attenuation that is heterogeneous or patchy, with a perivascular distribution (regions of hypoattenuation reflecting areas of hypoperfusion interposed with areas of hyperattenuation where there is normal or excessive perfusion); this differs from the typical segmental and well-defined distribution of mosaic attenuation associated with chronic pulmonary embolism

References

115

Pulmonary Veno-occlusive Disease • Rare subtype of pulmonary arterial hypertension, in which pulmonary venous thrombosis and fibrosis cause narrowing or occlusion of the pulmonary veins • Although the etiology is unknown, this condition has been associated with viral infection, chemotherapy, autoimmune disease, bone marrow transplantation, intracardiac shunts, radiation injury, and a genetic predisposition • Typically affects children and young adults • Classic triad of severe pulmonary artery hypertension, radiographic evidence of pulmonary edema, and normal wedge pressure (though not seen in many patients) Imaging (see Fig. e9.15) • The combination of smooth interlobular septal thickening and illdefined diffuse centrilobular ground-glass opacities in a patient with enlarged pulmonary arteries is highly suspicious for pulmonary veno-occlusive disease

References 1. Eisenberg RL. Clinical Imaging: An Atlas of Differential Diagnosis. 5th ed. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins; 2010. 2. Frazier AA, Galvin JR, Franks TJ, Rosado-de-Chrsitenson ML. Pulmonary vasculature: hypertension and infarction. Radiographics. 2000;20:491–524. 3. Wittram C, Maher MM, Yoo AJ.  CT angiography of pulmonary embolism: diagnostic criteria and causes of misdiagnosis. Radiographics. 2004;24:1219–38. 4. Arnold HR, Gardner JE, Goodman PH.  Amniotic pulmonary embolism. Radiology. 1961;77:629–43. 5. Restreppo CS, Carrillo JA, Martinez S, et  al. Pulmonary complications from cocaine and cocaine-based substances: imaging manifestations. Radiographics. 2007;27:941–56. 6. Gotway MR, Marder SR, Hanks DK, et al. Thoracic complications of illicit drug use: an organ system approach. Radiographics. 2002;22:S119–35. 7. Gladdish GW, Sabloff BM, Munden RF, et al. Pulmonary thoracic sarcomas. Radiographics. 2002;22:621–37.

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8. Ridge CA, Bankier AA, Eisenberg RL.  Mosaic attenuation. AJR. 2011;197:W970–7. 9. Peña E, Dennie C, Veinot J, Muñiz SH. Pulmonary hypertension: how the radiologist can help. Radiographics. 2012;32:7–32. 10. Gluecker T, Capasso P, Schnyder P, et al. Clinical and radiological features of pulmonary edema. Radiographics. 1999;19:1507–31.

Solitary Pulmonary Nodule (SPN)/ Pulmonary Neoplasms

10

Solitary round or oval pulmonary opacifications are common incidental findings on a chest radiograph or chest CT performed for another indication. They are especially common in smokers, up to half of whom have tiny nodules, almost all of which are benign. By definition, the opacification is termed a nodule if ≤3 cm in diameter and a mass if >3 cm. When encountering a solitary pulmonary nodule, the critical decision is whether this represents a benign or malignant process. Numerous criteria can be used to assess the risk of cancer. Age effect •  5 indicates an aggressive neoplasm with a poor prognosis) ○○ Can identify the site of an unknown primary in almost 50% of cases ○○ False positive – active inflammatory or granulomatous processes; primary lung malignancy ○○ False negative – small metastases (23 mm in women) on inspiration, with collapse on expiration • Corrugated appearance of the trachea and bronchial walls, with focal diverticular outpouchings along the bronchi • Thinning of the tracheal wall on CT • Evidence of such complications as recurrent pneumonia, bronchiectasis, and emphysematous changes with hyperinflation of the lungs and pulmonary fibrosis

Relapsing Polychondritis • Rare inflammatory disease, probably of autoimmune origin, that destroys cartilage of the ear, nose, upper respiratory tract, and joints (most common in middle-­aged women) • Inflammatory changes involve the pinna of the ear in about 90% of cases • Recurrent episodes of cartilage inflammation cause edema, granulation tissue, and eventually fibrosis • About half of patients demonstrate respiratory tract narrowing, which is the major cause of symptoms (recurrent infections and bronchiectasis related to impaired clearing of secretions) and death Imaging (Fig. 17.1; see Figs. e17.2–e17.4) • Diffuse smooth, symmetric wall thickening and luminal narrowing of the larynx, trachea, and main bronchi • Tracheal wall thickening that is anterior and lateral and spares the posterior membranous portion (which contains no cartilage) is virtually pathognomonic of relapsing polychondritis • Tracheal narrowing may be focal (usually in a subglottic location) or diffuse • Thickened airway wall has increased attenuation, and calcification frequently occurs • Dynamic scanning can demonstrate expiratory collapse of affected airways

Tracheomalacia

a

231

b

Fig. 17.1  Relapsing polychondritis. (a) End-inspiration and (b) end-expiration images show dynamic collapse of the trachea with expiration. Note the calcification and thickening of the cartilaginous parts of the trachea (arrow), with sparing of the posterior wall (arrowhead) [2]

Tracheomalacia • Excessive focal or generalized collapsibility of the trachea on expiration due to weakening of the supporting cartilage and muscles • Symptoms of stridor intensify during times of increased airflow, such as coughing, crying, or feeding • Associated inefficient coughing mechanism and retained secretions often lead to recurrent pulmonary infections and bronchiectasis • May be primary in children or secondary • In adults, tracheomalacia may be secondary to prior intubation, chest trauma, COPD, extrinsic compression (vascular ring or enlarged thyroid), chronic tracheobronchitis, or an intrinsic cartilage disorder (relapsing polychondritis) • Concomitant involvement of the bronchi is termed tracheobronchomalacia (TBM)

232

17  Trachea and Bronchi

Imaging (see Fig. e17.5) • Hyperinflation of the lungs with excessive narrowing of the tracheal lumen during expiration • CT ○○ Inspiration  – may be normal or only a “lunate” shape, with reduced AP diameter of the airway ○○ Expiration – substantial anterior bowing of the posterior membranous portion of the trachea (crescentic appearance with decreased space between the anterior and posterior walls, known as the frown sign) ○○ Tracheomalacia is now defined as narrowing >70% on expiration ○○ In severe disease, there may be touching of the anterior and posterior walls

Saber-Sheath Trachea • Narrowing of the intrathoracic trachea, caused by deformity of tracheal cartilage, is a highly specific sign of chronic obstructive pulmonary disease • Extrathoracic trachea is normal Imaging (Fig. 17.2; see Fig. e17.6) • Marked decrease in the coronal diameter of the intrathoracic trachea associated with an increase in its sagittal diameter (PA diameter of the trachea ≤2/3 thirds of the diameter on the lateral view)

Post-intubation Stenosis • Focal narrowing that represents a late complication of intubation • Reflects pressure necrosis of the wall of the trachea resulting from overdistension of the cuff (exceeding the pressure in the capillaries supplying the tracheal mucosa) or positioning the tip of the endotracheal tube against the tracheal wall • Most commonly, tracheal stenosis occurs at the level of a tracheostomy stoma, secondary to fibrosis and granulation tissue at the site

Post-intubation Stenosis

a

233

b

Fig. 17.2  Saber-sheath trachea. (a) In this patient with marked chronic obstructive pulmonary disease, there is severe coronal narrowing of the intrathoracic trachea (small arrows) with an abrupt change to a more rounded crosssectional shape at the thoracic outlet (large arrows). (b) Lateral view shows the sagittal diameter of the trachea to be within normal limits (arrow) [2]

• Presenting symptoms include cough, stridor, wheezing, and dyspnea on exertion (typically develop when narrowing of the lumen is >50% of the cross-sectional area) Imaging (Fig. 17.3) • Short segment of tracheal narrowing, typically with an hourglass configuration • Frequently not appreciated on chest radiographs, so that the diagnosis requires CT (multiplanar and 3D rendering can demonstrate narrowing not seen on axial images)

234

17  Trachea and Bronchi

a

b

c

Fig. 17.3  Tracheal stenosis after tracheostomy. (a) Frontal tomogram shows a well-defined tubular area of tracheal narrowing at the tracheostomy cuff site. (b) Lateral tomogram in a different patient demonstrates thickening of the anterior tracheal wall (arrows), secondary to fibrosis and granulation tissue, at the site of the tracheostomy stoma. This finding was of no clinical significance. (c) Coronal CT image shows severe tracheal narrowing after tracheostomy (arrows) [a, b from 2]

Bronchiectasis

235

Other Causes of Tracheal Stenosis and Wall Thickening • Amyloidosis – diffuse wall thickening/narrowing with focal nodular masses (see Fig. e15.34) • ANCA-associated granulomatous vasculitis – focal or diffuse wall thickening and narrowing (often renal and pulmonary involvement) (see Fig. e17.7) • Radiation fibrosis  – tracheal narrowing associated with traction bronchiectasis (see Fig. e17.8) • Sarcoidosis – wall thickening, often with irregular or nodular stenosis (may be enlarged lymph nodes compressing the airway) • Tuberculosis – irregular wall thickening in the hyperplastic stage, which leads to smooth narrowing in the fibrostenotic stage (usually also hilar lymphadenopathy and pulmonary findings)

Bronchiectasis • Progressive, irreversible localized or diffuse dilatation of the bronchi • Chronic cough with sputum production (often after severe pneumonia with incomplete clearing of symptoms), hemoptysis, recurrent pneumonia, or chronic atelectasis • Underlying mechanism – bronchial wall damage related to infection or inflammation, obstruction (Fig. 17.4), adjacent fibrosis, and failure to clear thick secretions leads to pooling of mucus and bacteria in the lungs and secondary inflammatory response (see Fig. e17.9) • Common causes include: ○○ Recurrent or chronic pneumonia (see Fig. e17.10) ○○ Chronic aspiration ○○ Cystic fibrosis (upper lobe predominance) (see Fig. e17.11) ○○ Kartagener syndrome (situs inversus, chronic sinusitis and/or nasal polyposis, and bronchiectasis due to ciliary dyskinesia) (see Fig. e17.12)

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17  Trachea and Bronchi

Fig. 17.4  Bronchiec­tasis (carcinoid). This predominantly endobronchial tumor, arising before the bifurcation of left upper and lower lobe bronchi, causes distal bronchiectasis (white arrows). Note the central carcinoid tumor (black arrow) [1]

○○ Allergic bronchopulmonary aspergillosis (increased immunologic response) (see page 180) ○○ Interstitial pulmonary fibrosis (loss of surrounding lung volume) ○○ Tuberculous scarring (upper lobes) ○○ Intrinsic bronchial disease (stenosis, extrinsic compression, endobronchial mass) • Classified into three categories (from least to most severe) (Fig. 17.5): ○○ Cylindrical – uniform bronchial dilatation without tapering and with parallel walls (Fig. 17.6)

Bronchiectasis

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Fig. 17.5  Normal bronchus (arrow) [1]

Fig. 17.6  Cylindrical bronchiectasis. Lack of bronchial tapering (arrow) [1]

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17  Trachea and Bronchi

Fig. 17.7  Varicose bronchiectasis. “String-of-­pearls” appearance (arrow) [1]

○○ Varicose – beaded appearance reflecting areas of bronchial dilatation and narrowing (Fig. 17.7) ○○ Cystic – severe bronchial enlargement and ballooning leading to the formation of a string of multiple cysts that extend to the pleural surface and often contain air-fluid levels (Fig. 17.8; see Fig e17.13) Imaging • Radiographs ○○ “Tram tracks” (parallel linear shadows representing the walls of cylindrically dilated bronchi) (Fig. 17.9) ○○ Areas of multiple thin-walled cysts that may have air-fluid levels and tend to be peripheral and cluster together in the distribution of a bronchovascular bundle (Fig. 17.10)

Bronchiectasis

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Fig. 17.8  Cystic bronchiectasis. Multiple cystic spaces, some with air-fluid levels (arrows), predominantly involve the left lung [2]

Fig. 17.9  Tram track sign. Coned view of the right lower lung demonstrates the characteristic parallel line shadows outside the boundary of the pulmonary hilum. Note the coarse increase in interstitial markings in this patient with chronic bronchitis [2]

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Fig. 17.10  Bronchiec­tasis. Diffuse increase in interstitial markings with multiple thin-walled cysts radiating in a bronchovascular distribution with tramlines (arrows) and peribronchial cuffing (arrowhead) [2]

• CT ○○ Multiple dilated, thin-walled circular lucencies (on cross-section) and parallel linear opacities (bronchial walls sectioned lengthwise) ○○ Signet ring sign – dilated bronchus adjacent to a normal pulmonary artery branch (generally the same size) (Fig. 17.11) ○○ Lack of normal bronchial tapering ○○ Bronchi visible in the peripheral 1  cm of the lungs (see Fig. e17.14) ○○ Mucoid impactions (simulating lung nodules or branching, finger-like opacities) ○○ Cystic bronchiectasis  – classic “cluster of grapes” appearance (see Fig. e17.15) ○○ Central varicose bronchiectasis  – highly suggestive of allergic bronchopulmonary aspergillosis (see Fig. e17.16)

Mucoid Impaction

241

Fig. 17.11  Signet ring sign. Multiple examples (arrows) in a patient with cystic bronchiectasis. (Courtesy of Ritu Gill, MD, Boston)

Mucoid Impaction • Airway filling by mucoid secretions that produce tubular or branching opacities that typically radiate from the hilum toward the periphery of the lung • Affects patients with bronchospasm (plugs present in dilated proximal segmental bronchi) and a sensitivity to Aspergillus fumigatus • Almost always associated with asthma or pre-existing chronic bronchial disease (especially cystic fibrosis) • May also develop distal to a bronchial obstruction due to either benign (tuberculosis, bronchostenosis) or malignant (lung cancer, bronchial carcinoid) disease • The affected portion of the lung remains aerated through collateral air drift through interalveolar (pores of Kohn) and bronchiole-alveolar (canals of Lambert) connections • Usually transient but may persist for months and even enlarge Imaging • Tubular or branching opacities that resemble fingers • May have Y- or V-shaped configuration if there is plugging of a bronchial bifurcation (Fig. 17.12; see Fig. e17.17) • CT  – bronchiectasis, low-attenuation mucus inspissated in the bronchi, and a clear connection with the central airways

242

a

17  Trachea and Bronchi

b

Fig. 17.12  Mucoid impaction. (a) V-shaped and (b) Y-shaped masses (arrows) [2]

Broncholithiasis • Calcified or ossified material within the bronchial lumen • Most commonly due to erosion or extrusion of a calcified adjacent lymph node into the bronchial lumen • Usually associated with a long-standing focus of necrotizing granulomatous lymphadenitis, especially following tuberculosis (but the frequency of broncholithiasis complicating granulomatous infection is quite low) • Most often involves the proximal right middle lobe bronchus and the origin of the anterior segmental bronchi of the upper lobes (because of airway anatomy and lymph node distribution) • May be recurrent pneumonias related to episodes of bronchial obstruction Imaging (Fig. 17.13; see Fig. e17.18) • Broncholiths vary in size and are usually irregular, often possessing spur-like projections or sharp edges • Post-obstructive atelectasis, bronchiectasis, and air trapping

Bronchopleural Fistula (BPF)

243

Fig. 17.13  Broncho­lithiasis. Innumerable calcified masses scattered throughout the lungs [2]

Bronchopleural Fistula (BPF) • Abnormal connection between an airway and the pleural space, which most commonly is a complication that develops after thoracic surgery (especially pneumonectomy) • High mortality rate, though about 1/3 of fistulas close spontaneously • Normal post-pneumonectomy appearance  – increasing fluid and decreasing air (should be 50–65% filled with fluid after 1 week, and completely fluid-filled by 2–4 months) • Any decrease in fluid (unless there has been instrumentation) suggests BPF (Fig. 17.14a, b) • CT may demonstrate the site of BPF (Fig. 17.14c; see Fig. e17.19), which is well shown on bronchoscopy

244

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a

b

c

Fig. 17.14  Bronchopleural fistula. (a) Several weeks after pneumonectomy for aspergillus infection, more than half of the right hemithorax is filled with fluid (air-fluid levels). (b) Four months later, the next follow-up image shows a dramatic increase in the amount of air within the hemithorax. (c) CT demonstrates a small focus of air immediately distal to the tracheal bifurcation (arrow), adjacent to the stump of the bronchus intermedius or right lower lobe bronchus, indicating the site of the leak

Foreign Body (Fig. 17.15) • Aspirated foreign bodies are most common in young children, especially under age 3 • In adults, they often occur in those with altered mental status or represent teeth or dental devices • Most frequently found in the lower lobe bronchi on the right, because of the more direct angle of the right main bronchus with the trachea

References

a

245

b

Fig. 17.15  Bronchial foreign body. (a, b) Aspirated dental crown appears as a dense metallic opacification (white arrow) causing collapse of the posterior basal segment of the right lower lobe (black arrow). (Courtesy of Jennifer Ni Mhuircheartaigh, MD, Boston)

Trauma • Tracheal tear is an uncommon injury that tends to be associated with fractures of the upper thorax, including the first three ribs, clavicle, sternum, and scapula • Bronchial tear, which may be a complication of surgical lobectomy, presents as persistent pneumothorax (despite adequate placement of one or more chest tubes), increasing subcutaneous emphysema postoperatively, and focal peribronchial collections of air (see Fig. e17.20) • Collapsed lung due to complete rupture of a main bronchus produces the fallen lung sign (see Fig. 5.27)

References 1. Cantin L, Bankier AA, Eisenberg RL.  Bronchiectasis. AJR. 2009;273: W158–71. 2. Eisenberg RL.  Clinical Imaging: An Atlas of Differential Diagnosis. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins; 2010. 3. Kaewlai R, Avery LL, Asrani AV, Novelline RA. Multidetector CT of blunt thoracic trauma. Radiographics. 2008;28:1555–70.

Aorta

18

Acute Aortic Injury • Serious complication of rapid deceleration injury or blunt chest trauma and associated with a high mortality rate • Cause of death in 15% of persons who die from motor vehicle accidents; of these, up to 90% are fatal before arrival at the hospital, and about half of short-­term survivors die within the first 24 hours • About 90% of acute aortic injuries visible on CT occur at the aortic isthmus, just distal to the origin of the left subclavian artery • About 2% of untreated cases eventually present as a chronic pseudoaneurysm Imaging • Radiographs (Figs. 18.1 and 18.2) ○○ Normal chest radiograph has a 98% negative predictive value for aortic injury ○○ Abnormal study has a low positive predictive value (4 mm) between intimal calcification and the outer border of the aortic shadow indicates widening of the aortic wall (see Fig. e18.5)

Aortic Dissection

a

251

b

Fig. 18.3  Huge aortic dissection. (a, b) Striking prominence of the entire descending thoracic aorta (arrows). Note the long intimal flap in b

• CT ○○ Double-barrel aorta with an intimal flap separating the true and false lumen (usually larger and more slowly filling) (Fig. 18.3b) ○○ Intimal tears spiral down the aorta, with the false lumen lying anterior and to the right in the ascending aorta and posterior and to the left in the descending aorta ○○ Interruption of the continuous intimal flap indicates entry and reentry points of the dissection (see Fig. e18.6) ○○ May be obstruction of one or more vessels arising from the aorta (especially the left renal artery) Management • Type A  – immediate surgical repair (because of a higher risk of aortic rupture and tendency to extend to the aortic root, coronary arteries, and pericardium) • Type B – medical therapy for hypertension (unless development of complications, especially rupture or occlusion of a major branch of the aorta)

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• Without treatment, there is a high mortality rate (1–2% per hour for the first 2 days) • With prompt appropriate surgical intervention, the long-term survival is about 50%

Aortic Aneurysm • Localized or diffuse dilatation of the aorta (≥50% of normal diameter) • Normal maximal aortic diameter: ○○ Ascending aorta – 3.5 cm ○○ Descending aorta – 3 cm • Shape of aneurysms: ○○ Saccular (20%) – focal outpouching (often secondary to trauma, infection) ○○ Fusiform (80%) – diffuse cylindrical dilatation of the entire circumference (usually atherosclerotic) • Integrity of the aortic wall: ○○ True – intact aortic wall (usually atherosclerotic) ○○ False (pseudoaneurysm) – disrupted aortic wall (typically infectious, post-traumatic) • Location: ○○ Ascending aorta – syphilis and cystic medial necrosis (may be associated with Marfan syndrome); frequently also caused by atherosclerosis ○○ Aortic arch/descending aorta  – atherosclerosis, mycotic infection, and trauma • Most patients are asymptomatic, and an unruptured aneurysm is usually an incidental finding on a routine chest radiograph • Large aneurysms may compress mediastinal structures (airways, esophagus, superior vena cava, pulmonary arteries, nerves) Imaging • Sharply marginated, saccular, or fusiform mass of homogeneous density (Fig. 18.4)

Aortic Aneurysm

a

253

b

Fig. 18.4  Aneurysm of the descending aorta. (a) Frontal view demonstrates a localized bulging of the descending aorta (arrows). (b) Lateral view in another patient shows aneurysmal dilatation of the lower thoracic aorta (arrows). Note the marked tortuosity of the remained of the descending aorta [1]

• Curvilinear calcification may occur in the outer wall (ascending aorta calcification suggests syphilis or hyperlipidemia and poses an embolic risk in patients scheduled for CABG) • CT: ○○ Crescent sign  – high attenuation of the aortic wall or mural thrombus on non-­contrast images suggests acute or impending rupture (see Fig. e18.7) ○○ Ruptured aneurysm produces high-attenuation blood in periaortic tissues (see Fig. e18.8) • MRI  – increased T1 signal in a saccular aneurysm is consistent with thrombosis or slow flow Management • Significant risk of rupture of a saccular aneurysm if: ○○ > 5.5 cm in the ascending aorta ○○ > 6.0 cm in the descending aorta • Annual growth rate of >1 cm/year (or >0.5 cm/6 months) also is an indication for surgical repair

254

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Pseudoaneurysm of the Aorta • Contained rupture in which the majority of the aortic wall has been breached and luminal blood is held in only by a thin rim of the remaining wall or adventitia • Typically secondary to focal aortic transection • About 85% result from penetrating trauma (gunshot or stab wounds); the remainder develops after blunt trauma (motor vehicle accidents or falls) • Relatively few develop from penetrating atherosclerotic ulcers Imaging (see Fig. 18.2b) • Generally occur along the undersurface of the aortic isthmus, at or near the site of the ductus arteriosus

Coarctation of the Aorta • Narrowing of the aortic arch with partial obstruction of blood flow • In the more common “adult” type, aortic narrowing occurs at or just distal to the level of the ductus arteriosus (double bulge represents prestenotic and poststenotic dilatation) • In the “infantile” variety, there is a long segment of narrowing lying proximal to the ductus (obligatory right-to-left shunt and early congestive heart failure) • Associated conditions include bicuspid aortic valve (75%), Turner syndrome (20%), and cerebral aneurysms (10%) • Characteristic difference in blood pressure between the upper and lower extremities with decreased femoral pulses Imaging • Enlargement of the left ventricle with a characteristic double bulge in the region of the aortic knob (figure-3 sign on plain chest radiographs and reverse figure-3, or figure-E, sign on the barium-filled esophagus) (see Fig. e18.9)

Reference

255

• Inferior rib notching (usually involving the posterior third to eighth ribs), which rarely develops before age 6 • Angiographic demonstration of a pressure gradient >20  mm Hg may indicate a need for intervention (surgery or balloon angioplasty with stent placement)

Reference 1. Eisenberg RL.  Clinical Imaging: An Atlas of Differential Diagnosis. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins; 2010.

Cardiac-Pericardial Disease

19

It is usually easy to determine whether the heart is enlarged or of normal size. When unsure, one can measure the cardiothoracic ratio (CTR). On a full inspiration PA image, the widest transverse diameter of the heart should be 90° (Fig. 19.4b) ○○ On the lateral view, bulge of the left atrial region (above the level of prominence related to an enlarged left ventricle) ○○ Posterior displacement of the esophagus (can cause dysphagia) (Fig. 19.5) • Right atrium (forms the right heart border)  – lateral bulging or elongation of the right heart border (Fig. 19.6; see Fig. e19.2)

260

a

19  Cardiac-Pericardial Disease

b

Fig. 19.4  Left atrial enlargement. (a, b) Gross cardiomegaly with enlargement of the left atrium and left ventricle in this patient with mitral regurgitation. Note the striking double contour configuration (arrows, a) and elevation of the left main bronchus (arrows, b), characteristic signs of left atrial enlargement. The aortic knob is normal in size, and there is no evidence of pulmonary vascular congestion [1]

If there is overall enlargement of the cardiac silhouette, an analysis of the size of the left atrium and the aorta can suggest the diagnosis of an underlying cardiac abnormality: • Enlarged left atrium – mitral regurgitation (see Fig. 19.4) • Enlarged aorta – aortic regurgitation (see Fig. 19.1) • Neither enlarged  – dilated cardiomyopathy, high-output state, or pericardial effusion (Fig. 19.7) Note: The radiographic appearance of a discordance between substantial enlargement of the cardiac silhouette and normal or minimally elevated pulmonary venous pressure should suggest two diagnostic possibilities – cardiomyopathy and pericardial effusion (see Fig. e19.3; see Fig. 2.1a) If the overall size of the cardiac silhouette is normal: • Enlarged left atrium – mitral stenosis (see Fig. e19.4) • Enlarged aorta – aortic stenosis or aneurysm (see Fig. e19.5) • Neither enlarged – hypertrophic cardiomyopathy, pulmonary artery hypertension, and acute myocardial infarction

19  Cardiac-Pericardial Disease

261

Fig. 19.5  Left atrial enlargement. The enlarged chamber produces a discrete posterior indentation (arrows) on the barium-filled esophagus in a patient with mitral stenosis [1]

a

b

Fig. 19.6  Right atrial enlargement. (a, b) Striking prominence of the right atrium in this patient with tricuspid insufficiency [1]

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19  Cardiac-Pericardial Disease

Fig. 19.7  Alcoholic cardiomyopathy. Generalized enlargement of the cardiac silhouette involving all chambers, without special prominence of the left atrium or aorta [1]

Mitral Annulus Calcification • Degenerative, non-inflammatory process that primarily occurs in persons over age 60, is more common in women, and usually is of no clinical significance • May be associated with aortic stenosis and hypertension (possibly related to increased strain on the mitral valve due to pressure overload on the left ventricle) and an increased risk of stroke Imaging (Fig. 19.8) • Bandlike calcification typically in a pattern resembling a reverse letter “C” or the letter “J” • Can also appear like the letter “O” if there is involvement of the anterior valve leaflet

Myocardial Infarction: Complications Ventricular Aneurysm (True) • Focal dyskinetic outpouching of the left ventricular wall that develops in fewer than 5% of ST elevation myocardial infarctions (STEMI). • Involvement of all layers of the muscular wall

Myocardial Infarction: Complications

263

Fig. 19.8  Mitral annulus calcification (arrows) [1]

a

b

Fig. 19.9  Ventricular aneurysm. (a, b) Bulging and curvilinear peripheral calcification (arrows) along the lower left border of the heart near the apex. Note the relatively anterior position of the aneurysm on the lateral view [1]

• Usually occurs along the anterolateral or apical wall of the left ventricle and is associated with occlusion of the left anterior descending coronary artery • Curvilinear calcification along the left ventricular contour (Fig. 19.9; see Fig. e19.6) Pseudoaneurysm (False) • Contained ventricular rupture in which there is no myocardium in the aneurysm wall, which is composed of pericardium

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• Typically occurs on the upper diaphragmatic and posterior wall and is associated with occlusion of the circumflex or right coronary artery • Danger of impending complete rupture, which is suggested by interval increase in size of the pseudoaneurysm over sequential images Dressler Syndrome • Autoimmune pericarditis, characterized by fever and pleuropericardial chest pain, beginning 1–6 weeks after an acute myocardial infarction • Striking response to steroid therapy • Pleural effusion (transudate), which is bilateral in 50% of patients (usually greater on the left), is the most common finding (80%) and may occur alone • Pericardial effusion

High-Output Failure • Uncommon condition in which there is elevated cardiac output and low systemic vascular resistance (due to peripheral vasodilatation or arteriovenous shunting) • May be associated with increased oxygen consumption that reflects increased metabolic demand • Most common causes: ○○ Anemia (especially sickle cell disease and thalassemia) ○○ Thyrotoxicosis (high metabolic rate) ○○ Paget’s disease (multiple microscopic arteriovenous malformations in affected bones) ○○ Pregnancy (increased blood volume and flow) Imaging • Enlargement of the heart with generalized engorgement of pulmonary vessels (see Fig. e19.7)

Pericardial Disease



265

Pericardial Disease

Normally, there is up to about 40 mL of fluid within the pericardial space, separating the parietal and visceral pericardial layers. An abnormal accumulation of pericardial fluid initially collects posterior to the left ventricle (dependent portion with the patient in a supine position). As the amount of pericardial effusion increases further, it tends to accumulate more along the right heart border until it fills the entire pericardial space and encircles the heart.

Pericardial Effusion • Severity of symptoms varies greatly depending on the underlying cause, the rate at which the pericardial fluid accumulates, and the total amount present • Faint, distant heart sounds on auscultation • Cardiac tamponade: ○○ May occur rapidly (trauma, myocardial rupture) or slowly (cancer) ○○ Rapid accumulation of as little as 100–200  mL of pericardial fluid can severely decrease ventricular filling during diastole ○○ Medical emergency because of such complications as pulmonary edema, shock, and death Causes • Congestive heart failure – evidence of venous congestion and frequently an associated pleural effusion (often unilateral on the right) • Infection – most commonly viral (coxsackievirus) or mycobacterial • Connective tissue disease – systemic lupus erythematosus, rheumatoid arthritis, scleroderma, and polyarteritis nodosa • Neoplasm – lymphoma and lung, breast, or melanoma metastases • Drug-induced – procainamide, hydralazine, and phenytoin • Uremia – pericardial effusion develops in about 15% of patients on prolonged hemodialysis (may collect rapidly and be life threatening)

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• Myxedema • Trauma – rapid development may produce severe alteration of cardiac function with minimal change in the radiographic cardiac silhouette • Idiopathic (diagnosis of exclusion) Imaging • Radiographs ○○ Rapid increase in the size of the cardiac silhouette on serial chest films (suggests pericardial effusion rather than cardiomyopathy as the cause of a large heart with normal pulmonary vascularity) ○○ The heart often assumes a globular, water-bottle, or flask-shaped configuration (both sides of the heart appearing rounded and displaced laterally), especially when the lungs remain clear (Fig. 19.10; see Fig. e19.8) ○○ Epicardial fat pad sign • On a lateral projection, virtually pathognomonic widening (>4 mm) of the normally thin soft-tissue opacity of the pericardium between the lucent stripes representing the anterior mediastinal and subepicardial fat (Oreo cookie sign) (Fig. 19.11) • Low sensitivity but high specificity for pericardial effusion

Fig. 19.10  Uremic pericardial effusion. Globular enlargement of the cardiac silhouette in a child on prolonged hemodialysis [1]

Pericardial Disease

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• CT/MRI ○○ Sensitive modalities for detecting and confirming pericardial effusion (see Fig. e19.9) ○○ CT attenuation measurements and signal characteristics at MRI can characterize pericardial effusions as serous or hemorrhagic/ proteinaceous (see Figs. e19.10 and e19.11)

a

b

Fig. 19.11  Epicardial fat pad sign in pericardial effusion, (a) On the lateral view in a normal patient, a thin, relatively dense line (arrow) representing the normal pericardium may be seen between the anterior mediastinal and subepicardial fat. (b) In this patient, there is a wide soft-tissue density separating the subepicardial fat stripe (arrows) from the anterior mediastinal fat. This is a virtually pathognomonic sign of pericardial effusion or thickening [1]

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○○ Signs of pericardial tamponade include: • Compression of the right heart chambers • Flattening or inversion of the wall of the right ventricle • Inverted interventricular septum • Enlargement of the SVC and IVC

Constrictive Pericarditis • Fibrotic pericardial thickening limiting the ability of the heart to function normally and leading to clinical signs of heart failure • Most frequent causes are cardiac surgery and radiation therapy • Less common etiologies include infection (viral or tuberculous), connective tissue disease, uremia, and neoplasm Imaging • Pericardial thickening (≥4 mm) with a reduced cardiac volume and a narrowed, tubular configuration of the right ventricle • CT is exquisitely sensitive for detecting often-associated pericardial calcification, which predominantly is seen in an inferior and right-sided location • MRI is more sensitive in distinguishing between pericardial effusion and thickening (but cannot detect calcification) • Contrast enhancement of the pericardium suggests an active inflammatory process

Pericardial Calcification • Usually related to prior pericarditis (most commonly viral or uremic) or trauma • Occurs in about 50% of cases of constrictive pericarditis (strong evidence to distinguish this condition from restrictive cardiomyopathy, which can have a similar clinical appearance) Imaging • Curvilinear calcification that conforms to the margins of the pericardial sac and often is best visualized on lateral chest radiographs (Fig. 19.12)

References

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Fig. 19.12  Chronic constrictive pericarditis. Dense calcification in the pericardium (arrows) surrounding a normal-sized heart [1]

• If thin and linear – typically viral or uremic pericarditis, but could be prior trauma or surgery, or a connective tissue disorder • If thick, irregular, and amorphous  – most likely old tuberculous pericarditis or asbestos plaques (as in pleural disease)

References 1. Eisenberg RL.  Clinical Imaging: An Atlas of Differential Diagnosis. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins; 2010. 2. Shahrzad M, Le TSN, Silva M, Bankier AA, Eisenberg RL. Anterior mediastinal masses. AJR. 2014;203:W128–38. 3. Wang ZJ, Reddy GP, Gotway MB, et al. CT and MR imaging of pericardial disease. Radiographics. 2003;23:S167–80.

Diaphragm

20

The two hemidiaphragms separate the thoracic and abdominal cavities. At times, a small basilar pneumonia or pleural effusion may not be seen on the frontal view and only can be visualized as silhouetting one hemidiaphragmatic contour on the lateral view. To determine which hemidiaphragm is involved, the classic teaching is that the right hemidiaphragm is usually higher and visible for its entire length from front to back, whereas the left hemidiaphragm disappears anteriorly where it abuts the heart. However, the left hemidiaphragm is higher in up to 10% of cases. If two sets of ribs are clearly visible posteriorly on the lateral view, it is easy to distinguish between the two hemidiaphragms. Virtually always, the technologist obtains a standard left lateral view, with the cassette touching the left side of the patient so as to decrease magnification of the heart. This means that the right ribs (farther from the cassette) will be magnified and thus appear larger (big rib sign; Fig. 20.1) and also displaced posteriorly. Consequently, the hemidiaphragm that extends to the larger ribs is always on the right.

Electronic Supplementary Material The online version of this chapter (https://doi.org/10.1007/978-3-030-16826-1_20) contains supplementary material, which is available to authorized users. © Springer Nature Switzerland AG 2020 R. L. Eisenberg, What Radiology Residents Need to Know: Chest Radiology, https://doi.org/10.1007/978-3-030-16826-1_20

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Fig. 20.1  Big rib sign. (a) Lateral view shows that the magnified right ribs appear larger and are projected more posteriorly (black arrows) when compared with the smaller and more anterior left ribs (white arrow). Note that the lower thoracic vertebrae appear whiter than those above, the opposite of the normal pattern (spine sign), indicating an abnormality at the base. The hemidiaphragm extending to the larger ribs (right) is sharply seen, unlike the other hemidiaphragm (left) that is not well visualized posteriorly. Therefore, the spine sign should be resulting from an abnormality at the left base. (b) Frontal view confirms the left basilar abnormality, representing a combination of pleural fluid and underlying volume loss in the lower lung

Eventration

273

Eventration (Fig. 20.2; See Fig. e20.1) (All electronic images (Figs. e20.1–e20.4) can be found on this chapter’s website on SpringerLink: https://doi.org/10.1007/978-3-030-16826-1_20) • Congenital elevation of a portion of the hemidiaphragm due to a thin and weakened membranous sheet replacing a portion of the normal diaphragmatic muscle • Usually involves only the anteromedial portion of the right hemidiaphragm, through which a portion of the right lobe of the liver bulges (unlike paralysis or weakness of the hemidiaphragm, which generally affects the entire muscle uniformly) • In a posterior eventration, upward displacement of the kidney can produce a rounded mass • Frontal view may show a “double diaphragm” appearance, which can be confirmed as an eventration on the lateral projection • No clinical significance

Fig. 20.2  Partial eventration. Elevation of the central portion of the right hemidiaphragm (arrow) [1]

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20 Diaphragm

Phrenic Nerve Paralysis (Fig. 20.3; See Fig. e20.2) • Causes of phrenic nerve paralysis include: ○○ Process interfering with the normal function of the phrenic nerve (inadvertent surgical transaction, primary bronchogenic carcinoma, or mediastinal metastases) ○○ Intrinsic neurologic disease (poliomyelitis, Erb’s palsy, peripheral neuritis, hemiplegia) ○○ Injury to the phrenic nerve, thoracic cage, cervical spine, or brachial plexus ○○ Pressure from a substernal thyroid or aneurysm ○○ Lung or mediastinal infection (paralysis may be temporary) Imaging • Unilateral (infrequently bilateral) diaphragmatic elevation with characteristic paradoxical motion of the affected hemidiaphragm (tends to ascend rather than descend with inspiration and the fluoroscopic “sniff test”)

a

b

Fig. 20.3  Phrenic nerve palsy. (a, b) Images in two separate patients show paralysis of the elevated right hemidiaphragm due to a primary bronchogenic carcinoma (arrows) involving the phrenic nerve (a From Ref. [1]; b From Ref. [2])

Traumatic Rupture of Hemidiaphragm

275

 raumatic Rupture of Hemidiaphragm (Figs. 20.4 and T 20.5; See Fig. e20.3) • Uncommon, but serious, complication of blunt and penetrating trauma that predominantly occurs in young men • Much more frequent on the left (ascribed to either the protective effect of the liver on the right hemidiaphragm or relative weakness of the left hemidiaphragm) • Initial chest radiograph is nondiagnostic in up to 50% of cases • Rapid diagnosis is necessary to prevent such serious complications as bowel obstruction and strangulation • Congenital diaphragmatic hernia typically occurs on the left (see Fig. e20.4)

Fig. 20.4  Left diaphragmatic rupture (motor vehicle accident). Initial radiograph shows intrathoracic herniation of the stomach (S), a pleural effusion, a pulmonary contusion, and contralateral mediastinal shift [3]

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20 Diaphragm

Fig. 20.5  Left diaphragmatic tear. Sagittal CT demonstrates a large defect (arrows) with herniation of the stomach (∗) into the thorax [4]

Imaging • CT ○○ Multiplanar imaging and speed of acquisition make this the preferred modality to directly demonstrate a defect or discontinuity of the hemidiaphragm in the setting of acute trauma • Radiographs – indirect signs of left hemidiaphragm injury ○○ Nasogastric tube coiled in the thorax above the left hemidiaphragm ○○ Presence of gas-filled stomach or bowel in the thorax ○○ Apparently elevated hemidiaphragm with an unusual contour (loss of normal dome shape) ○○ Changing hemidiaphragm levels on serial radiographs ○○ Shift of the mediastinum to the right

Diaphragmatic Herniation • • • •

Hiatal – see page 219 Paraesophageal Morgagni – see page 216 Bochdalek – see page 219

References

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Juxtaphrenic Peak (Fig. 20.6) • Peak arising from the medial part of the hemidiaphragm, most commonly caused by traction from the accessory oblique fissure in patients with volume loss in the upper lobe related to collapse or lobectomy

a

b

Fig. 20.6  Juxtaphrenic peak. (a) Preoperative radiograph shows that the right hemidiaphragm has a normal appearance. (b) After right upper lobectomy, the patient developed a classic juxtaphrenic peak (arrow)

References 1. Eisenberg RL.  Clinical Imaging: An Atlas of Differential Diagnosis. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins; 2010. 2. Nason LK, Walker CM, McNeeley MF, et  al. Imaging of the diaphragm: anatomy and function. Radiographics. 2012;32:E51–70. 3. Iochum S, Ludig WF, et al. Imaging of diaphragmatic injury: a diagnostic challenge? Radiographics. 2002;22:S103–18. 4. Kaewlai R, Avery LL, Asrani AV, Novelline RA. Multidetector CT of blunt thoracic trauma. Radiographics. 2008;28:1555–70.

Esophagus

21

Achalasia • Functional obstruction of the distal esophagus with proximal dilatation caused by incomplete relaxation of the lower esophageal sphincter, related to a paucity or absence of ganglion cells in the myenteric plexuses (Auerbach) of the distal esophageal wall • A similar appearance (secondary achalasia) may be produced by any generalized or localized interruption of the reflex arc controlling normal esophageal motility: ○○ Diseases of the medullary nuclei ○○ Abnormality of the vagus nerve ○○ Destruction of myenteric ganglion cells by inflammatory disease (e.g., trypanosomes in Chagas disease) or by carcinoma of the distal esophagus or the gastric cardia • Patients with classic achalasia are typically aged 20–40 and present with dysphagia for solids and liquids, nocturnal regurgitation of undigested food, and aspiration (recurrent pneumonia) • Similar imaging appearance on chest radiographs may be caused by other esophageal motility disorders and surgical bypass procedures for esophageal cancer (gastric pull-through/colonic interposition)

Electronic Supplementary Material The online version of this chapter (https://doi.org/10.1007/978-3-030-16826-1_21) contains supplementary material, which is available to authorized users. © Springer Nature Switzerland AG 2020 R. L. Eisenberg, What Radiology Residents Need to Know: Chest Radiology, https://doi.org/10.1007/978-3-030-16826-1_21

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Imaging • Dilatation and tortuosity of the esophagus can produce a widened mediastinum (double contour) (Fig. 21.1) • Often an air-fluid level in the retrotracheal region, which on the frontal view projects to the right side adjacent to the cardiac shadow (see Fig. e21.1a) (All electronic images (Figs. e21.1–e21.7) can be found on this chapter’s website on SpringerLink: https://doi.org/10.1007/​ 978-3-030-16826-1_21) • Anterior bowing of the trachea (see Fig. e21.1b) • Small or absent gastric air bubble • Esophagram – characteristic smoothly tapered, conical narrowing of the distal esophagus (beak sign) (Fig. 21.2) • CT – filling of the dilated esophagus with food (see Figs. e21.2 and e21.3)

a

b

Fig. 21.1  Achalasia. (a) The margin of the dilated, tortuous esophagus (arrows) parallels the right border of the heart. (Courtesy of James Heilman, MD, Vancouver, Canada). (b) In another patient, a lateral view shows dramatic dilatation of the esophagus (arrows) [1]

Boerhaave Syndrome

281

Fig. 21.2  Achalasia. Beak sign (arrow) [1]

Boerhaave Syndrome • Transmural perforation of the distal esophagus (relatively unsupported by connective tissue), which is related to severe vomiting that produces a sudden increase in intraluminal pressure • Most frequently occurs in males and usually follows heavy drinking and a large meal • The tear is classically vertical and involves the posterolateral wall of the esophagus • Patients usually present with sudden retrosternal or epigastric pain, which often radiates to the neck or shoulder blades and is associated with fever and leukocytosis • Frequently misdiagnosed as myocardial infarction, aortic dissection, pulmonary embolism, pancreatitis, or perforated peptic ulcer • High morbidity and mortality (70%) if there is a delay of more than 24 hours in making the diagnosis and instituting appropriate treatment (intravenous volume resuscitation, broad-spectrum antibiotics, and generally prompt surgical intervention)

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Fig. 21.3  Boerhaave syndrome. Pneumomediastinum along the outer margin of the descending thoracic aorta (white arrows) and extending into the soft tissues of the neck (black arrows). (https://commons.wikimedia.org/wiki/ File:CXR_Pneumomediastinum.jpg to410/Wikimedia)

Imaging • Pneumomediastinum that surrounds the aorta and extends into the soft tissues of the neck (Fig. 21.3; see Fig. e21.4) • Characteristic V-shaped appearance of gas, which corresponds to the fascial planes of the mediastinal and diaphragmatic pleuras in the region of the lower esophagus (see Fig. e21.5) • Diffuse mediastinal widening and left hydropneumothorax • If untreated, late complications may include abscess formation and fistulas to the tracheobronchial tree and pleural spaces • Esophagram  – water-soluble contrast demonstrates extravasation through the transmural perforation (though false negatives occur in about 10% of cases) (Fig. 21.4; see Fig. e21.6)

Foreign Body • If large enough, a foreign body may become impacted in the esophagus, predominantly in the cervical region (at or just about the level of the thoracic inlet) or proximal to an esophageal stricture

Foreign Body

283

Fig. 21.4  Boerhaave syndrome. Esophagram with water-soluble contrast shows substantial extravasation (white arrow) through the transmural perforation of the esophagus (black arrow). (Courtesy of Gillian Lieberman, MD, Boston)

• Sharp swallowed objects that transiently lodge in the esophagus can abrade the esophageal mucosa, so that patient symptoms can persist long after the foreign material has passed (until the mucosal abrasion has healed) Imaging (Fig. 21.5; see Fig. e21.7) • Radiographs easily demonstrate metallic objects (pins, coins, small toys) that are frequently swallowed by infants and young children • Two views are always necessary to make certain the dense object projected over the esophagus that truly lies within it • Nonopaque objects made of wood or aluminum (and some light alloys) are usually impossible to detect radiographically because the density of these structures is almost equal to that of soft tissue

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21 Esophagus

a

b

Fig. 21.5  Foreign body. (a) Frontal and (b) lateral views of a child show a coin lodged in the esophagus. (Courtesy of Edward Lee, MD, Boston, MA)

References 1. Eisenberg RL, Johnson NM, editors. Comprehensive Radiographic Pathology. 6th ed. St Louis: Elsevier/Mosby; 2016. 2. Franquet T, Erasmus JJ, Giménez A, et al. The retrotracheal space: normal anatomic and pathologic appearances. Radiographics. 2002;22:S231–46. 3. Eisenberg RL.  Clinical Imaging: An Atlas of Differential Diagnosis. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins; 2010.

Abnormal Air

22

Pneumothorax • Air in the pleural space that produces volume loss in the ipsilateral lung Common causes • Spontaneous (rupture of a small, usually apical bleb, especially in tall, asthenic individuals) (Fig. 22.1) • Trauma (penetrating or blunt, rib fracture, tracheobronchial injury) • Complication of mechanical ventilation (barotrauma) • Chronic obstructive pulmonary disease • Chronic pulmonary disease (e.g., sarcoidosis, Langerhans cell histiocytosis) • Pneumocystis jiroveci pneumonia (formerly Pneumocystis carinii) and other infections (see Figs. e22.1 and e22.2) (All electronic images (Figs. e22.1–e22.11) can be found on this chapter’s website on SpringerLink: https://doi.org/10.1007/​ 978-3-030-16826-1_22) • Lung abscess with bronchopleural fistula • Rupture of the esophagus (Boerhaave syndrome) Electronic Supplementary Material The online version of this chapter (https://doi.org/10.1007/978-3-030-16826-1_22) contains supplementary material, which is available to authorized users. © Springer Nature Switzerland AG 2020 R. L. Eisenberg, What Radiology Residents Need to Know: Chest Radiology, https://doi.org/10.1007/978-3-030-16826-1_22

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a

22  Abnormal Air

b

Fig. 22.1  Spontaneous pneumothorax. Complete collapse of the right (a) and left (b) lungs in two different patients [1]

• Iatrogenic (surgery, lung or pleural biopsy, thoracentesis, central line placement) (see Figs. e22.3 and e22.4) Imaging • Most commonly apical and lateral air without peripheral lung markings, which parallels the curvature of the lateral chest wall and is separated from normal lung by a sharp pleural margin (Fig. 22.2) • Accentuated on expiration views, as the volume of the normal lung decreases and gas fills the pleural space (see Fig. e22.5) • Supine view: ○○ Deep sulcus sign – air in the pleural space predominantly collects in the anteromedial and subpulmonic portions of the chest and may produce an unusually deep and lucent costophrenic sulcus or upper abdomen (may be the only finding on supine radiographs); highly specific, though not sensitive (Fig.  22.3; see Fig. e22.6) ○○ Pneumothorax also may cause an unusually sharp outline of the cardiac and mediastinal contours (because of adjacent free air rather than aerated lung), or air may accumulate in a subpulmonic location to produce a sharply defined hemidiaphragm

Pneumothorax

287

Fig. 22.2  Small pneumothorax. Collection of air in the left apex and along the left lateral chest wall. The pleural line (arrows) is somewhat difficult to visualize on this image. (Courtesy of Jeffrey Klein, MD, Burlington, VT)

Fig. 22.3  Pneumothorax. Deep sulcus sign on the left (arrows) representing an anterior pneumothorax in a supine patient

288

a

22  Abnormal Air

b

Fig. 22.4  Hydropneumothorax. (a, b) Multiple air-fluid levels (black arrows) in the right hemithorax representing areas of loculated pneumothorax related to bronchopleural fistula. The large right superior mediastinal mass (white arrow) reflects metastatic spread from a previously resected carcinoma of the right lung [1]

• Hydropneumothorax – presence of an air-fluid level in the pleural space on an upright view (Fig. 22.4) • Selective resorption of pleural fluid can result in a loculated pneumothorax (see Fig. e22.7) • Size of pneumothorax – in general, if the distance between the lung margin and the apex of the chest wall is 2 cm) • Note that the decision whether to insert a chest tube is primarily based on the clinical status of the patient

Mimics of Pneumothorax • Apparent pleural line simulating pneumothorax • Skin fold (relatively unsharp and thicker band of opacity rather than the thin white line of visceral pleura) (Fig. 22.5a–c) • Monitoring or support lines (Fig. 22.5d) • Medial margin of the scapula • Bullous emphysema (margin of a large cyst may simulate a pleural line, and CT may be necessary to make this distinction)

Mimics of Pneumothorax

289

b a

c

d

Fig. 22.5  Skin fold. (a) Curvilinear line (arrows) mimicking a right pneumothorax. (b) Image obtained 1 minute later shows that there is no pneumothorax, indicating that the previous finding represented only a skin fold. (c) Prominent skin fold on the left (white arrows) mimics a pneumothorax in a patient who has a small right pneumothorax (black arrow) after a biopsy. The opaque area medial to the pneumothorax represents post-procedure hemorrhage. (d) Outer margin of a chest tube mimics a left pneumothorax (arrows). (c, Courtesy of Ritu Gill, MD, Boston)

290

22  Abnormal Air

Tension Pneumothorax • Medical emergency, in which there is shift of mediastinal structures to the contralateral side • Continually increasing intrathoracic pressure may compromise venous return to the heart and lead to cardiopulmonary collapse (Fig. 22.6) • Note that there may be complete collapse of a lung without any midline shift to suggest tension (Fig. 22.7)

Fig. 22.6  Tension pneumothorax. Substantial collapse of the right lung (white arrows) with shift of the mediastinum to the contralateral side. Black arrow points to a malpositioned endotracheal tube in the right main bronchus, with early volume loss in the left lower lung

Fig. 22.7  Total pneumothorax. Complete collapse of the right lung, without any midline shift to suggest tension

Pneumomediastinum

291

Pulmonary Interstitial Emphysema (See Fig. e22.8) • Alveolar rupture due to increased pressure/volume, which primarily develops in patients with assisted mechanical ventilation and often is not visible on radiographs • Cystic or linear lucencies in the affected segment (best seen on CT), which may be hyperexpanded • Substantial increase in intrathoracic pressure may cause the heart to become smaller and decrease venous return • Tracking of air (Fig. 22.8): ○○ Backward along the perivascular connective tissue to the hilum – may produce pneumomediastinum and then extend into the neck and subcutaneous tissues of the chest and abdominal wall ○○ If near a pleural surface, may extend outward and cause a pneumothorax

Fig. 22.8  Pulmonary interstitial emphysema. After intubation and positivepressure ventilation in a child with hydrocarbon poisoning, there is the development of a pneumomediastinum (white arrows) and small right pneumothorax (black arrow). Note that the stiffness of the lungs has prevented substantial collapse [1]

Pneumomediastinum • Air within the mediastinum

292

22  Abnormal Air

Causes of air within the mediastinum • Extension of pulmonary interstitial emphysema (in about one of three patients) • Trauma ○○ Chest wall  – closed chest trauma causing abrupt increase in intrathoracic pressure ○○ Esophagus – most frequently occurs during episodes of severe vomiting (Boerhaave syndrome), with the tear typically involving the posterolateral wall of the lower portion of the esophagus (relatively unsupported by connective tissue) ○○ Bronchi/trachea – caused by shearing force or a sudden increase in pressure against a closed glottis • Iatrogenic – surgery or instrumentation of the esophagus, trachea, bronchi, or neck; overinflation during anesthesia and respiratory therapy • Extension of gas from the neck or retroperitoneum – trauma, surgical procedures, or penetrating cervical lesions • Asthma – primarily in children

Fig. 22.9  Pneumomediastinum. The mediastinal pleura is displaced laterally and appears as a long linear opacity (arrows) parallel to the heart border but separated from it by air [3]

Pneumopericardium

a

293

b

Fig. 22.10  Severe pneumomediastinum. (a, b) Large amounts of mediastinal air (white arrow) along with extensive subcutaneous air, both anteriorly and laterally (black arrows)

Images • Linear, streak-like lucencies surrounding mediastinal structures (Figs. 22.9, 22.10; see Figs. e22.9 and e22.10) ○○ Most commonly parallel to the left heart border or outlining the great vessels, aorta, SVC, or carotid arteries ○○ Parallel to the spine in the upper thorax and extending to the neck to surround the esophagus and trachea ○○ Continuous diaphragm sign (between the base of the heart and diaphragm) • If there is a small collection of gas adjacent to the heart border and the precise diagnosis is in doubt, a decubitus view can be performed (pneumomediastinum will not shift in position, whereas pneumothorax and pneumopericardium do)

Pneumopericardium • Air surrounding the heart, which usually develops from cardiac surgery or penetrating trauma Images (Fig. 22.11, see Fig. e22.11) • Continuous band of lucency surrounding the heart • To distinguish from pneumomediastinum, pneumopericardium does not extend beyond the root of the great vessels at the level of the main pulmonary artery (upper limit of the parietal pericardial layer)

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Fig. 22.11  Pneumopericardium. Gas filling the pericardial sac causes cardiac tamponade. This newborn with respiratory distress syndrome developed pneumopericardium associated with barotrauma from mechanical ventilation [4]

Subcutaneous Emphysema • Dissection of air into the soft tissues of the chest wall, which can extend upward into the neck and downward into the upper abdominal wall • Usually related to a thoracotomy drainage tube or penetrating chest wall injury (including surgery) Images (Fig. 22.12) • Streaks of air outlining muscle bundles produce a striated appearance along the chest wall • Involvement of the pectoral muscles causes streaks projected across the chest, making it difficult to evaluate the underlying lung • No clinical significance and typically resolves within a few days • Progressive increase in subcutaneous emphysema after thoracic surgery is worrisome for bronchial leak

References

295

Fig. 22.12  Subcutaneous emphysema. Streaks and bubbles of subcutaneous air (black arrows) are evident in the soft tissues along the lateral borders of the thorax, especially on the right. Broad lucencies outlining pectoral muscle bundles (open arrows) overlie the anterior chest wall. Note the fracture of the left scapula (white closed arrow) and multiple rib fractures [3]

References 1. Eisenberg RL.  Clinical Imaging: An Atlas of Differential Diagnosis. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins; 2010. 2. Agrons GA, Courtney SE, Stocker JT, Markowitz RI.  Lung disease in premature neonates: radiologic-pathologic correlation. Radiographics. 2005;25:1047–73. 3. Eisenberg RL, Johnson NM, editors. Comprehensive Radiographic Pathology. 6th ed. St. Louis: Elsevier/Mosby; 2016. 4. Restropo CS, Lemos DF, Lemos JA, et al. Imaging findings in cardiac tamponade with emphasis on CT. Radiograpics. 2007;27:1595–610.

Abnormalities Outside the Thorax

23

Although the vast majority of abnormalities on chest radiographs and CT scans involve the heart and lungs, it is important to also examine all other areas on the images. The following are examples of the broad spectrum of pathology outside the heart and lungs that may be evident on chest examinations.

Mass Impressing/Displacing the Lower Cervical Trachea (Fig. 23.1) • Most commonly a thyroid adenoma or goiter (95% benign and of no clinical significance) • Usually detected as an incidental finding on a frontal chest radiograph (confirmation can be made clinically by palpation of the neck) • Peripheral rim of calcification suggests a benign lesion (adenoma) • Ultrasound, CT, or radionuclide studies can indicate the precise nature of the mass

Electronic Supplementary Material The online version of this chapter (https://doi.org/10.1007/978-3-030-16826-1_23) contains supplementary material, which is available to authorized users. © Springer Nature Switzerland AG 2020 R. L. Eisenberg, What Radiology Residents Need to Know: Chest Radiology, https://doi.org/10.1007/978-3-030-16826-1_23

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23  Abnormalities Outside the Thorax

298

a

b Fig. 23.1  Thyroid goiter. (a) Right thyroid mass (arrows) impresses the lower cervical trachea and displaces it to the left. (b) Left thyroid mass impresses the trachea (arrow)

Cervical Rib (See Fig. e23.1) (All electronic images (Figs. e23.1–e23.22) can be found on this chapter’s website on SpringerLink: https://doi.org/10.1007/​ 978-3-030-16826-1_23)

Gastrointestinal Abnormalities

299

• Extra rib arising from the seventh cervical vertebra (less than 0.5% of the population) • Usually of no clinical significance and discovered incidentally • Pressure on underlying vessels and nerves can cause thoracic outlet syndrome

Gastrointestinal Abnormalities • Enlarged spleen – soft-tissue mass in the left upper abdomen causing medial displacement of the stomach (Fig. 23.2) • Gallstones – characteristic opacifications in the right upper quadrant of the abdomen (see Fig. e23.2)

a

b

Fig. 23.2  Splenomegaly. (a) Marked medial displacement of the gastric air shadow (arrows), consistent with enlargement of the spleen. (b) CT confirms the presence of a huge spleen in this patient with cirrhosis

300

23  Abnormalities Outside the Thorax

Fig. 23.3  Gastric outlet obstruction. Severe dilatation of the gas-filled stomach (arrows)

• • • • •

Dilated stomach (Fig. 23.3) Gastric pull-through following esophagectomy (Fig. 23.4) Pseudopolyposis in ulcerative colitis (see Fig. e23.3) Opaque foreign body (Fig. 23.5; see Fig. e23.4) Chilaiditi syndrome (Fig. 23.6) ○○ Interposition of the colon between the liver and right hemidiaphragm ○○ Demonstration of haustra eliminates the possibility that the air density is due to pneumoperitoneum

Pneumoperitoneum (Figs. 23.7–23.9; See Figs. e23.5–e23.8) • Characteristic curvilinear collection of air beneath one or both hemidiaphragms • Double wall (Rigler) sign on supine view, caused by peritoneal gas outlining both the inner mucosal and outer serosal margins of the bowel wall (the latter normally obscured by adjacent mesentery)

Pneumoperitoneum

301

Fig. 23.4  Gastric pull-through following esophagectomy (arrows)

Fig. 23.5  Foreign body. Retention of a swallowed dental crown (arrow) in a gastric fundal diverticulum

• Supine view (no air-fluid level in the gastric fundus) can confirm pneumoperitoneum, but not exclude it • If there is strong clinical suspicion of free intraperitoneal gas, the report should indicate that an upright image or CT is needed to eliminate the possibility of pneumoperitoneum

302

23  Abnormalities Outside the Thorax

Fig. 23.6  Chilaiditi syndrome. Interposition of colon (arrows) between the liver and hemidiaphragm. Note the haustral markings within the dilated colon

Fig. 23.7  Pneumoperitoneum. Gas accumulating beneath the dome of the right hemidiaphragm appears as a sickle-shaped lucency (arrow) on this erect chest radiograph

Pneumoperitoneum

303

Fig. 23.8  Rigler sign of pneumoperitoneum. The white arrow points to the outer wall of the stomach, which is seen because there is air both within the stomach and outside it (a massive pneumoperitoneum). The patient suffered an esophageal perforation during a dilation procedure. There is extensive subcutaneous gas in the right lower neck (black arrow) and a small medial pneumothorax (gray arrow)

Fig. 23.9  Massive pneumoperitoneum (black arrows). This developed following insertion of a PEG tube (white arrow)

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23  Abnormalities Outside the Thorax

• If pneumoperitoneum is detected, it is essential to check whether the patient has undergone recent surgery, peritoneal dialysis, or insertion of a percutaneous endoscopic gastrostomy (PEG) tube; if not, must worry about a perforated viscus

Injuries to the Bones of the Thorax • Ribs (Fig. 23.10) ○○ On frontal radiographs, rib fractures are only seen when they are displaced

a

b

Fig. 23.10  Rib fracture. (a) Displaced right rib fracture (arrow) (Courtesy of Jim Wu, MD, Boston). (b) CT image in another patient shows a displaced left posterior rib fracture (arrow) with a subpleural hematoma (arrowheads) [2]

Injuries to the Bones of the Thorax

305

○○ In patients from the emergency room, artifacts from a trauma board make it even more difficult to detect a rib fracture ○○ If there is a strong clinical suspicion of rib fracture, dedicated oblique views can be obtained ○○ Always check for an associated pneumothorax or visceral injury, which are serious complications of rib fracture (much better demonstrated on CT) ○○ Flail chest (Fig. 23.11; see Figs. e23.9 and e23.10) • Three or more contiguous rib fractures that are segmental (fractures in two or more places) • This disrupts the normal respiratory mechanics of the chest wall and leads to inadequate ventilation of the underlying lung • Prompt identification of a flail chest is critical, and open reduction and internal plate fixation of the rib fractures appear to speed the recovery process

Fig. 23.11  Flail chest. Note the associated right-­sided pulmonary contusion and subcutaneous emphysema (https://commons.wikimedia.org/wiki/File: Pulmonary_contusion.jpg)

306

23  Abnormalities Outside the Thorax

• Sternum and clavicle (Figs.  23.12 and 23.13; see Figs. e23.11– e23.13) ○○ Radiographs are notoriously poor for detecting nondisplaced sternal fractures ○○ Lateral view may demonstrate a displaced fracture ○○ If there is strong clinical suspicion for a radiographically occult sternal fracture, CT is far more sensitive for making the diagnosis ○○ Clavicular fractures are easily demonstrated on radiographs

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Fig. 23.12  Sternal fracture. (a) On the lateral radiograph, the fracture (arrow) is very difficult to see. (b) Corresponding sagittal CT image clearly shows the fracture (arrow). (Courtesy of Jennifer Ni Muircheartaigh, MD, Boston)

Injuries to the Bones of the Thorax

a

307

b

Fig. 23.13  Clavicle fracture. (a) Frontal radiograph and (b) coned mage show a comminuted fracture of the midshaft of the clavicle (arrow). (Courtesy of Jeffrey Klein, MD, Burlington, VT)

○○ Acromioclavicular (AC) dislocation: • Widening of the AC joint ○○ Normal distance is 5–8 mm ○○ Concerning if >2–4 mm asymmetry when compared to the contralateral side • >5  mm asymmetry of coracoclavicular distance (normal, 10–13 mm) • Superior displacement of the clavicle (normally, the undersurfaces of the clavicle and acromion are at the same level, though mild clavicular elevation can be normal) • If there is a strong clinical suspicion of AC separation, stress views with weight-bearing can be performed ○○ The sternoclavicular articulation is difficult to assess on radiographs, and CT is far more sensitive for detecting fractures and dislocations in this region • Thoracic spine (Fig. 23.14) ○○ Radiographic signs: • Loss of vertebral body height (usually anterior wedge compression fracture) • Displaced paraspinal line (reflecting bleeding in the paravertebral space) • Widened interpedicular distance • Absence of a pedicle ○○ Often fractures of multiple vertebral bodies (frequently noncontiguous)

308

a

23  Abnormalities Outside the Thorax

b

Fig. 23.14  Spinal fracture. (a) Compression fracture of a lower dorsal vertebral body. (b) CT image shows loss of height of a mid-thoracic vertebral body (arrow) with mild retropulsion. Note the vertical striations in the vertebral body above it, characteristic of a hemangioma (of no clinical significance). (Courtesy of Jim Wu, MD, Boston)

○○ Burst fracture – compression fracture of a vertebral body with posteriorly displaced fragment(s) that may injure the spinal cord ○○ CT clearly demonstrates the extent of the fracture and injury to the spinal cord ○○ MRI is the best imaging modality for evaluating the full extent of spinal cord and ligamentous injury ○○ If unclear whether an isolated thoracic spinal collapse represents fracture (post-traumatic or postmenopausal) or metastatic disease, radionuclide bone imaging is the least expensive imaging modality of choice for further work-­up. Although all three conditions will produce increased isotope uptake, the key is to assess for multiple lesions, which strongly suggest metastases. If only the one vertebral fracture shows isotope uptake, MRI can assess the underlying marrow and determine whether the process is benign or malignant

Miscellaneous

309

Miscellaneous • Mastectomy – unilateral absence of a breast shadow (Fig. 23.15) • Bullet fragments – metallic opacities (Fig. 23.16) • Pectus excavatum – can silhouette the right hear border and mimic a middle lobe abnormality (see Fig. e23.14) • Sickle cell disease (see Fig. e23.15) a

b

Fig. 23.15  Mastectomy. Asymmetric loss of the breast shadow on the right (a) and left (b). The arrows point to the normal breast shadows. (Courtesy of Jennifer Ni Muircheartaigh, MD, Boston)

a

b

Fig. 23.16  Bullet fragments. (a) Metallic opacifications overlie the lower left chest (circle). (b) Lateral view shows that the fragments are in the posterior soft tissues (circle)

310

• • • •

23  Abnormalities Outside the Thorax

○○ Localized steplike central depressions of multiple vertebral end plates (“H” vertebrae) due to sludging of red blood cells ○○ Circulatory stasis and ischemic infarcts retard growth in the central portion of the vertebral cartilaginous growth plate (while the periphery of the growth plate, which has a different blood supply, continues to grow at a more normal rate) ○○ Jail bars sign (dense osteosclerosis of ribs, resulting in horizontal bands fancifully likened to bars in a prison window) Sternal dehiscence (see Fig. e23.16) Rugger-jersey spine (Fig. 23.17) Disseminated idiopathic skeletal hyperostosis (DISH) (Fig. 23.18) Malignancy (metastatic or primary) (see Figs. e23.17–e23.19)

Fig. 23.17  Rugger-jersey spine. Alternating regions of lucency and sclerosis in multiple vertebral bodies in this patient with secondary hyperparathyroidism related to chronic renal disease

Miscellaneous

311

Fig. 23.18  DISH. (https://commons.wikimedia.org/wiki/File:Forestier%27s_ disease,_X-ray_of_thoracic_column.jpg)

• Carotid artery calcification (See Fig. e23.20) • Expansile rib lesion – fibrous dysplasia, myeloma • Rotator cuff calcification – homogeneous opacification, often globular and amorphous with poor margins, adjacent to the greater tuberosity of the humerus (see Fig. e23.21a) • Shoulder fracture (see Fig. e23.21b) • Hair/hair band – can produce an artifact in the upper lungs (see Fig. e23.22)

312

23  Abnormalities Outside the Thorax

References 1. Eisenberg RL.  Clinical Imaging: An Atlas of Differential Diagnosis. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins; 2010. 2. Kaewlai R, Avery LL, Asrani AV, Novelline RA. Multidetector CT of blunt thoracic trauma. Radiographics. 2008;28:1555–70. 3. Restropo CS, Martinez S, Lemos DF, et al. Imaging appearances of the sternum and sternoclavicular joints. Radiographics. 2009;29:839–59.

Index

A Abnormal air pneumomediastinum, 291 pneumopericardium, 293–294 pneumothorax, 285–291 pulmonary interstitial emphysema, 291–293 subcutaneous emphysema, 294–295 Achalasia, 222 Acute interstitial pneumonia (AIP), 166–167 Acute radiation pneumonitis, 197 Adult respiratory distress syndrome (ARDS), 101–103 Allergic bronchopulmonary aspergillosis (ABPA), 180–182 Alveolar sarcoidosis, 188 Amiodarone toxicity, 197 Amniotic fluid emboli, 110 Amyloidosis, 201 ANCA-associated granulomatous vasculitis, 126, 191–193 Anterior junction line, 8–9 Aorta acute aortic injury, 247–250 aneurysm, 252–253 ascending thoracic, 216 descending thoracic, 225–226 coarctation, 254–255 dissection, 250–252 pseudoaneurysm, 254 Aorticopulmonary (AP) window, 11 Apical pleural cap, 86 ARDS, 101–103 Asbestosis, 176–177 Automatic implantable cardiac defibrillator (AICD), 38 Azygoesophageal line and recess, 15–16

B Bochdalek hernia, 220–221 Boerhaave syndrome, 281–282 Bronchogenic cyst, 219–220 Bronchopleural fistula (BPF), 243–244 C Carcinoid tumor, 133–135 Cardiac edema vs. noncardiac edema, 98 Cardiothoracic ratio (CTR), 257 Cardiac chamber enlargement left atrium, 259 left ventricle, 257 right atrium, 259 right ventricle, 259 Carotid artery calcification, 311 Cervical rib, 299 Cervicothoracic sign, 207 Chest tube, 40–42 Chylothorax, 91 Coccidioidomycosis, 124 Community-acquired pneumonia (CAP), 56 Crack lung, 182 Cryptogenic organizing pneumonia (COP), 164–166 Cystic fibrosis, 194–195 D Desquamative interstitial pneumonia (DIP), 168–169 Diaphragm eventration, 273–274 herniation, 276 juxtaphrenic peak, 277 phrenic nerve paralysis, 274 traumatic rupture, 275–276 Dobhoff (feeding) tube, 36–39 Drug toxicity, 195–197

© Springer Nature Switzerland AG 2020 R. L. Eisenberg, What Radiology Residents Need to Know: Chest Radiology, https://doi.org/10.1007/978-3-030-16826-1

313

Index

314 E Emphysema alpha-1 antitrypsin deficiency, 158 bullous disease, 157–158 centrilobular, 153–154 congenital lobar, 158–159 panlobular (panacinar), 154–155 paraseptal, 155–157 Endotracheal (ET) tube, 25–27 Enlarged spleen, 299 Epicardial fat pad, 217 Esophagus achalasia, 279–281 Boerhaave syndrome, 281–282 dilatation, 221–222 foreign body, 282–284 neoplasm, 222 varices, 223 Expansile rib lesion, 311 Extramedullary hematopoiesis, 224–225 F Fallen lung sign, 52 Fat embolism syndrome, 110, 111 Fissural pseudotumor, 90 Fissures, 7–8 Fleischner sign, 107 Focal oligemia, 106 Foregut duplication cyst, 221 Foreign body emboli, 110 G Galaxy sign, 187 H Hamartoma, 125 Hampton hump sign, 106 Hemorrhage, 215–216 Hemothorax, 90, 91 Hiatal hernia, 220 High-output failure, 264 Hilum convergence sign, 113 Hilum overlay sign, 9 Histoplasmosis, 124 Hospital-acquired pneumonia (HAP), 57 Hypersensitivity pneumonitis, 177–180 I Intra-aortic balloon pump (IABP), 34

K Kaposi’s sarcoma, 144 L Lipoma, 214–215 Lobar collapse, 46–53 left upper lobe, 50–51 lingula, 48 lower lobe, 48–50 right middle lobe, 48 right upper lobe, 46 total lung, 51–53 Loculated effusion, 89, 90 Lung cancer adenocarcinoma, 127–130 carcinoid tumor, 133–135 large cell carcinoma, 133 metastases, 136 direct spread, 141–142 hematogenous spread, 136–139 Kaposi sarcoma, 144–145 lymphangitic spread, 139–141 lymphoma, 142–144 pancoast (superior sulcus) tumor, 135–136 small cell carcinoma (SCLC), 132–133 squamous cell carcinoma, 130–132 Lymphadenopathy, 218–219 Lymphangioleiomyomatosis (LAM), 188–190 Lymphoid interstitial pneumonia (LIP), 199–200 Lymphoma, 142, 143, 214 M Mass impressing/displacing the lower cervical trachea, 297–299 Mediastinal hemorrhage, 215 Mediastinal lipomatosis, 226 Mediastinal masses anterior mediastinum, 203, 207–218 cervicothoracic sign, 206 diffuse mediastinum, 226–227 middle mediastinum, 203, 218–220 posterior mediastinum, 204–205, 220–226 Mediastinitis acute, 226 fibrosing, 226–227 Meningocele, 224 Mitral annulus calcification, 262 Morgagni hernia, 217–218 Mosaic attenuation, 21–22 Mounier-Kuhn syndrome, 229

Index Myocardial infarction complications, 262–264 Dressler syndrome, 264 pseudoaneurysm, 263 ventricular aneurysm, 262 N Nasogastric/orogastric tube, 35 Neurogenic tumor, 223 Nonspecific interstitial pneumonia (NSIP), 163–164 O Obstructive atelectasis, 45 P Pacemaker, 38 Pancoast tumor, 135–136 Paraspinal lines, 11–14 Pericardial cyst, 216–217 Pericardial disease, 265 calcification, 268–269 constrictive pericarditis, 268 effusion, 265–268 Peripherally inserted central catheters (PICC lines), 28–32 Pleural effusion, 52, 83, 85 causes, 84 chylothorax, 91 fissural pseudotumor, 90 hemothorax, 90, 91 lateral decubitus view, 86 layering, 86 loculated effusion, 89 subpulmonic effusion, 88 supine view, 85 ultrasound, 88 Pleural neoplasms fibrous tumor, 150–151 mesothelioma, 147–149 metastases, 149–150 pleural lipoma, 151–152 Pneumoconioses, 173 Pneumonia, 56–57 aspiration, 60–62 bacterial pneumonia chronic eosinophilic pneumonia, 69 klebsiella, 66–67 Loeffler’s syndrome, 68–69 septic emboli, 67 community-acquired pneumonia, 56 complications, 62–66

315 empyema, 64–66 lung abscess, 63–64 pneumatocele, 62–63 follow-up of, 62 fungal pneumonia, 70–74 actinomycosis, 72 aspergillosis, 70, 72 candidiasis, 72 coccidioidomycosis, 72 histoplasmosis, 72 mucormycosis, 72 pneumocystis jiroveci, 72–73 sporotrichosis, 72 hospital-acquired pneumonia, 57 interstitial pneumonia, 59 lobar pneumonia, 57–58 lobular pneumonia, 58 round pneumonia, 59–60 ventilator-acquired pneumonia, 57 viral pneumonia, 74–75 infectious mononucleosis, 74 tree-in-bud pattern, 75 varicella (chickenpox) pneumonia, 74 Pneumoperitoneum, 300 Port-a-Cath and other tunneled catheters, 32 Posterior junction line, 9 Posterior tracheal stripe, 14–15 Pulmonary alveolar proteinosis, 191 Pulmonary arterial hypertension, 112–114 Pulmonary arteriovenous fistula (AVM), 125 Pulmonary artery hypertension, 113 Pulmonary edema, 5 cardiac, 93–97 neurogenic, 97–101 Pulmonary embolism, 105–109 Pulmonary hemorrhage, 101 Pulmonary Langerhans cell histiocytosis (PLCH), 169–171 Pulmonary veno-occlusive disease, 115 R Radiation-induced lung disease, 197–199 Relaxation (compressive) atelectasis, 44 Respiratory bronchiolitis-interstitial lung disease (RB-ILD), 167–168 Retrosternal stripe, 14 Rheumatoid necrobiotic nodule, 125–126 Rib expansile lesion, 311 fracture, 304 Right paravertebral stripe, 9–11 Rotator cuff calcification, 311 Round atelectasis, 45–46

Index

316 S Saddle embolus, 109 Sarcoidosis, 183–188 Scleroderma, 193–194 Sequestration, 145–146 Shoulder fracture, 312 Silhouette sign, 22 Silicosis, 174–176 Sinus of Valsalva, 216 Solitary pulmonary nodule (SPN), 117 age effect, 117 air bronchogram, 123 calcification, 119 cavitation, 122 clinical risk factors, 118 doubling time, 122 Fleischner criteria, 124 granuloma, 124–125 hamartoma, 125 margins, 118 mimics, 123–124 PET-CT, 123 size effect, 117 Spinal neoplasm, 223–224 Spine (vertebral fade-off) sign, 22–23 Subsegmental/discoid/platelike atelectasis, 43–44 Swan-Ganz catheters, 32

thymoma, 207–210 Thyroid mass, 213–214 Trachea and bronchi amyloidosis, 235 ANCA-associated granulomatous vasculitis, 235 bronchiectasis, 235–241 broncholithiasis, 242–243 bronchopleural fistula, 243–244 foreign body, 244–245 mucoid impaction, 241–242 post-intubation stenosis, 232–235 radiation fibrosis, 235 relapsing polychondritis, 230–231 saber-sheath trachea, 232 sarcoidosis, 235 tracheobronchomegaly, 229–230 tracheomalacia, 231–232 trauma, 245 tuberculosis, 235 Tracheostomy tube, 27 Tree-in-bud pattern, 20–21 Tuberculosis miliary, 80 postprimary (reactivation/active), 78–80 primary, 75–77 Tuberculous osteomyelitis, 223 Tumor emboli, 110

T Teratoma, 211–213 Thorax bone injuries ribs, 304 soft-tissue abnormalities, 309 sternum and clavicle, 306 thoracic spine, 307 Thymus carcinoid, 209 carcinoma, 209–210 cyst, 210–211 hyperplasia, 210

U Usual interstitial pneumonia (UIP), 161–163 V Ventilator-acquired pneumonia (VAP), 57 W Westermark sign, 107