Junzi Shi_ Jacob Mandell_ Ellen X. Sun_ Jacob Mandell - Core radiology _ A Visual Approach To Diagnostic Imaging. 2 Volume Set-Cambridge University Press (2021).pdf

Core Radiology Second Edition Painting by Jacqueline Liu Core Radiology A Visual Approach to Diagnostic Imaging Second Edition Volume 1 and 2 Ellen X. Sun Brigham & Women’s Hospital, Boston, MA Junzi Shi Brigham & Women’s Hospital, Boston, MA Jacob C. Mandell Brigham & Women’s Hospital, Bo...

Core Radiology Second Edition Painting by Jacqueline Liu Core Radiology A Visual Approach to Diagnostic Imaging Second Edition Volume 1 and 2 Ellen X. Sun Brigham & Women’s Hospital, Boston, MA Junzi Shi Brigham & Women’s Hospital, Boston, MA Jacob C. Mandell Brigham & Women’s Hospital, Boston, MA University Printing House, Cambridge CB2 8BS, United Kingdom One Liberty Plaza, 20th Floor, New York, NY 10006, USA 477 Williamstown Road, Port Melbourne, VIC 3207, Australia 314–321, 3rd Floor, Plot 3, Splendor Forum, Jasola District Centre, New Delhi – 110025, India 103 Penang Road, #05–06/07, Visioncrest Commercial, Singapore 238467 Cambridge University Press is part of the University of Cambridge. It furthers the University’s mission by disseminating knowledge in the pursuit of education, learning, and research at the highest international levels of excellence. www.cambridge.org Information on this title: www.cambridge.org/9781108965910 DOI: 9781108966450 © Ellen X. Sun, Junzi Shi, and Jacob C. Mandell 2021 This publication is in copyright. Subject to statutory exception and to the provisions of relevant collective licensing agreements, no reproduction of any part may take place without the written permission of Cambridge University Press. Second edition published 2021 First edition published 2013 Printed in Singapore by Markono Print Media Pte Ltd A catalogue record for this publication is available from the British Library. 2 volume set: SET ISBN 9781108965910 Volume 1: ISBN 9781108984447 Volume 2: ISBN 9781108984454 Cambridge University Press has no responsibility for the persistence or accuracy of URLs for external or third-party internet websites referred to in this publication and does not guarantee that any content on such websites is, or will remain, accurate or appropriate. Every effort has been made in preparing this book to provide accurate and up-to-date information that is in accord with accepted standards and practice at the time of publication. Although case histories are drawn from actual cases, every effort has been made to disguise the identities of the individuals involved. Nevertheless, the authors, editors, and publishers can make no warranties that the information contained herein is totally free from error, not least because clinical standards are constantly changing through research and regulation. The authors, editors, and publishers therefore disclaim all liability for direct or consequential damages resulting from the use of material contained in this book. Readers are strongly advised to pay careful attention to information provided by the manufacturer of any drugs or equipment that they plan to use.  CONTENTS Volume 1 List of contributors vii Acknowledgements x 1 THORACIC IMAGING 1 Khushboo Jhala, Junzi Shi, and Mark M. Hammer 2 GASTROINTESTINAL IMAGING 95 Cory Robinson-Weiss, Fiona E. Malone, Ellen X. Sun, Junzi Shi, Khushboo Jhala, and Shanna A. Matalon 3 GENITOURINARY IMAGING 229 Cory Robinson-Weiss, Madhvi Deol, Fiona E. Malone, Khushboo Jhala, Junzi Shi, Ellen X. Sun, Michael A. Buckner, Jose M. Lopez, Khanant M. Desai, and Daniel Souza 4 OBSTETRICAL IMAGING 324 Ellen X. Sun, Junzi Shi, Robin Perlmutter-Goldenson, and Mary C. Frates 5 BREAST IMAGING 368 Aaron Jen, Ellen X. Sun, and Christine M. Denison 6 NUCLEAR AND MOLECULAR IMAGING 444 Ellen X. Sun, Christopher G. Sakellis, and Hyewon Hyun 7 CARDIAC IMAGING 486 E llen X. Sun, Junzi Shi, Sharmila Dorbala, Ayaz Aghayev, and Michael L. Steigner 8 VASCULAR IMAGING 539 Junzi Shi, Ellen X. Sun, and Ayaz Aghayev 9 INTERVENTIONAL RADIOLOGY 588 Leigh Casadaban, Colette Martin Glaser, Junzi Shi, Ellen X. Sun, Steven Morales-Rivera, Sharath Bhagavatula, Regina Maria Koch, and Timothy P. Killoran  CONTENTS Volume 2 10 NEUROIMAGING: BRAIN 650 Francis Deng, Shruti Mishra, Ellen X. Sun, and Raymond Y. Huang 11 NEUROIMAGING: HEAD AND NECK 753 Francis Deng, Shruti Mishra, Jeffrey P. Guenette, and Raymond Y. Huang 12 SPINE IMAGING 860 Francis Deng, Shruti Mishra, Nityanand Miskin, Ellen X. Sun, Raymond Y. Huang, and Jacob Mandell 13 MUSCULOSKELETAL IMAGING 908 Yuntong Ma, and Jacob Mandell 14 PEDIATRIC IMAGING 1084 Ngoc-Anh T. Tran, Ellen X. Sun, Sanjay P. Prabhu, and Michael P. George 15 IMAGING PHYSICS 1195 Junzi Shi, Ellen X. Sun, and Jacob Mandell Index 1222  full list of references, resources and further reading can be found online at A www.cambridge.org/coreradiology CONTRIBUTORS Ayaz Aghayev, MD Sharmila Dorbala, MD Staff Radiologist, Division of Director of Nuclear Cardiology, Cardiovascular Imaging, Division of Cardiovascular Imaging, Brigham and Women’s Hospital Brigham and Women’s Hospital Instructor of Radiology, Associate Professor of Radiology, Harvard Medical School Harvard Medical School Sharath Bhagavatula, MD Mary C. Frates, MD Staff Radiologist, Abdominal Assistant Director, Division of Ultrasound, Imaging and Intervention, Brigham and Women’s Hospital Brigham and Women’s Hospital Professor of Radiology, Instructor of Radiology, Harvard Medical School Harvard Medical School Michael P. George, MD Michael A. Buckner, MD Staff Pediatric Radiologist, Resident in Radiology, Boston Children’s Hospital Brigham and Women’s Hospital Instructor of Radiology, Harvard Medical School Harvard Medical School Leigh Casadaban, MD MS Colette Martin Glaser, MD Clinical Fellow in Interventional Radiology, Resident in Radiology, University of California, Los Brigham and Women’s Hospital Angeles Medical Center Harvard Medical School David Geffen School of Medicine Robin Perlmutter-Goldenson, MD, MPH Francis Deng, MD Staff Radiologist, Division of Ultrasound, Resident in Radiology, Brigham and Women’s Hospital Massachusetts General Hospital Assistant Professor of Radiology, Harvard Medical School Harvard Medical School Christine M. Denison, MD Jeffrey P. Guenette, MD Staff Radiologist, Division of Breast Imaging, Director of Head and Neck Imaging, Brigham and Women’s Hospital Division of Neuroradiology Assistant Professor of Radiology, Associate Program Director, Diagnostic Harvard Medical School Radiology Residency Brigham and Women’s Hospital Madhvi Deol, MD Assistant Professor of Radiology, Resident in Radiology, Harvard Medical School Brigham and Women’s Hospital Harvard Medical School Mark M. Hammer, MD Thoracic Imaging Fellowship Director, Khanant M. Desai, MD Brigham and Women’s Hospital Clinical Fellow in Interventional Radiology, Assistant Professor of Radiology, University of Virginia Medical Center Harvard Medical School Raymond Y. Huang, MD, PhD Jacob Mandell, MD Assistant Division Chief, Division of Neuroradiology Musculoskeletal Imaging and Intervention Brigham and Women’s Hospital Fellowship Director, Associate Professor of Radiology Brigham and Women’s Hospital Harvard Medical School Assistant Professor of Radiology, Harvard Medical School Hyewon Hyun, MD Program Director, Joint Program in Nuclear Shanna A. Matalon, MD Medicine and Molecular Imaging, Staff Radiologist, Division of Abdominal Brigham and Women’s Hospital Imaging and Intervention, Assistant Professor of Radiology, Associate Program Director, Radiology Residency, Harvard Medical School Brigham and Women’s Hospital Assistant Professor of Radiology, Aaron Jen, MD Harvard Medical School Resident in Radiology, Brigham and Women’s Hospital Shruti Mishra, MD Harvard Medical School Resident in Radiology, Brigham and Women’s Hospital Khushboo Jhala, MD Harvard Medical School Resident in Radiology, Brigham and Women’s Hospital Nityanand Miskin, MD Harvard Medical School Clinical Fellow in Neuroradiology, Timothy P. Killoran, MD Massachusetts General Hospital Integrated and Independent Interventional Harvard Medical School Radiology Residency Director, Steven Morales-Rivera, MD Brigham and Women’s Hospital Resident in Radiology, Assistant Professor of Radiology, Brigham and Women’s Hospital Harvard Medical School Harvard Medical School Regina Maria Koch, MD Sanjay P. Prabhu, MBBS, DCH, FRCR Staff Radiologist, Interventional Radiology, Staff Pediatric Neuroradiologist, Brigham and Women’s Hospital Director, Advanced Image Analysis Lab, Instructor of Radiology, Medical Director, Imaging Informatics Harvard Medical School Boston Children’s Hospital Jose M. Lopez, MD, MBA Assistant Professor of Radiology, Resident in Radiology, Harvard Medical School Brigham and Women’s Hospital Cory Robinson-Weiss, MD Harvard Medical School Clinical Fellow in Abdominal Imaging, Yuntong Ma, MD Massachusetts General Hospital Resident in Radiology, Harvard Medical School Brigham and Women’s Hospital Christopher G. Sakellis, MD Harvard Medical School Staff Radiologist, Division of Nuclear Fiona E. Malone, MD Medicine, Resident in Radiology, Brigham and Women’s Hospital Brigham and Women’s Hospital Assistant Professor of Radiology, Harvard Medical School Harvard Medical School List of contributors Junzi Shi, MD Michael L. Steigner, Clinical Fellow in Musculoskeletal Radiology, Staff Radiologist, Division of Cardiovascular Brigham and Women’s Hospital Imaging, Harvard Medical School Brigham and Women’s Hospital Associate Professor of Radiology, Daniel Souza, MD, MSc Harvard Medical School Fellowship Program Director, Abdominal Imaging and Intervention, Ngoc-Anh T. Tran, MD Brigham and Women’s Hospital Resident in Radiology, Instructor of Radiology, Brigham and Women’s Hospital Harvard Medical School Harvard Medical School Ellen X. Sun, MD Staff Radiologist, Division of Emergency Radiology, Brigham and Women’s Hospital Instructor of Radiology, Harvard Medical School List of contributors ACKNOWLEDGEMENTS Frontispiece painting by Jaqueline Liu Chapter cover page cinematic renderings by Khushboo Jhala  Khushboo Jhala, Junzi Shi, Mark M. Hammer Thoracic Imaging Introductory concepts..............................2 Patterns of lung disease............................8 Pulmonary infection...............................21 Pulmonary edema and ICU imaging........32 Lung cancer............................................34 Pulmonary vascular disease....................46 Diffuse lung disease................................54 Mediastinum..........................................70 Airways..................................................83 Pleura.....................................................92 Chest: 1 Introductory concepts Anatomy Lobar and segmental anatomy apical apical posterior anterior posterior superior lingula right upper lobe left upper lobe anterior inferior lateral lingula right middle lobe bronchus medial intermedius e superior lob superior lef er tl w ow lo ht er rig lo be medial basal medial basal posterior posterior basal basal lateral anterior anterior lateral basal basal basal basal Interlobar fissures The minor fissure separates the right upper lobe (RUL) from the right middle lobe (RML) and is seen on both the frontal and lateral views as a fine horizontal line. The major (oblique) fissures are seen only on the lateral radiograph as oblique lines. However, if they are fluid-filled, the major fissures can be seen on the frontal view as concave curvilinear opacities in the lateral hemithorax. On the right, the major fissure separates the RUL and RML from the right lower lobe. On the left, the major fissure separates the left upper lobe (LUL) from the left lower lobe (LLL). Accessory fissures The azygos fissure is an accessory fissure present in less than 1% of patients, seen in the presence of an azygos lobe. An azygos lobe is an anatomic variant where a portion of the apical right upper lobe is encased in its own parietal and visceral pleura. The superior accessory fissure is seen in approximately 5% of patients and separates the superior and basal segments of the right lower lobe. The inferior accessory fissure is seen in approximately 12% of patients, more commonly in the right lung, and divides the medial basal segment from the other basal segments. The left minor fissure is present in approximately 8% of patients and separates the lingula from the left upper lobe. Chest: 2 Overview of atelectasis Atelectasis is loss of lung volume due to decreased aeration. Atelectasis is synonymous with collapse. Atelectasis may be caused by bronchial obstruction, mucus plugging, or external compression (e.g., by small lung volumes or pleural effusions). Direct signs of atelectasis are from lobar volume loss and include: Displacement of the fissures. Vascular crowding. Plate-like or triangular opacity from the collapsed lung itself. Indirect signs of atelectasis are due to the effect of volume loss on adjacent structures and include: Elevation of the diaphragm. Overinflation of adjacent or contralateral lobes. Rib crowding on the side with volume loss. Hilar displacement. Mediastinal shift to the side with volume loss. Air bronchograms are not seen in atelectasis when the cause of the atelectasis is central bronchial obstruction, but air bronchograms can be seen in atelectasis caused by external compression. Mechanisms of atelectasis Obstructive atelectasis occurs when alveolar gas is absorbed by blood circulating through alveolar capillaries but is not replaced by inspired air due to bronchial obstruction. Obstructive atelectasis can cause lobar atelectasis, which is complete collapse of a lobe, discussed on the following pages. Obstructive atelectasis occurs more quickly when the patient is breathing supplemental oxygen since oxygen is absorbed from the alveoli more rapidly than nitrogen. In children, airway obstruction is most often due to an aspirated foreign object. In contrast to adults, the affected side becomes hyperexpanded in children due to a ball-valve effect. Subsegmental atelectasis is a subtype of obstructive atelectasis commonly seen after surgery or general illness, due to mucus obstruction of the small airways. Relaxation (passive) atelectasis is caused by relaxation of lung adjacent to an intrathoracic lesion causing mass effect, such as a pleural effusion, pneumothorax, or pulmonary mass. Adhesive atelectasis is due to surfactant deficiency. Adhesive atelectasis is seen most commonly in neonatal respiratory distress syndrome, but can also be seen in acute respiratory distress syndrome (ARDS). Cicatricial atelectasis is volume loss from architectural distortion of lung parenchyma by fibrosis. Lobar atelectasis Lobar atelectasis is usually caused by central bronchial obstruction (obstructive atelectasis), which may be secondary to mucus plugging or an obstructing neoplasm. If the lobar atelectasis occurs acutely, mucus plugging is the most likely cause. Mucus plugging is most common in the lower lobes, least common in the left upper lobe. If lobar atelectasis is seen in an outpatient, an obstructing central tumor must be ruled out. Lobar atelectasis, or collapse of an entire lobe, has characteristic appearances depending on which of the five lobes is collapsed, as discussed on the following pages. Chest: 3 Patterns of lobar atelectasis frontal schematic RUL LUL RML LLL RLL right lung left lung lateral schematic RUL LUL RML RLL LLL right lung left lung Illustration showing direction of collapse for each of the five lobes. Chest: 4 Left upper lobe atelectasis Left upper lobe collapse and luftsichel sign: Frontal radiograph (left image) shows veil-like opacity with obscured left cardiac margin, a characteristic finding of left upper lobe collapse on frontal view; note the crescent of air lateral to the aortic arch representing the luftsichel sign (yellow arrow). The lateral view (right image) shows the anterior displacement of the left major fissure and collapsed left upper lobe (red arrows). Key imaging findings include the veil-like opacity on frontal radiograph, anterior displacement of major fissure and anterior collapsed lung on lateral radiograph. The luftsichel (air-sickle in German) sign is a crescent of air seen on the frontal radiograph, which represents the interface between the aorta and the hyperexpanded superior segment of the left lower lobe. However, this sign is not always present. It is important to recognize left upper lobe collapse and not mistake the left lung opacity for pneumonia or pleural effusion, since a mass obstructing the airway may be the cause of the lobar atelectasis. Right upper lobe atelectasis Right upper lobe collapse: Frontal radiograph (left image) shows a right upper lobe opacity with superior displacement of the minor fissure (blue arrow) and a convex mass (Golden S sign; yellow arrow). Lateral radiograph (right image) shows the wedge-shaped collapsed RUL projecting superiorly (red arrows). The reverse S sign of Golden is seen in right upper lobe collapse caused by an obstructing mass. The central convex margins of the mass form a reverse S. Although the sign describes a reverse S, it is also commonly known as the Golden S sign. Similar to left upper lobe collapse, a right upper lobe collapse should raise concern for an underlying malignancy in adults or mucus plugging, particularly common in children. Chest: 5  The juxtaphrenic peak sign is a peridiaphragmatic triangular opacity caused by diaphragmatic traction from an inferior accessory fissure or an inferior pulmonary ligament, seen in upper lobe volume loss from any cause. Left lower lobe atelectasis Left lower lobe collapse: Frontal radiographs demonstrate a triangular retrocardiac opacity representing the collapsed left lower lobe (yellow arrows). Lateral radiograph shows posterior hazy opacity (red arrows). Triangular retrocardiac opacity is the main imaging feature of left lower lobe collapse. The flat waist sign describes the flattening of the left heart border due to posterior shift of hilar structures and resultant cardiac rotation. Right lower lobe atelectasis Right lower lobe collapse: Frontal radiograph shows a triangular opacity at the right lower zone with apex pointing towards the right hilum and obscuration of the medial right hemidiaphragm (blue arrow). Note there is preservation of the right heart border. Lateral radiograph shows a hazy posterior opacity of the collapsed right lower lobe (red arrows). Right lower lobe atelectasis is the mirror-image of left lower lobe atelectasis. Lower lobe collapse is not well-seen on lateral view since the lobes mostly collapse medially. The collapsed lower lobe appears as a triangular retrocardiac opacity. Chest: 6  Right middle lobe atelectasis Right middle lobe atelectasis: Frontal chest radiograph shows an indistinct opacity in the right lung with focal silhouetting of the right heart border (blue arrows). There is elevation of the right hemidiaphragm due to volume loss. The lateral radiograph shows a triangular opacity (red arrow) projecting over the mid-heart representing the collapsed right middle lobe. The findings of right middle lobe atelectasis can be subtle on the frontal radiograph. Silhouetting of the right heart border by the collapsed medial segment of the middle lobe may be the only clue. The lateral radiograph shows a triangular opacity anteriorly. Collapse of both right middle and lower lobes occurs from obstruction of the bronchus intermedius, and it causes obscuration of both the right heart border and right hemidiaphragm, with a linear superior margin directed towards the hilum. Round atelectasis Round atelectasis is focal atelectasis with a round morphology that is always associated with an adjacent pleural abnormality (e.g., pleural effusion, pleural thickening or plaque). Round atelectasis is most common in the posterior lower lobes. All five of the following findings must be present to diagnose round atelectasis: 1) Adjacent pleura must be abnormal. 2) Opacity must be peripheral and in contact with the pleura. Round atelectasis: Noncontrast CT shows a rounded opacity in 3) Opacity must be round or elliptical. the medial right lower lobe (red arrows). This example meets 4) Volume loss must be present in the all five criteria for round atelectasis including adjacent pleural affected lobe. abnormality (effusion), opacity in contact with the pleura, round 5) Pulmonary vessels and bronchi shape, volume loss in the affected lobe, and the comet tail sign leading into the opacity must be (yellow arrows) representing curved vessels and bronchi leading curved — this is the comet tail sign. to the focus of round atelectasis. Chest: 7 Patterns of lung disease Essential anatomy Secondary pulmonary lobule (SPL) acinus, not visible on CT (approximately 12 per secondary lobule) acinar artery and respiratory bronchiole centrilobular bronchus and artery 1 cm 2 cm 3 cm approximate scale pulmonary veins (and lymphatics, not pictured) run in the interlobular septa The secondary pulmonary lobule (SPL) is the elemental unit of lung function. Each SPL contains a central artery (the aptly named centrilobular artery) and a central bronchus, each branching many times to ultimately produce acinar arteries and respiratory bronchioles. On CT, the centrilobular artery is often visible as a faint dot. The centrilobular bronchus is not normally visible. The acinus is the basic unit of gas exchange, containing several generations of branching respiratory bronchioles, alveolar ducts, and alveoli. There are generally 12 or fewer acini per secondary lobule. Pulmonary veins and lymphatics collect in the periphery of each SPL. Connective tissue, called interlobular septa, encases each SPL. Thickening of the interlobular septa can be seen on CT and suggests pathologic enlargement of either the venous or lymphatic spaces, as discussed on subsequent pages. Each SPL is between 1 and 2.5 cm in diameter. Chest: 8 Abnormalities of the secondary pulmonary lobule Consolidation and ground glass Consolidation and ground glass opacification are two very commonly seen patterns of lung disease caused by abnormal alveoli. The alveolar abnormality may represent either filling of the alveoli with fluid or incomplete alveolar aeration. Consolidation can be described on either a chest radiograph or CT, while ground glass is generally reserved for CT. Although consolidation often implies pneumonia, both consolidation and ground glass are nonspecific findings with a broad differential depending on chronicity (acute versus chronic) and distribution (focal versus patchy or diffuse). Consolidation Consolidation: Contrast-enhanced CT shows bilateral consolidative opacities, more densely consolidated on the left. There are bilateral air bronchograms. Although these imaging findings are nonspecific, this was a case of multifocal consolidative adenocarcinoma. Consolidation is histologically due to complete filling of affected alveoli (commonly remembered as blood, pus, water, or cells). Pulmonary vessels are not visible through the consolidation on an unenhanced CT. Air bronchograms are often present if the airway is patent. An air bronchogram represents a lucent air-filled bronchus (or bronchiole) seen within a consolidation. Consolidation causes silhouetting of adjacent structures on conventional radiography. Acute consolidation is most commonly due to pneumonia, but the differential includes: Pneumonia (by far the most common cause of acute consolidation). Aspiration, consolidation may appear heterogeneous from mucus plugging. Pulmonary hemorrhage (primary pulmonary hemorrhage or aspiration of hemorrhage). Adult respiratory distress syndrome (ARDS), which is noncardiogenic pulmonary edema seen in critically ill patients and thought to be due to increased capillary permeability. Pulmonary edema may cause consolidation if severe. The differential diagnosis of chronic consolidation includes: Adenocarcinoma, previously bronchioloalveolar carcinoma Lymphoma. Organizing pneumonia, which is a nonspecific response to injury characterized by granulation polyps which fill the distal airways, producing peripheral rounded and nodular consolidation. Chronic eosinophilic pneumonia, an inflammatory process characterized by eosinophils causing alveolar filling in an upper-lobe distribution. Chest: 9 Ground glass opacification (GGO) Ground glass opacification: Noncontrast CT shows diffuse ground glass opacification (GGO). The pulmonary architecture, including vasculature and bronchi, can be still seen, which is characteristic for GGO. Although these imaging findings are nonspecific, this was a case of acute respiratory distress syndrome (ARDS). Ground glass opacification is histologically due to either partial filling of the alveoli (by blood, pus, water, or cells), alveolar wall thickening, or reduced aeration of alveoli (atelectasis). Ground glass is usually a term reserved for CT. CT shows a hazy, gauze-like opacity, through which pulmonary vessels are still visible. Acute ground glass opacification has a similar differential to acute consolidation, since many of the entities that initially cause partial airspace filling can progress to completely fill the airspaces later in the disease. The differential of acute ground glass includes: Pulmonary edema, which is usually central or dependent. Pneumonia. Unlike consolidation, ground glass is more commonly seen in atypical pneumonia such as viral or Pneumocystis jiroveci pneumonia. Pulmonary hemorrhage, seen as pure ground glass in acute phase, but subacute phase shows peripheral sparing and crazy paving. Adult respiratory distress syndrome (ARDS). Chronic ground glass opacification has a similar but broader differential diagnosis compared to chronic consolidation. In addition to all of the entities which may cause chronic consolidation, the differential diagnosis of chronic ground glass also includes: Lung adenocarcinoma, which can be focal or multifocal. Organizing pneumonia, typically presenting as rounded, peripheral opacities. Chronic eosinophilic pneumonia, usually with an upper-lobe predominance. Interstitial lung disease, including desquamative interstitial pneumonia (DIP), nonspecific interstitial pneumonia (NSIP), and hypersensitivity pneumonitis (HP). Hypersensitivity pneumonitis (HP) is a type III hypersensitivity reaction to inhaled organic antigens. In the subacute phase there is ground glass, centrilobular nodules, and mosaic attenuation. Chest: 10 Peripheral ground glass or consolidation Coronal schematic demonstrates peripheral Axial CT shows peripheral and subpleural ground glass ground glass. attenuation. This was a case of organizing pneumonia. The differential diagnosis for peripheral consolidation or ground glass includes: Organizing pneumonia. Chronic eosinophilic pneumonia, typically with an upper lobe predominance. Pulmonary infarction. Interlobular septal thickening – smooth Schematic demonstrates smooth Smooth interlobular septal thickening: CT demonstrates smooth interlobular septal thickening. thickening of the interlobular septa (arrows) in pulmonary edema. Courtesy Ritu R. Gill, MD, MPH, Brigham and Women’s Hospital. Conditions that dilate the pulmonary veins cause smooth interlobular septal thickening. By far the most common cause of smooth interlobular septal thickening is pulmonary edema; however, the differential diagnosis for smooth interlobular septal thickening is: Pulmonary edema. Lymphangitis carcinomatosis. Chest: 11 Interlobular septal thickening – nodular, irregular, or asymmetric Schematic demonstrates irregular and Axial CT shows a diffuse nodular septal thickening (yellow arrows). nodular interlobular septal thickening. This was a case of lymphangitic carcinomatosis. Nodular, irregular, or asymmetric septal thickening tends to be caused by processes that infiltrate the peripheral lymphatics, most commonly by lymphangitic carcinomatosis and sarcoidosis: Lymphangitic carcinomatosis is tumor spread through the lymphatics. Sarcoidosis rarely causes septal thickening. Crazy paving Schematic demonstrates interlobular Axial CT shows interlobular septal thickening in regions of ground septal thickening and ground glass glass opacification, representing crazy paving. This was a case opacification. of alveolar proteinosis, the entity in which crazy paving was first described. Crazy paving describes interlobular septal thickening with superimposed ground glass opacification, which is thought to resemble the appearance of a stone path. Although nonspecific, this pattern was first described for alveolar proteinosis, where the ground glass opacification is caused by filling of alveoli by proteinaceous material and the interlobular septal thickening is caused by lymphatics taking up the same material. Chest: 12  The differential diagnosis for crazy paving includes: Pulmonary edema, by far the most common cause. Pulmonary hemorrhage. Acute respiratory distress syndrome. Pulmonary alveolar proteinosis (PAP), an idiopathic disease characterized by alveolar filling by a proteinaceous substance. PAP is almost always seen with a crazy paving pattern. Pneumocystis jiroveci pneumonia. Adenocarcinoma, uncommon cause Lipoid pneumonia, an inflammatory pneumonia caused by reaction to aspirated lipids, uncommon cause. Approach to multiple micronodules Tree-in-Bud Centrilobular Perilymphatic Random (Form of centrilobular) Viral pneumonia Infectious bronchiolitis: Sarcoidosis Hematogenous metastases Hypersensitivity pneumonitis Mycobacterial infections Pneumoconiosis Disseminated mycobacteria Aspiration Viral infections Lymphangitic carcinomatosis Disseminated fungal infections Pulmonary capillary hemangiomatosis Bacterial pneumonia Metastatic calcification Aspiration Occasionally, pulmonary edema Rarely, lymphangitic carcinomatosis and vascular abnormalities (endovascular metastases and pulmonary arterial aneurysms) Table for Micronodular Patterns. KB pg14 Micronodules No subpleural nodules Subpleural nodules Peribronchial nodules, Uniform non-uniform distribution distribution Centrilobular Perilymphatic Random aspiration sarcoid/silicosis metastases inflammatory (HP, RB) lymphangitic carcinomatosis infection (miliary TB, fungal) infection (viral, mycobacterial) Chest: 13 Centrilobular nodules Schematic demonstrates a centrilobular Axial CT demonstrates diffuse faint centrilobular opacities (arrows), nodule, located at the center of the none of which extend to the pleural surface, which is typical of a pulmonary lobule. centrilobular distribution. This was a case of pulmonary capillary hemangiomatosis. Centrilobular nodules represent opacification of and around the centrilobular bronchiole (or less commonly the centrilobular artery) at the center of each secondary pulmonary lobule. On CT, multiple small nodules are seen in the centers of secondary pulmonary lobules. Centrilobular nodules never extend to the pleural surface. The nodules may be solid or of ground glass attenuation, and range in size from tiny up to a centimeter. Centrilobular nodules may be caused by infectious or inflammatory conditions. Infectious causes of centrilobular nodules include viral pneumonias. The most common inflammatory cause of centrilobular nodules is hypersensitivity pneumonitis (HP), an exposure-related lung disease. HP is a type III hypersensitivity reaction to an inhaled organic antigen. The acute or subacute presentation of HP is primarily characterized by centrilobular nodules. Pulmonary capillary hemangiomatosis is a vascular pathology characterized by abnormal capillary proliferation leading to pulmonary hypertension. Viral pneumonias. Aspiration is dependent. Metastatic calcification most commonly occurs in the lung apices, typically in patients with renal failure. Chest: 14 Perilymphatic nodules Perilymphatic nodules: Schematic of the secondary pulmonary lobule (left image) demonstrates gray nodules located along the bronchovascular bundle and white nodules located along the interlobular septa. Axial CT (right image) demonstrates multiple subpleural nodules and nodules along the bronchovascular bundles (arrows). This was a case of sarcoidosis. Perilymphatic nodules follow the anatomic locations of pulmonary lymphatics, which can be seen in three locations in the lung: 1. Subpleural. 2. Peribronchovascular. 3. Septal (within the interlobular septa separating the secondary pulmonary lobules). Sarcoidosis is the most common cause of perilymphatic nodules, typically with an upper- lobe distribution. The nodules may become confluent creating the galaxy sign in which many tiny nodules surround a central lesion. Pulmonary sarcoidosis with galaxy sign: Axial and coronal CT images demonstrate extensive upper-lobe predominant confluent perilymphatic nodules. The galaxy sign is most apparent on the axial image, where the confluent nodules appear like the confluence of stars forming a galaxy. The differential of perilymphatic nodules includes: Sarcoidosis. Pneumoconioses (silicosis and coal workers’ pneumoconiosis) are reactions to inorganic dust inhalation. The imaging may look identical to sarcoidosis with perilymphatic nodules, but there is usually a history of exposure (e.g., a sandblaster who develops silicosis). Lymphangitic carcinomatosis. Chest: 15 Random nodules Random nodules: Schematic of the secondary pulmonary lobule (top left image) demonstrates nodules distributed randomly throughout the SPL. Schematic of the lungs (bottom left image) demonstrates nodules scattered randomly. Some of the nodules are in close contact with the pleural surface. Axial CT (top right image) demonstrates multiple random nodules. Some of the nodules abut the pleural surface. This was a case of metastatic colon cancer. Randomly distributed nodules usually occur via hematogenous spread. The differential of random nodules includes: Hematogenous metastases. Disseminated mycobacteria. Disseminated fungal infection. A miliary pattern is innumerable tiny random nodules the size of millet seeds. Miliary nodules: Axial CT shows innumerable tiny nodules distributed randomly throughout both lungs in a miliary pattern. This was a case of miliary tuberculosis. Case courtesy Ritu R. Gill, MD, MPH, Brigham and Women’s Hospital Chest: 16 Tree-in-bud nodules Schematic shows several nodules centered on an opacified small airway. Tree-in-bud nodularity: Axial CT shows numerous small nodules (arrows) “budding” off of linear branching structures in the right middle lobe. This case was secondary to atypical mycobacteria. Tree-in-bud nodules are multiple small nodules connected to linear branching structures, which resemble a budding tree branch in springtime. The linear branching structures represent mucus-impacted bronchioles, which are normally invisible on CT, and the nodules represent impacted terminal bronchioles. Tree-in-bud nodules are due to mucus, pus, or fluid impacting bronchioles and terminal bronchioles. Tree-in-bud nodules are almost always associated with small airways infection or inflammation, such as endobronchial spread of tuberculosis. The differential of tree-in-bud nodules includes: Mycobacterium tuberculosis and atypical mycobacteria. Viral pneumonia. Aspiration pneumonia. Rarely, lymphangitic carcinomatosis and vascular abnormalities (endovascular metastases and pulmonary arterial aneurysms). Chest: 17 Cavitary and cystic lung disease Solitary cavitary nodule/mass Coronal schematic demonstrates a single cavitary Axial CT shows a single spiculated cavitary lesion in the lesion. left upper lobe (arrow). This was a case of squamous cell carcinoma. A cavitary lesion represents development of air within a pre-existing lesion (nodule, mass, or consolidation). It typically has a thick, irregular wall, often with a solid mural component. Although the findings of benign and malignant cavitary nodules overlap, a maximum wall thickness of ≤4 mm is usually benign and a wall thickness >15 mm is usually malignant. Spiculated margins also suggest malignancy. A solitary cavitary lesion is most likely cancer or infection. Primary bronchogenic carcinoma. While both squamous cell and adenocarcinoma can cavitate, squamous cell cavitates more frequently. Small cell carcinoma is never known to cavitate. Tuberculosis classically produces an upper-lobe cavitary consolidation. Fungal pneumonia. Cavitary bacterial pneumonia. Multiple cavitary nodules Coronal schematic shows numerous cavitary Axial CT shows numerous cavitary and non-cavitary lesions lesions bilaterally. bilaterally, in a random distribution. This was a case of polysubstance abuse and septic emboli. The differential diagnosis for multiple cavitary lesions includes: Septic emboli, typically peripheral. Vasculitis, including granulomatosis with polyangiitis (GPA). Metastases, classically squamous cell carcinoma but any metastatic lesion can cavitate. Chest: 18 Cystic lung diseases Coronal schematic shows numerous thin-walled Axial CT shows bilateral thin-walled cysts that are of cystic lesions bilaterally. varying sizes but are predominantly regular in shape. There is a small left pleural effusion. This was a case of lymphangioleiomyomatosis. A cyst is an air-containing space with a thin wall. The differential diagnosis for multiple lung cysts includes: Lymphangioleiomyomatosis (LAM), a diffuse cystic lung disease due to smooth muscle proliferation of the distal airways. LAM causes uniformly distributed, thin-walled cysts in a diffuse distribution. It may be associated with chylous effusion, as demonstrated in the above right case. Pulmonary Langerhans cell histiocytosis, which features irregular cysts and nodules predominantly in the upper lungs. Lymphoid interstitial pneumonia (LIP), a rare disease usually associated with Sjögren syndrome and characterized by lymphocytic infiltrate and multiple cysts. Amyloid which appears similar to LIP. Birt-Hogg-Dube syndrome which is an autosomal dominant genetic disorder characterized by renal tumors (most commonly chromophobe renal carcinoma and renal oncocytoma), and renal and pulmonary cysts. Spontaneous pneumothoraxes can occur as a sequela of pulmonary cysts. Pneumocystis jiroveci pneumonia, which features cysts in late-stage disease. Of note, it is important to distinguish cysts from emphysema. The latter typically does not have walls and may have central vessels, whereas cysts classically do not have anything inside. The differential for a single cyst includes: Bulla. A bulla is an air-filled emphysematous space measuring >1 cm. A giant bulla occupies at least 30% of the volume of the thorax. Bleb. A bleb is an air-filled cystic structure contiguous with the pleura measuring 2 day hospitalization over the past 90 days. Pathogens are similar to HAP. Ventilator-associated pneumonia (VAP) Ventilator-associated pneumonia is caused by infectious agents not present at the time mechanical ventilation was started. Most infections are polymicrobial and primarily involve gram-negative rods such as Pseudomonas and Acinetobacter. Pneumonia in the immunocompromised patient Any of the above pathogens, plus opportunistic infections including Pneumocystis, fungi such as Aspergillus, Nocardia, CMV, etc., can be seen in immunocompromised patients. Different types of immunocompromise can lead to different infections. In particular, neutropenia predisposes to fungal pneumonia. Radiographic patterns of infection Lobar pneumonia Lobar pneumonia is consolidation of a single lobe. It is usually bacterial in origin and is the most common presentation of community-acquired pneumonia. The larger bronchi remain patent, causing air bronchograms. Bronchopneumonia Bronchopneumonia is patchy peribronchial consolidation with air-space opacities, usually involving several lobes, and may be caused by both bacterial and viral pneumonias as well as aspiration. Interstitial pneumonia Interstitial pneumonia is a misnomer, a finding on CXR that usually corresponds to ground glass on CT. Generally it can be caused by atypical (e.g., Mycoplasma, Chlamydia), viral, or Pneumocystis pneumonia. Round pneumonia Round pneumonia is an infectious mass-like opacity seen in children, most commonly due to S. pneumoniae. Infection remains confined due to incomplete formation of pores of Kohn. Chest: 21 Complications of pneumonia Pulmonary abscess Pulmonary abscess is necrosis of the lung parenchyma typically due to Staphylococcus aureus, Pseudomonas, or anaerobic bacteria. An air-fluid level is often present. An abscess is usually spherical, with equal dimensions on frontal and lateral views. Empyema Empyema is infection within the pleural space. There are three stages in the development of an empyema: 1) Free-flowing exudative effusion: Can be treated with needle aspiration or simple drain. 2) Development of fibrous strands: Requires large-bore chest tube and fibrinolytic therapy. 3) Fluid becomes solid and jelly-like: Usually requires surgery. Although pneumonia is often associated with a parapneumonic effusion, most pleural effusions associated with pneumonia are not empyema, but are instead a sterile effusion caused by increased capillary permeability. An empyema conforms to the shape of the pleural space, causing a longer air-fluid level on the lateral radiograph. This is in contrast to an abscess, discussed above, which typically is spherical and has the same dimensions on the frontal and lateral radiographs. The split pleura sign describes enhancing parietal and visceral pleura of an empyema seen on contrast-enhanced study. Split pleura sign: Contrast-enhanced CT shows enhancement of the thickened visceral and parietal pleural layers (arrows), which encase a pleural fluid collection. The split pleura sign is seen in the majority of exudative effusions, although it is not specific. Similar findings can be seen in malignant effusion, mesothelioma, fibrothorax, and after talc pleurodesis. Case courtesy Ritu R. Gill, MD, MPH, Brigham and Women’s Hospital. Empyema necessitans Empyema necessitans is extension of an empyema to the chest wall, most commonly secondary to tuberculosis. Other causative organisms include Actinomyces. Pneumatocele A pneumatocele is a thin-walled, gas-filled cyst that may be post-traumatic or develop as a sequela of pneumonia, typically from Staphylococcus aureus or Pneumocystis. Bronchopleural fistula (BPF) Bronchopleural fistula (BPF) is an abnormal communication between the airway and the pleural space. It is caused by rupture of the visceral pleura. By far the most common cause of BPF is surgery; however, other etiologies include lung abscess, empyema, and trauma. On imaging, new or increasing gas is present in a pleural effusion. A connection between the bronchial tree and the pleura is not always apparent, but is helpful when seen. The treatment of BPF is controversial and highly individualized. Chest: 22 Tuberculosis (TB) Tuberculosis (TB), caused by Mycobacterium tuberculosis, remains an important disease despite remarkable progress in public health and antituberculous therapy over the past century. Tuberculosis remains a significant problem in developing countries. In the United States, TB is seen primarily in immigrant, institutionalized, and immunocompromised individuals. Initial exposure to TB can lead to two clinical outcomes: 1) Contained disease (90%) results in calcified granulomas and/or calcified hilar lymph nodes. In a patient with normal immunity, the tuberculous bacilli are sequestered with a caseating granulomatous response. 2) Primary tuberculosis results when the host cannot contain the organism. Primary tuberculosis is seen more commonly in children and immunocompromised patients. Reactivation (post-primary) TB is reactivation of a previously latent infection. Primary tuberculosis Primary TB: Chest radiograph (left image) shows a vague right upper lung opacity (arrow). CT shows a patchy opacification (arrow) in the lower portion of the right upper lobe with adjacent tree-in-bud nodularity. The patient's sputum grew Mycobacterium tuberculosis. Case courtesy Ritu R. Gill, MD, MPH, Brigham and Women’s Hospital. Primary TB represents infection from the first exposure to TB. Primary TB may involve the pulmonary parenchyma, the airways, and the pleura. Primary TB often causes adenopathy. As many as 15% of patients infected with primary TB have no radiographic changes and the imaging appearance of primary TB is nonspecific. The typical imaging manifestation of primary TB is lobar consolidation +/- pleural effusion and lymphadenopathy, although not all of these need to be present. Primary TB may occur in any lobe. Both primary and reactivation TB can also present as isolated pleural disease or miliary disease, see next section on miliary TB. Classic imaging findings are not always seen, but include: Ghon focus: Initial focus of parenchymal infection, usually located in the upper part of the lower lobe or the lower part of the upper lobe. Ranke complex: Ghon focus and lymphadenopathy. Cavitation is rare in primary TB, in contrast to reactivation TB. Chest: 23  Adenopathy is common in primary TB, typically featuring central low-attenuation and peripheral enhancement, especially in children. Tuberculous adenopathy: Contrast-enhanced neck CT shows marked right-sided adenopathy (arrows) with peripheral enhancement and central necrosis. Case courtesy Ritu R. Gill, MD, MPH, Brigham and Women’s Hospital. Reactivation (post-primary) tuberculosis Reactivation TB, also called post-primary TB, usually occurs in adolescents and adults and is caused by reactivation of a dormant infection acquired earlier in life. Clinical manifestations of reactivation TB include chronic cough, low-grade fever, hemoptysis, and night sweats. Reactivation TB most commonly occurs in the upper lobe apical and posterior segments and superior segments of the lower lobes. Reactivation TB: Frontal chest radiograph (left image) shows a cavitary lesion in the left upper lobe (arrow), confirmed by CT (arrow). There was no significant mediastinal adenopathy. The differential diagnosis of this appearance would include cavitary primary lung cancer, which would be expected to feature a thicker wall. Case courtesy Michael Hanley, MD, University of Virginia Health System. In an immunocompetent patient, the imaging hallmarks of reactivation TB are upper-lobe predominant consolidation with cavitation. Tree-in-bud nodules are common and suggest active endobronchial spread. Low-attenuation adenopathy is a common additional finding, seen more often in immunocompromised patients. A tuberculoma is a well-defined rounded opacity consisting of an encapsulating fibrous wall with central caseation, usually in the upper lobes. Chest: 24 Healed tuberculosis Healed TB: Radiograph shows scarring, volume loss, and superior hilar retraction (arrows). CT shows apical scarring. Case courtesy Ritu R. Gill, MD, MPH, Brigham and Women’s Hospital. Healed TB is evident on radiography as apical scarring, usually with upper lobe volume loss and superior hilar retraction. Calcified granulomas may be present as well, which indicate containment of the initial infection by a delayed hypersensitivity response. Miliary tuberculosis Miliary TB: Radiograph and CT show innumerable tiny nodules in a random pattern, reflecting hematogenous seeding of TB. Case courtesy Ritu R. Gill, MD, MPH, Brigham and Women’s Hospital. Miliary TB is a diffuse random distribution of tiny nodules seen in hematogenously disseminated TB. Miliary TB can occur in primary or reactivation TB. Chest: 25 Atypical mycobacteria Atypical mycobacteria infection Mycobacterium avium intracellulare infection: Coronal (left image) and axial CT show right upper lobe and lingular tree-in-bud opacities and bronchiectasis, with more focal consolidation in the lingula (arrow). There are three types of atypical mycobacterial infection: (1) “Classic” or nodular cavitary form that simulates TB; typically seen in patients with chronic lung disease. (2) Non-classic or bronchiectatic form (more common). (3) Disseminated form, typically lymphadenopathy in immunocompromised patients (usually AIDS). The presentation of bronchiectatic atypical mycobacteria is an elderly woman with cough, low-grade fever, and weight loss, called Lady Windermere syndrome. Mycobacterium avium intracellulare and M. kansasii are the two most common organisms. Radiographic findings are bronchiectasis and tree-in-bud nodules, most common in the right middle lobe and lingula. “Hot-tub” lung “Hot-tub” lung is a hypersensitivity pneumonitis in response to atypical mycobacteria, which are often found in hot tubs. There is no active infection and the typical patient is otherwise healthy. Imaging is similar to other causes of hypersensitivity pneumonitis, featuring centrilobular nodules. Endemic fungi Endemic fungi can cause pneumonia in normal individuals, with each subtype having a specific geographic distribution. Histoplasma capsulatum Histoplasma capsulatum is localized to the Ohio and Mississippi river valleys, in soil contaminated with bat or bird guano. Acute infection usually produces nodules and lymphadenopathy. Chronic sequela of infection is a calcified granuloma. A less common radiologic manifestation is a pulmonary nodule (histoplasmoma), which can mimic a neoplasm. Fibrosing mediastinitis is a rare complication of Histoplasma infection of mediastinal lymph nodes leading to pulmonary venous obstruction, bronchial stenosis, and pulmonary artery stenosis. Affected lymph nodes tend to calcify. Chest: 26  Coccidioides immitis and Blastomyces dermatitidis Coccidioides immitis is found in the southwestern United States and has a variety of radiologic appearances, including multifocal consolidation, multiple pulmonary nodules, and miliary nodules. Blastomyces dermatitidis is found in the central and southeastern United States. Infection is usually asymptomatic, but may present as flu-like illness that can progress to multifocal consolidation, ARDS, or miliary disease. Viral pneumonia In general, viral pneumonias have a large overlap with bacterial pneumonias in imaging appearance. Classic imaging findings on CT include centrilobular or tree-in-bud nodules, patchy ground glass opacities, and bronchopneumonia (peribronchial consolidations). Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Severe acute respiratory syndrome coronavirus 2 SARS-CoV-2 (i.e., COVID-19) is a respiratory viral disease that became a pandemic in early 2020. Imaging findings are nonspecific, however bilateral, dependent, lower-lobe predominant ground glass opacities or consolidations are classic features. Pleural effusions, centrilobular nodules, and tree-in-bud nodules are typically not associated. COVID-19 infection: Chest radiograph (left image) shows bilateral peripheral opacities (arrows). Chest CT (right) in a different patient shows peripheral ground glass and consolidations in both lungs (arrows). Chest: 27 Infections in the immunocompromised Immunosuppressed patients are susceptible to the same organisms that infect immunocompetent patients; however, one must be aware of several additional opportunistic organisms that may present in the immunocompromised. An immunocompromised patient with a focal air space opacity is most likely to have a bacterial pneumonia (most commonly pneumococcus), but TB should also be considered if the CD4 count is low. In contrast, multifocal opacities have a wider differential diagnosis including Pneumocystis pneumonia and opportunistic fungal infection such as Cryptococcus or Aspergillus. Pneumocystis jiroveci pneumonia Pneumocystis jiroveci (previously called Pneumocystis carinii) is an opportunistic fungus that may cause pneumonia in individuals with CD4 counts 3 cm). Amyloidosis Tracheal amyloid: Axial CT images show nodular and irregular thickening of the trachea (arrows). This pattern is not specific, and the differential diagnosis would also include sarcoidosis, multifocal adenoid cystic carcinoma, and tracheal metastases. Case courtesy Ritu R. Gill, MD, MPH, Brigham and Women’s Hospital. Amyloidosis causes irregular narrowing of the airways due to submucosal amyloid deposition, which may be calcified. Involvement may be mass-like or segmental. Tracheal amyloidosis is very rare. The posterior membranous trachea is not spared. Chest: 84  Granulomatosis with polyangiitis (GPA) Large airway involvement is seen in approximately 20% of patients with GPA, most commonly manifesting as subglottic tracheal stenosis with circumferential mucosal thickening. The posterior membranous trachea is not spared. Calcifications are not seen. Sarcoidosis Tracheal involvement by sarcoid is rare and usually seen in advanced disease. Tracheal sarcoid has a variable appearance ranging from smooth stenosis to a nodular or mass-like appearance. The posterior membranous trachea is not spared. Large airways Bronchiectasis Bronchiectasis is progressive, irreversible dilation of cartilage-containing bronchi. Three etiologies of bronchiectasis have been described, with a final common pathway of mucus plugging, superimposed bacterial colonization, and inflammatory response. Bronchial wall injury, typically from infection or inflammation. Bronchial lumen obstruction. Traction from adjacent fibrosis. Morphologic classification of bronchiectasis is most useful as a rough gauge of severity. Cylindrical bronchiectasis (least severe): Mild bronchial dilation. Varicose bronchiectasis (moderately severe): Bronchi may become beaded and irregular. Cystic bronchiectasis (most severe): Bronchi are markedly enlarged and ballooned. Radiographic findings depend on severity. In mild cases only tram tracks may be visible, representing thickened bronchial walls causing parallel radiopaque lines resembling tram tracks. In more severe cases there can be extensive cystic change. CT findings include the signet ring sign, which describes a dilated bronchus adjacent to a normal pulmonary artery branch. Normally each bronchus should be approximately the same size as the adjacent pulmonary artery branch. Other CT findings of bronchiectasis include lack of bronchial tapering, bronchial wall thickening, and mucus-filled bronchi. Often, adjacent tree-in-bud nodules are present, likely representing associated small-airways infection. Traction bronchiectasis occurs secondary to lung fibrosis (see earlier discussion of ILD). Patterns of primary bronchiectasis can be divided into lung zones and central to peripheral distribution: Upper lung: cystic fibrosis, ABPA. Mid lung: atypical mycobacteria. Lower lung: chronic aspiration, post-infectious, immotile cilia, immunodeficiency. Central: ABPA, Mounier-Kuhn (tracheobronchomegaly). Mid-order bronchi: Williams-Campbell (fourth to sixth order bronchi). Chest: 85 Bronchiectasis (continued) Chronic aspiration is the most common cause of bronchiectasis. Bronchiectasis from chronic aspiration: Axial and coronal CT show bronchial wall thickening in the bilateral lower lobes due to dependent aspiration (arrows). Bronchocentric infections, such as tuberculosis and atypical mycobacteria. Bronchiectasis of the right middle lobe and lingula (arrows) due to Mycobacterium avium intracellulare infection. Ineffective clearing of secretions – cystic fibrosis and Kartagener (primary ciliary dyskinesia). Bronchiectasis from cystic fibrosis with superimposed pneumonia: Radiograph shows upper-lobe bronchiectasis with a focal left upper lobe opacity (yellow arrow). CT confirms bronchiectasis (red arrows) and a left upper lobe consolidation (yellow arrow), representing pneumonia. Congenital connective tissue disorders – Mounier-Kuhn (a connective tissue disorder causing tracheobronchomegaly leading to recurrent pneumonia), or Williams-Campbell (a rare disorder of the fourth to sixth mid-order bronchial cartilage, which may be congenital or acquired as a sequela of viral infection). Mounier-Kuhn: Chest radiograph (left image) shows severe diffuse bronchiectasis. CT shows tracheal dilation (calipers) up to 3 cm and severe cystic bronchiectasis. Chest: 86  Broncholithiasis Broncholithiasis is a rare disorder of calcified/ossified material within the bronchial lumen, caused by erosion of an adjacent calcified granulomatous lymph node. Broncholithiasis clinically presents with nonproductive cough, hemoptysis, and air trapping. Focal non-neoplastic tracheal stenosis/wall thic ening Intubation/tracheostomy There is approximately 1% risk of tracheal stenosis after intubation, but approximately 30% risk of stenosis after long-standing tracheostomy. Rare causes of focal tracheal stenosis Extremely uncommon causes of focal tracheal stenosis include Behçet and Crohn disease. Airway tumors Primary tumors of the trachea and central bronchi are rare. In adults, the vast majority of tumors are malignant, while in children most are benign. Squamous cell carcinoma and adenoid cystic carcinoma are by far the two most common primary central airway tumors in adults. Squamous cell carcinoma (SCC) Endotracheal squamous cell carcinoma: Radiograph shows a tracheal luminal narrowing (arrow) at the level of the thoracic inlet. On CT there is an eccentric enhancing mass invading the left tracheal wall and markedly narrowing the tracheal lumen (arrow). Squamous cell carcinoma is the most common primary tracheal malignancy. It is strongly associated with cigarette smoking. The typical CT appearance of tracheal squamous cell carcinoma is a polypoid intraluminal mass. The contours of the mass can be irregular, smooth, or lobulated. The tumor can occasionally invade into the esophagus, causing tracheoesophageal fistula. Chest: 87 Adenoid cystic carcinoma (ACC) Tracheal adenoid cystic carcinoma: CT (left image) shows irregular circumferential tracheal thickening (arrow). Post-contrast coronal T1-weighted MRI (right image) shows an enhancing nodular mass extending into the tracheal lumen (arrows). Case courtesy Ritu R. Gill, MD, MPH, Brigham and Women’s Hospital. Adenoid cystic carcinoma (ACC) is a relatively low grade malignancy that usually affects patients in their forties, a decade or two younger than the typical SCC patient. It is not associated with cigarette smoking. ACC has a propensity for perineural and submucosal spread. It may spread over a long segment of the trachea, complicating the ability to resect the lesion. The typical CT appearance of ACC is a submucosal mass that infiltrates the tracheal wall and surrounding mediastinal fat. ACC may also present as circumferential tracheal or bronchial thickening causing airway stenosis. Carcinoid Endobronchial carcinoid: Chest radiograph shows right lower lobe atelectasis (arrows) and volume loss. Axial contrast-enhanced CT shows a mildly enhancing well-circumscribed endobronchial mass (arrow) in the right mainstem bronchus just distal to the carina. Carcinoid almost always occurs distal to the carina. CT shows an endoluminal bronchial mass that may calcify and often enhances avidly. Note that carcinoid tumors tend to have a larger extrinsic component than endobronchial component. In addition to carcinoid, the differential diagnosis of an enhancing endobronchial mass includes mucoepidermoid carcinoma and very rare entities such as hemangioma and glomus tumor. Chest: 88 Mucoepidermoid carcinoma Mucoepidermoid carcinoma is a rare tumor that originates from tiny salivary glands lining the tracheobronchial tree. Mucoepidermoid carcinoma tends to affect younger patients than adenoid cystic carcinoma. CT appearance is a round or oval endobronchial mass, indistinguishable from carcinoid. Tracheal lymphoma Tracheal lymphoma is rare. It is usually associated with mucosa-associated lymphoid tissue (MALT), a low-grade malignancy. Endobronchial metastasis Endobronchial metastasis: Coronal contrast-enhanced CT demonstrates a heterogeneously enhancing mass, which invades the right mainstem bronchus (arrows). This was a spindle-cell carcinoma, but the imaging appearance is nonspecific. Breast cancer, renal cell carcinoma, thyroid cancer, lung cancer, melanoma, and sarcoma are the most common malignancies to metastasize to the central airways. The mnemonic BReTh Lung may be helpful to remember the four most common airway metastases (breast, renal cell, thyroid, and lung). Direct invasion of the central airways by adjacent malignancy Direct central airway invasion occurs more commonly than endobronchial metastases. Aggressive laryngeal, thyroid, esophageal, and lung cancer may cause direct airway invasion. Benign endobronchial lesions Papilloma is a benign but potentially pre-malignant lesion that may transform into carcinoma. Suspected papillomas are typically closely followed. A single papilloma is usually caused by chronic irritation. Multiple papillomas (laryngotracheal papillomatosis) is caused by HPV, which may be acquired at birth. Distribution is usually centered in the larynx, with tracheobronchial involvement in 1–5% of cases. Papillomas may spread to the lungs, where they will form multiple cavitary nodules with dependent distribution. Chondroma is a benign cartilaginous tumor that rarely may occur in the airways. Other benign endobronchial lesions include schwannoma, adenoma, hamartoma, hemangioma, lipoma, and leiomyoma. Chest: 89 Emphysema Emphysema is the destruction of alveolar walls resulting in irreversible enlargement of the distal airspaces. Elastase is produced by alveolar macrophages and neutrophils, both of which are increased in smokers. Elastase is a powerful destructive enzyme which functions in the host defense mechanism, but excess elastase can be highly harmful to the native tissues. Alpha-1- antitrypsin normally neutralizes elastase. Either a surplus of elastase (in smoking-related emphysema) or insufficient neutralizing enzyme (in alpha-1-antitrypsin deficiency) can cause lung destruction and resultant emphysema. Centrilobular emphysema Centrilobular and paraseptal emphysema: Coronal (left image) and axial CT demonstrates both centrilobular and paraseptal emphysema. Centrilobular emphysema is predominant in the upper lobes (yellow arrows) and paraseptal emphysema is seen anteromedially (blue arrows). Centrilobular emphysema is a smoking-related lung disease. Centrilobular emphysema predominantly affects the upper lobes. Like RB-ILD, another smoking-related lung disease, centrilobular emphysema primarily affects the center of the secondary pulmonary lobule. All smoking-related lung disease (RB, RB-ILD, DIP, PLCH, and emphysema) may be within the same spectrum of disease caused by macrophage-mediated inflammation in reaction to inhaled particles and toxins. Paraseptal emphysema Paraseptal emphysema is usually seen in combination with other forms of emphysema. It is also usually smoking related. Paraseptal emphysema is subpleural in location and may predispose to pneumothorax. Chest: 90 Panacinar (panlobular) emphysema Panacinar (also called panlobular) emphysema affects the entire acinus diffusely throughout the lung. The emphysematous changes are usually more severe at the lung bases. Alpha-1-antitrypsin deficiency is the main cause of panacinar emphysema. Panacinar emphysema due to alpha-1-antitrypsin deficiency: Frontal radiograph and coronal CT show diffuse emphysematous changes most severely affecting the lower lobes, with flattening of the diaphragms (arrows). Chest: 91 Pleura Pleural malignancy Metastatic disease Metastatic disease is the most common cause of pleural malignancy. Lung and breast cancer, gastrointestinal and genitourinary adenocarcinoma, and invasive thymoma can metastasize to the pleura. Chest wall metastases: Axial CT image shows a heterogeneously enhancing mass invading the chest wall and adjacent pleural of the left lung. This was a case of breast cancer metastasis. Features to help differentiate malignant pleural effusions Unexplained recurrent pleural effusions should raise suspicion for underlying malignancy regardless of associated visualized pleural nodularity. The split pleura sign is characteristic of an empyema, formed by fibrin coating both parietal and visceral pleuras resulting in in-growth of blood vessels. Although rare, empyema can be seen in lung cancer. Features of malignant effusion include: Nodular pleural thickening. Large or recurrent effusion without etiology. Thickening of mediastinal (medial) pleura. Multiple myeloma/plasmacytoma Osseous metastases may have soft tissue components that are extrapleural, which may secondarily invade the pleura. Chest: 92 Mesothelioma Mesothelioma: Contrast-enhanced CT through the thorax (left image) shows extensive nodular pleural thickening of the left hemithorax (arrows). Images through the upper abdomen show extensive soft tissue abnormality with invasion of the chest wall (arrows). Mesothelioma (in different patient from above): Axial (left image) and coronal T1-weighted post-contrast fat- suppressed MR images demonstrate circumferential nodular thickening of the left pleura. Mesothelioma is a highly aggressive neoplasm arising from the pleura. Most cases are due to prior asbestos exposure, with a latency of >20 years. The epithelial subtype is more common and has a slightly better prognosis. Sarcomatoid and mixed subtypes are more aggressive. CT of mesothelioma typically shows nodular concentric pleural thickening, often with an associated pleural effusion. The role of surgery is evolving, with the goal to resect all visible tumor. Trimodality therapy involving surgery, intraoperative heated chemotherapy, and radiation has been shown to provide benefit for a subset of patients. Chest: 93  Fibrous tumor of the pleura (FTP) Fibrous tumor of the pleura (FTP), also known as solitary fibrous tumor, is a focal pleural mass not related to asbestos or mesothelioma. It is not mesothelial in origin. Approximately 20–30% of FTP are malignant, so all are excised. Malignant potential is determined by number of mitoses seen at pathology. FTP may be associated with hypoglycemia or hypertrophic pulmonary osteoarthropathy, although these associated conditions are uncommon (5%). FTP may be pedunculated. A pleural-based mass that changes position is suggestive of FTP. FTP tends to have low FDG uptake on PET. Fibrous tumor of the pleura: CT topogram (left image) shows a round opacity (arrow) with a circumscribed medial margin and indistinct lateral margin, suggesting a pleural-based mass. CT confirms that the mass (arrow) is pleural-based, with a broad attachment to the pleura. Case courtesy Ritu R. Gill, MD, MPH, Brigham and Women’s Hospital. Pleural effusion Transudate A transudative effusion is caused by systemic or local imbalances in hydrostatic and oncotic forces. Common causes include systemic low-protein states, heart failure, and nephrotic syndrome. Exudate An exudative effusion is distinguished from a transudate by thoracentesis. There are no reliable imaging features to distinguish between transudative and exudative effusions. The presence of an exudate implies pleural disease causing increased permeability of pleural capillaries, which may be due to: Pneumonia with parapneumonic effusion, empyema, or tuberculous pleuritis. Mesothelioma or pleural metastasis. Rheumatoid arthritis or other collagen vascular diseases. Chylothorax A chylothorax is a pleural effusion consisting of intestinal lymph, most commonly caused by iatrogenic injury, less commonly neoplastic obstruction of the thoracic duct. Chylothorax is also associated with lymphangioleiomyomatosis (LAM). The thoracic duct originates at the cisterna chyli in the upper abdomen and drains into the left brachiocephalic or subclavian vein. Chest: 94  Cory Robinson-Weiss, Fiona E. Malone, Ellen X. Sun, Junzi Shi, Khushboo Jhala, Shanna A. Matalon Gastrointestinal Imaging Liver.......................................................96 Hepatic Doppler...................................123 Biliary imaging......................................130 Pancreas...............................................148 Spleen..................................................163 Esophagus............................................173