Diagnostic Imaging Chest 3Rd Edition Melissa L Rosado de Christenson Full Chapter

Diagnostic Imaging: Chest 3rd Edition
Melissa L. Rosado-De-Christenson
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THIRD EDITION
Rosado-de-Christenson
Martmez-Jimenez
Restrepo I Betancourt-Cuellar
Carter I Lichtenberger
Heeger I Ternes
Carrillo-Bayona I Frazier
Silva I Garrana
Alegria I Fuss
Diagnostic Imaging
THIRD EDITION
Martínez-Jiménez
Restrepo | Betancourt-Cuellar
Carter | Lichtenberger
Heeger | Ternes
Carrillo-Bayona | Frazier
Silva | Garrana
Alegría | Fuss
THIRD EDITION
Melissa L. Rosado-de-Christenson, MD, FACR

Section Chief, Thoracic Radiology
Department of Radiology
Saint Luke's Hospital of Kansas City
Professor of Radiology
University of Missouri-Kansas City School of Medicine
Kansas City, Missouri
Santiago Martínez-Jiménez, MD
iii
Elsevier
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DIAGNOSTIC IMAGING: CHEST, THIRD EDITION ISBN: 978-0-323-79663-7

Inkling: 978-0-323-79664-4
Copyright © 2022 by Elsevier. All rights reserved.
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Previous edition copyrighted 2012.
Library of Congress Control Number: 2021944546
Printed in Canada by Friesens, Altona, Manitoba, Canada
Last digit is the print number: 9 8 7 6 5 4 3 2 1
iv
Dedications
To my wonderful family – Paul, Jennifer, Heather, David, Mike, and Juniper,
for your unconditional love and support. You are everything to me.
MLR
To Isabela and Lucas. You are simply the best. Just keep smiling and
remember that monsters were never under the bed.
SMJ
v
Contributing Authors
Carlos S. Restrepo, MD Jorge Alberto Carrillo-Bayona, MD
Professor of Radiology Professor of Radiology
Director of Cardiothoracic Imaging Universidad Nacional de Colombia
Department of Radiology Hospital Universitario Mayor Mederi
The University of Texas RIMAB
Health Science Center at San Antonio Bogotá, Colombia
San Antonio, Texas
Aletta Ann Frazier, MD
Sonia L. Betancourt-Cuellar, MD Section Chief, Cardiothoracic Imaging
Professor of Thoracic Imaging ACR Institute for Radiologic Pathology (AIRP)
Department of Thoracic Imaging Silver Spring, Maryland
The University of Texas MD Anderson Cancer Center Professor of Diagnostic Radiology
Houston, Texas University of Maryland School of Medicine
Baltimore, Maryland
Brett W. Carter, MD, CPPS
Director of Clinical Operations Claudio Silva, MD, MSc, MBA
Chief Patient Safety and Associate Professor of Radiology
Quality Officer, Diagnostic Imaging Clínica Alemana - Universidad del Desarrollo
Professor of Thoracic Imaging School of Medicine
The University of Texas MD Anderson Cancer Center Cardiothoracic Imaging Division, Radiology Department
Houston, Texas Clínica Alemana de Santiago
Santiago, Chile
John P. Lichtenberger, III, MD
Chief of Thoracic Imaging Sherief H. Garrana, MD
Associate Professor of Radiology Assistant Professor of Radiology
Department of Radiology Department of Radiology
George Washington University Medical Saint Luke’s Hospital of Kansas City
Faculty Associates University of Missouri-Kansas City School of Medicine
Washington, D.C. Kansas City, Missouri
Allen Heeger, DO Julia Alegría, MD

Thoracic Radiologist Chief, Cardiothoracic Imaging Division
West County Radiological Group Radiology Department
Mercy Hospital Clínica Alemana de Santiago
St. Louis, Missouri Santiago, Chile
Assistant Professor of Radiology
Tyler H. Ternes, MD Clínica Alemana - Universidad del Desarrollo School of
Section Chief, Thoracic Imaging Medicine
Clinical Assistant Professor
University of Kansas School of Medicine Cristina Fuss, MD
Wichita Diagnostic Radiology Associate Professor and Section Chief
Wichita, Kansas Cardiothoracic Imaging
Department of Diagnostic Radiology
Oregon Health & Science University
Portland, Oregon
vi
Additional Contributing Authors
Gerald F. Abbott, MD, FACR
Jonathan Hero Chung, MD
Florian J. Fintelmann, MD, FRCPC
Tomás Franquet, MD, PhD
Terrance Healey, MD
Laura E. Heyneman, MD
Jeffrey P. Kanne, MD
Kyung Soo Lee, MD
Diane C. Strollo, MD, FACR
Christopher M. Walker, MD
Helen T. Winer-Muram, MD
Carol C. Wu, MD
vii
Preface
We proudly present the 3rd edition of Diagnostic Imaging: Chest. It is hard to believe
that 9 years have elapsed since the publication of the 2nd edition. I am immensely
grateful to the Elsevier team for giving me the opportunity to, once again, serve as
lead author of this work, and to my good friend, colleague, and practice partner, Dr.
Santiago Martínez-Jiménez, for serving as co-lead author.
The 3rd edition is similar to the 2nd in both style and appearance, with a succinct,
bulleted text format and image-rich depictions of a large number of cardiothoracic
diseases. The content is organized based on both anatomic location and category of
disease. The work is enhanced by a wealth of new material that includes:
• 13 updated and illustrated section introductions that set the stage for
the specific diagnoses that follow
• Updated sections that define and illustrate thoracic imaging terminology,
including many entities from the Fleischner Society glossary of terms, as well
as classic signs in chest imaging
• An updated section on posttreatment changes in the thorax and the
effects of novel therapies that include surgery, radiotherapy, chemotherapy,
immunotherapy, and ablation procedures
• New chapters on emerging diseases, including coronavirus disease-2019
(COVID-19) and e-cigarette or vaping product use-associated lung injury
(EVALI)
• A total of 344 chapters supplemented with updated material and references
• In all, 2,640 images and 2,536 online-only images that include radiographic,
CT,
MR, and PET/CT images, as well as gross photographs and
photomicrographs where appropriate
• Updated graphics that illustrate the anatomic/pathologic basis of various
imaging abnormalities
We were fortunate to recruit a world-class team of authors who delivered

meticulously researched content in all areas of thoracic imaging, including both
seasoned authors from the 2nd edition and promising early-career cardiothoracic
radiologists destined to lead this project in the future. We were privileged to work
with Terry W. Ferrell, MS, an outstanding lead editor whose suggestions and edits
enhanced each and every chapter, and with Lane R. Bennion, MS, a gifted medical
illustrator whose artistry greatly enriched the imaging content. We gratefully
acknowledge the tireless work of the Elsevier production staff, who sustained us
through each step of the work. Finally, we express our heartfelt gratitude to Karen
E. Concannon, PhD, senior manager of content, for her enthusiastic leadership and
thoughtful guidance through the entire process.
viii
Melissa L. Rosado-de-Christenson, MD, FACR
Section Chief, Thoracic Radiology
ix
Acknowledgments
LEAD EDITOR
Terry W. Ferrell, MS
LEAD ILLUSTRATOR
Lane R. Bennion, MS
TEXT EDITORS
Arthur G. Gelsinger, MA
Rebecca L. Bluth, BA
Nina Themann, BA
Megg Morin, BA
Kathryn Watkins, BA
ILLUSTRATIONS
Richard Coombs, MS
Laura C. Wissler, MA
IMAGE EDITORS
Jeffrey J. Marmorstone, BS
Lisa A. M. Steadman, BS
ART DIRECTION AND DESIGN

Tom M. Olson, BA
PRODUCTION EDITORS
Emily C. Fassett, BA
John Pecorelli, BS
xi
Sections
SECTION 1:
Overview of Chest Imaging
SECTION 2:
Developmental Abnormalities
SECTION 3:
Airway Diseases
SECTION 4:
Infections
SECTION 5:
Pulmonary Neoplasms
SECTION 6:
Interstitial, Diffuse, and Inhalational Lung Disease
SECTION 7:
Connective Tissue Disorders, Immunological Diseases, and Vasculitis
SECTION 8:
Mediastinal Abnormalities
SECTION 9:
Cardiovascular Disorders
SECTION 10:
Trauma
SECTION 11:
Post-Treatment Chest
SECTION 12:
Pleural Diseases
SECTION 13:
Chest Wall and Diaphragm
xiii
TABLE OF CONTENTS
26 Peribronchovascular
SECTION 1: OVERVIEW OF CHEST Santiago Martínez-Jiménez, MD
IMAGING 27 Perilobular Pattern
INTRODUCTION AND OVERVIEW Santiago Martínez-Jiménez, MD
28 Perilymphatic
4 Approach to Chest Imaging Santiago Martínez-Jiménez, MD
Melissa L. Rosado de Christenson, MD, FACR 29 Pneumatocele
Melissa L. Rosado de Christenson, MD, FACR
ILLUSTRATED TERMINOLOGY 30 Reticular Pattern
6 Approach to Illustrated Terminology Melissa L. Rosado de Christenson, MD, FACR
Melissa L. Rosado de Christenson, MD, FACR 31 Secondary Pulmonary Lobule
8 Acinar Nodules Melissa L. Rosado de Christenson, MD, FACR
Melissa L. Rosado de Christenson, MD, FACR and Tyler H. 32 Traction Bronchiectasis
Ternes, MD Melissa L. Rosado de Christenson, MD, FACR
9 Air Bronchogram 33 Tree-in-Bud Opacities
Tyler H. Ternes, MD Melissa L. Rosado de Christenson, MD, FACR
10 Air-Trapping
Tyler H. Ternes, MD CHEST RADIOGRAPHIC AND CT SIGNS
11 Airspace 34 Approach to Chest Radiographic and CT Signs
Tyler H. Ternes, MD Santiago Martínez-Jiménez, MD
12 Architectural Distortion 40 Air Crescent Sign
13 Bulla/Bleb 41 Cervicothoracic Sign
14 Cavity 42 Comet Tail Sign
Melissa L. Rosado de Christenson, MD, FACR Santiago Martínez-Jiménez, MD
15 Centrilobular 43 CT Halo Sign
Santiago Martínez-Jiménez, MD and Melissa L. Rosado de Santiago Martínez-Jiménez, MD
Christenson, MD, FACR 44 Deep Sulcus Sign
16 Consolidation Santiago Martínez-Jiménez, MD
Melissa L. Rosado de Christenson, MD, FACR 45 Fat Pad Sign
17 Cyst Santiago Martínez-Jiménez, MD
Melissa L. Rosado de Christenson, MD, FACR 46 Finger-in-Glove Sign
18 Ground-Glass Opacity Santiago Martínez-Jiménez, MD
Melissa L. Rosado de Christenson, MD, FACR 47 Hilum Convergence Sign
19 Honeycombing Santiago Martínez-Jiménez, MD
Santiago Martínez-Jiménez, MD 48 Hilum Overlay Sign
20 Interlobular Septal Thickening Santiago Martínez-Jiménez, MD
Melissa L. Rosado de Christenson, MD, FACR 49 Incomplete Border Sign
21 Intralobular Lines Santiago Martínez-Jiménez, MD
Melissa L. Rosado de Christenson, MD, FACR 50 Luftsichel Sign
22 Mass Santiago Martínez-Jiménez, MD
Melissa L. Rosado de Christenson, MD, FACR 51 Reversed Halo Sign
23 Miliary Pattern Santiago Martínez-Jiménez, MD
Melissa L. Rosado de Christenson, MD, FACR 52 Rigler and Cupola Signs
24 Mosaic Attenuation Santiago Martínez-Jiménez, MD
Melissa L. Rosado de Christenson, MD, FACR 53 S-Sign of Golden
25 Nodule Santiago Martínez-Jiménez, MD
Melissa L. Rosado de Christenson, MD, FACR 54 Signet Ring Sign
xiv
TABLE OF CONTENTS
55 Silhouette Sign
SYSTEMIC CIRCULATION
110 Accessory Azygos Fissure
ATELECTASIS AND VOLUME LOSS Sherief H. Garrana, MD
56 Approach to Atelectasis and Volume Loss 112 Azygos and Hemiazygos Continuation of the IVC
Melissa L. Rosado de Christenson, MD, FACR and Gerald F. Sherief H. Garrana, MD
Abbott, MD, FACR 116 Persistent Left Superior Vena Cava
60 Atelectasis Claudio Silva, MD, MSc, MBA
Tomás Franquet, MD, PhD 120 Aberrant Subclavian Artery
64 Cicatricial Atelectasis Sherief H. Garrana, MD
Brett W. Carter, MD, CPPS 122 Right Aortic Arch
65 Rounded Atelectasis Santiago Martínez-Jiménez, MD
Brett W. Carter, MD, CPPS 126 Double Aortic Arch
Carlos S. Restrepo, MD and Diane C. Strollo, MD, FACR
SECTION 2: DEVELOPMENTAL 130 Aortic Coarctation
ABNORMALITIES Tyler H. Ternes, MD and Santiago Martínez-Jiménez, MD
INTRODUCTION AND OVERVIEW CARDIAC, PERICARDIAL, AND VALVULAR

DEFECTS
68 Approach to Developmental Abnormalities
Melissa L. Rosado de Christenson, MD, FACR 134 Atrial Septal Defect
AIRWAYS 138 Ventricular Septal Defect
70 Tracheal Bronchus and Other Anomalous Bronchi Brett W. Carter, MD, CPPS
Melissa L. Rosado de Christenson, MD, FACR and Tomás 142 Bicuspid Aortic Valve
Franquet, MD, PhD Santiago Martínez-Jiménez, MD and Carlos S. Restrepo,
74 Paratracheal Air Cyst MD
Allen Heeger, DO 146 Pulmonic Stenosis
76 Bronchial Atresia Brett W. Carter, MD, CPPS
Tyler H. Ternes, MD 150 Heterotaxy
Tyler H. Ternes, MD
LUNG 154 Absence of the Pericardium
80 Extralobar Sequestration
Tyler H. Ternes, MD CHEST WALL AND DIAPHRAGM
82 Intralobar Sequestration
Tyler H. Ternes, MD 156 Poland Syndrome
86 Diffuse Pulmonary Lymphangiomatosis Sherief H. Garrana, MD
Tyler H. Ternes, MD 158 Pectus Deformity
88 Apical Lung Hernia Sherief H. Garrana, MD and Tomás Franquet, MD, PhD
Sonia L. Betancourt-Cuellar, MD 160 Kyphoscoliosis
Carlos S. Restrepo, MD and Helen T. Winer-Muram, MD
PULMONARY CIRCULATION 164 Morgagni Hernia
90 Proximal Interruption of the Pulmonary Artery 166 Bochdalek Hernia
Tyler H. Ternes, MD Aletta Ann Frazier, MD
94 Aberrant Left Pulmonary Artery
Carlos S. Restrepo, MD and Diane C. Strollo, MD, FACR SECTION 3: AIRWAY DISEASES
96 Pulmonary Arteriovenous Malformation
Sherief H. Garrana, MD INTRODUCTION AND OVERVIEW
98 Partial Anomalous Pulmonary Venous Return
170 Approach to Airways Disease
102 Scimitar Syndrome
Santiago Martínez-Jiménez, MD BENIGN NEOPLASMS
106 Pulmonary Varix
Carlos S. Restrepo, MD 172 Tracheobronchial Hamartoma
108 Meandering Pulmonary Vein Sherief H. Garrana, MD and Christopher M. Walker, MD
Melissa L. Rosado de Christenson, MD, FACR 174 Tracheobronchial Papillomatosis
xv
TABLE OF CONTENTS
248 Infectious Bronchiolitis
MALIGNANT NEOPLASMS John P. Lichtenberger, III, MD and Laura E. Heyneman, MD
178 Squamous Cell Carcinoma, Airways 252 Constrictive Bronchiolitis
Sonia L. Betancourt-Cuellar, MD Brett W. Carter, MD, CPPS
182 Adenoid Cystic Carcinoma 256 Swyer-James-MacLeod Syndrome
Sonia L. Betancourt-Cuellar, MD Allen Heeger, DO
186 Mucoepidermoid Carcinoma 260 Asthma
Sonia L. Betancourt-Cuellar, MD Carlos S. Restrepo, MD and Santiago Martínez-Jiménez,
190 Metastasis, Airways MD
Sonia L. Betancourt-Cuellar, MD
SECTION 4: INFECTIONS
AIRWAY NARROWING AND WALL
THICKENING INTRODUCTION AND OVERVIEW
192 Saber-Sheath Trachea 266 Approach to Infections
Brett W. Carter, MD, CPPS Santiago Martínez-Jiménez, MD
194 Tracheal Stenosis
Aletta Ann Frazier, MD GENERAL
196 Tracheobronchomalacia 268 Bronchopneumonia
Aletta Ann Frazier, MD Sherief H. Garrana, MD
200 Middle Lobe Syndrome 270 Community-Acquired Pneumonia
Santiago Martínez-Jiménez, MD Claudio Silva, MD, MSc, MBA and Jeffrey P. Kanne, MD
206 Airway Granulomatosis With Polyangiitis 274 Hospital-Acquired Pneumonia
Jorge Alberto Carrillo-Bayona, MD Jorge Alberto Carrillo-Bayona, MD
208 Tracheobronchial Amyloidosis 276 Lung Abscess
John P. Lichtenberger, III, MD and Jeffrey P. Kanne, MD Carlos S. Restrepo, MD and Helen T. Winer-Muram, MD
210 Tracheobronchopathia Osteochondroplastica 280 Septic Emboli
Sonia L. Betancourt-Cuellar, MD John P. Lichtenberger, III, MD and Carol C. Wu, MD
212 Relapsing Polychondritis
Jorge Alberto Carrillo-Bayona, MD BACTERIA
214 Rhinoscleroma 284 Pneumococcal Pneumonia
288 Staphylococcal Pneumonia
BRONCHIAL DILATATION AND IMPACTION
Jorge Alberto Carrillo-Bayona, MD
216 Bronchitis 292 Klebsiella Pneumonia
Carlos S. Restrepo, MD and Carol C. Wu, MD Jorge Alberto Carrillo-Bayona, MD
218 Bronchiectasis 294 Pseudomonas Pneumonia
Sherief H. Garrana, MD and Laura E. Heyneman, MD Sherief H. Garrana, MD
222 Cystic Fibrosis 296 Legionella Pneumonia
Aletta Ann Frazier, MD Carlos S. Restrepo, MD and Jeffrey P. Kanne, MD
226 Allergic Bronchopulmonary Aspergillosis 298 Nocardiosis
Allen Heeger, DO Carlos S. Restrepo, MD and Helen T. Winer-Muram, MD
230 Primary Ciliary Dyskinesia 300 Actinomycosis
Melissa L. Rosado de Christenson, MD, FACR and Carlos S. Carlos S. Restrepo, MD and Tomás Franquet, MD, PhD
Restrepo, MD 302 Melioidosis
234 Mounier-Kuhn Syndrome Jorge Alberto Carrillo-Bayona, MD
Sonia L. Betancourt-Cuellar, MD and Carlos S. Restrepo, 304 Tuberculosis
MD Melissa L. Rosado de Christenson, MD, FACR
236 Williams-Campbell Syndrome 308 Nontuberculous Mycobacterial Infection
Sonia L. Betancourt-Cuellar, MD Kyung Soo Lee, MD
238 Broncholithiasis 312 Mycoplasma Pneumonia
Santiago Martínez-Jiménez, MD Jorge Alberto Carrillo-Bayona, MD
EMPHYSEMA AND SMALL AIRWAY DISEASES VIRUSES

240 Centrilobular Emphysema 314 Viral Pneumonia
Allen Heeger, DO Tomás Franquet, MD, PhD
244 Paraseptal Emphysema 318 Influenza Pneumonia
Allen Heeger, DO Carlos S. Restrepo, MD and Helen T. Winer-Muram, MD
246 Panlobular Emphysema
Allen Heeger, DO
xvi
TABLE OF CONTENTS
320 Cytomegalovirus Pneumonia
Carol C. Wu, MD and Carlos S. Restrepo, MD
UNCOMMON NEOPLASMS
324 COVID-19 398 Pulmonary Hamartoma
Santiago Martínez-Jiménez, MD and Sherief H. Garrana, Allen Heeger, DO
MD 402 Bronchial Carcinoid
FUNGI 406 Neuroendocrine Carcinoma
328 Histoplasmosis Cristina Fuss, MD and Sonia L. Betancourt-Cuellar, MD
Carlos S. Restrepo, MD and Helen T. Winer-Muram, MD 410 Kaposi Sarcoma
332 Coccidioidomycosis Carlos S. Restrepo, MD and Brett W. Carter, MD, CPPS
334 Blastomycosis
LYMPHOMA AND LYMPHOPROLIFERATIVE
DISORDERS
336 Cryptococcosis 414 Follicular Bronchiolitis
Brett W. Carter, MD, CPPS Jorge Alberto Carrillo-Bayona, MD
338 Paracoccidioidomycosis 418 Lymphoid Interstitial Pneumonia
340 Aspergillosis 422 Nodular Lymphoid Hyperplasia
Allen Heeger, DO Santiago Martínez-Jiménez, MD
346 Zygomycosis 424 Post-Transplant Lymphoproliferative Disease
Sonia L. Betancourt-Cuellar, MD John P. Lichtenberger, III, MD and Christopher M. Walker,
348 Pneumocystis jirovecii Pneumonia MD
Sherief H. Garrana, MD 428 Pulmonary Lymphoma
PARASITES
352 Dirofilariasis
METASTATIC DISEASE
Carlos S. Restrepo, MD and Tomás Franquet, MD, PhD 432 Hematogenous Metastases
354 Hydatidosis Aletta Ann Frazier, MD
Carlos S. Restrepo, MD and Tomás Franquet, MD, PhD 436 Lymphangitic Carcinomatosis
356 Strongyloidiasis Sonia L. Betancourt-Cuellar, MD
Carlos S. Restrepo, MD and Brett W. Carter, MD, CPPS 440 Tumor Emboli
358 Amebiasis Carlos S. Restrepo, MD and Florian J. Fintelmann, MD,
Carlos S. Restrepo, MD FRCPC
362 Schistosomiasis
Carlos S. Restrepo, MD SECTION 6: INTERSTITIAL, DIFFUSE, AND
INHALATIONAL LUNG DISEASE
SECTION 5: PULMONARY NEOPLASMS
INTRODUCTION AND OVERVIEW
INTRODUCTION AND OVERVIEW 446 Approach to Interstitial, Diffuse, and Inhalational
366 Approach to Pulmonary Neoplasms Lung Disease
Melissa L. Rosado de Christenson, MD, FACR Santiago Martínez-Jiménez, MD
LUNG CANCER IDIOPATHIC INTERSTITIAL LUNG DISEASES

372 Solitary Pulmonary Nodule 448 Acute Respiratory Distress Syndrome (ARDS)
Melissa L. Rosado de Christenson, MD, FACR Julia Alegría, MD
378 Adenocarcinoma 450 Acute Interstitial Pneumonia
Tyler H. Ternes, MD and Santiago Martínez-Jiménez, MD Carlos S. Restrepo, MD
384 Squamous Cell Carcinoma 454 Idiopathic Pulmonary Fibrosis
Sonia L. Betancourt-Cuellar, MD Julia Alegría, MD
388 Small Cell Carcinoma 458 Nonspecific Interstitial Pneumonia
Sonia L. Betancourt-Cuellar, MD Tyler H. Ternes, MD
392 Multifocal Lung Cancer 462 Organizing Pneumonia
Tyler H. Ternes, MD Jorge Alberto Carrillo-Bayona, MD
394 Lung Cancer Screening 466 Sarcoidosis
Sonia L. Betancourt-Cuellar, MD Sonia L. Betancourt-Cuellar, MD
472 Pleuropulmonary Fibroelastosis
xvii
TABLE OF CONTENTS
548 Dendriform Pulmonary Ossification
SMOKING-RELATED DISEASES Jorge Alberto Carrillo-Bayona, MD
474 Respiratory Bronchiolitis and RBILD
Jorge Alberto Carrillo-Bayona, MD SECTION 7: CONNECTIVE TISSUE
476 Desquamative Interstitial Pneumonia DISORDERS, IMMUNOLOGICAL
Jorge Alberto Carrillo-Bayona, MD DISEASES, AND VASCULITIS
480 Pulmonary Langerhans Cell Histiocytosis
Tyler H. Ternes, MD INTRODUCTION AND OVERVIEW
484 Combined Pulmonary Fibrosis and Emphysema 552 Approach to Connective Tissue Disorders,
Aletta Ann Frazier, MD Immunological Diseases, and Vasculitis
PNEUMOCONIOSIS
486 Asbestosis IMMUNOLOGICAL AND CONNECTIVE TISSUE
Carlos S. Restrepo, MD and Helen T. Winer-Muram, MD DISORDERS
490 Silicosis and Coal Worker's Pneumoconiosis 554 Interstitial Pneumonia With Autoimmune Features
Brett W. Carter, MD, CPPS and Julia Alegría, MD (IPAF)
494 Hard Metal Pneumoconiosis Santiago Martínez-Jiménez, MD
Carlos S. Restrepo, MD 558 Rheumatoid Arthritis
496 Berylliosis Sonia L. Betancourt-Cuellar, MD
Sonia L. Betancourt-Cuellar, MD 562 Scleroderma
500 Silo-Filler's Disease Julia Alegría, MD and Jonathan Hero Chung, MD
Tyler H. Ternes, MD 566 Mixed Connective Tissue Disease
Julia Alegría, MD and Laura E. Heyneman, MD
OTHER INHALATIONAL DISORDERS 568 Polymyositis/Dermatomyositis
502 Hypersensitivity Pneumonitis Julia Alegría, MD and Carlos S. Restrepo, MD
Julia Alegría, MD 572 Systemic Lupus Erythematosus
506 Smoke Inhalation Julia Alegría, MD and Laura E. Heyneman, MD
John P. Lichtenberger, III, MD and Terrance Healey, MD 576 Sjögren Syndrome
510 E-Cigarette or Vaping Product Use-Associated Lung Sonia L. Betancourt-Cuellar, MD
Injury (EVALI) 582 Ankylosing Spondylitis
Carlos S. Restrepo, MD Tyler H. Ternes, MD
512 Aspiration 586 Inflammatory Bowel Disease
Carlos S. Restrepo, MD Sonia L. Betancourt-Cuellar, MD
516 Excipient Lung Disease 590 Erdheim-Chester Disease
Santiago Martínez-Jiménez, MD Carlos S. Restrepo, MD
EOSINOPHILIC LUNG DISEASE THORACIC COMPLICATIONS IN

520 Acute Eosinophilic Pneumonia IMMUNOCOMPROMISED PATIENTS
Jorge Alberto Carrillo-Bayona, MD 592 Hematopoietic Stem Cell Transplantation
522 Chronic Eosinophilic Pneumonia Sonia L. Betancourt-Cuellar, MD
Jorge Alberto Carrillo-Bayona, MD 596 Solid Organ Transplantation
524 Hypereosinophilic Syndrome Sonia L. Betancourt-Cuellar, MD
Jorge Alberto Carrillo-Bayona, MD 600 HIV/AIDS
METABOLIC DISEASES AND MISCELLANEOUS 604 Neutropenia
CONDITIONS Sonia L. Betancourt-Cuellar, MD
526 Alveolar Microlithiasis
Jorge Alberto Carrillo-Bayona, MD PULMONARY HEMORRHAGE AND
528 Metastatic Pulmonary Calcification VASCULITIS
Tyler H. Ternes, MD 608 Idiopathic Pulmonary Hemosiderosis
532 Lymphangioleiomyomatosis Allen Heeger, DO
Melissa L. Rosado de Christenson, MD, FACR 610 Goodpasture Syndrome
536 Pulmonary Amyloidosis Aletta Ann Frazier, MD
Laura E. Heyneman, MD 614 Pulmonary Granulomatosis With Polyangiitis
540 Pulmonary Alveolar Proteinosis Aletta Ann Frazier, MD
Julia Alegría, MD and Jorge Alberto Carrillo-Bayona, MD 618 Eosinophilic Granulomatosis With Polyangiitis
544 Lipoid Pneumonia Carlos S. Restrepo, MD and Jonathan Hero Chung, MD
xviii
TABLE OF CONTENTS
620 Behçet Syndrome 688 Coronary Artery Aneurysm
Aletta Ann Frazier, MD Julia Alegría, MD and John P. Lichtenberger, III, MD
622 Necrotizing Sarcoid Granulomatosis 690 Paraesophageal Varices
Aletta Ann Frazier, MD John P. Lichtenberger, III, MD
692 Mediastinal Lymphangioma
SECTION 8: MEDIASTINAL Aletta Ann Frazier, MD
ABNORMALITIES 694 Mediastinal Hemangioma
626 Approach to Mediastinal Abnormalities GLANDULAR ENLARGEMENT
Melissa L. Rosado de Christenson, MD, FACR 696 Thymic Hyperplasia
PRIMARY NEOPLASMS 700 Mediastinal Goiter
630 Thymoma Santiago Martínez-Jiménez, MD
634 Thymic Neuroendocrine Neoplasm DISEASES OF THE ESOPHAGUS
Sherief H. Garrana, MD 704 Achalasia
636 Thymic Carcinoma Julia Alegría, MD
Sherief H. Garrana, MD 706 Esophageal Diverticula
638 Thymolipoma Julia Alegría, MD and Tomás Franquet, MD, PhD
Melissa L. Rosado de Christenson, MD, FACR 708 Esophageal Stricture
640 Mediastinal Teratoma Claudio Silva, MD, MSc, MBA and Santiago Martínez-
John P. Lichtenberger, III, MD Jiménez, MD
644 Mediastinal Seminoma 710 Esophageal Carcinoma
Aletta Ann Frazier, MD Sonia L. Betancourt-Cuellar, MD
646 Nonseminomatous Malignant Germ Cell Neoplasm
Aletta Ann Frazier, MD MISCELLANEOUS CONDITIONS
648 Neurogenic Neoplasms of the Nerve Sheath 714 Mediastinal Lipomatosis
Sherief H. Garrana, MD Claudio Silva, MD, MSc, MBA
652 Neurogenic Neoplasms of the Sympathetic Ganglia 716 Mediastinitis
John P. Lichtenberger, III, MD Claudio Silva, MD, MSc, MBA
654 Neurofibromatosis 720 Mediastinal Fat Necrosis
Sonia L. Betancourt-Cuellar, MD Allen Heeger, DO
724 Extramedullary Hematopoiesis
LYMPHADENOPATHY
Claudio Silva, MD, MSc, MBA and Santiago Martínez-
656 Metastatic Disease, Lymphadenopathy Jiménez, MD
Brett W. Carter, MD, CPPS 726 Hiatal Hernia
660 Mediastinal Lymphoma Tyler H. Ternes, MD
Sherief H. Garrana, MD
664 Fibrosing Mediastinitis SECTION 9: CARDIOVASCULAR
Sherief H. Garrana, MD DISORDERS
668 Castleman Disease
Brett W. Carter, MD, CPPS INTRODUCTION AND OVERVIEW
732 Approach to Cardiovascular Disorders
CYSTS Santiago Martínez-Jiménez, MD
672 Bronchogenic Cyst
Aletta Ann Frazier, MD DISEASES OF THE AORTA AND GREAT
676 Esophageal Duplication Cyst VESSELS
Aletta Ann Frazier, MD 736 Atherosclerosis
678 Pericardial Cyst Carlos S. Restrepo, MD and Santiago Martínez-Jiménez,
Aletta Ann Frazier, MD MD
682 Thymic Cyst 740 Aortic Aneurysm
Aletta Ann Frazier, MD Carlos S. Restrepo, MD and Santiago Martínez-Jiménez,
MD
VASCULAR LESIONS
742 Acute Aortic Syndromes
684 Mediastinal Vascular Masses Santiago Martínez-Jiménez, MD and Julia Alegría, MD
xix
TABLE OF CONTENTS
748 Marfan Syndrome 820 Cardiac Myxoma
Claudio Silva, MD, MSc, MBA and Santiago Martínez- John P. Lichtenberger, III, MD
Jiménez, MD 824 Cardiac Sarcoma
750 Takayasu Arteritis Brett W. Carter, MD, CPPS
Brett W. Carter, MD, CPPS 826 Pulmonary Artery Sarcoma
752 Superior Vena Cava Obstruction Brett W. Carter, MD, CPPS
Allen Heeger, DO 828 Aortic Sarcoma
PULMONARY EDEMA
756 Pulmonary Edema SECTION 10: TRAUMA
Melissa L. Rosado de Christenson, MD, FACR INTRODUCTION AND OVERVIEW
PULMONARY HYPERTENSION AND 832 Approach to Chest Trauma
THROMBOEMBOLIC DISEASE Melissa L. Rosado de Christenson, MD, FACR
762 Pulmonary Artery Hypertension AIRWAYS AND LUNG
766 Pulmonary Venoocclusive Disease/Pulmonary 834 Tracheobronchial Laceration
Capillary Hemangiomatosis Cristina Fuss, MD and Terrance Healey, MD
Claudio Silva, MD, MSc, MBA 836 Lung Trauma
768 Acute Pulmonary Thromboembolic Disease Allen Heeger, DO
Allen Heeger, DO
772 Chronic Pulmonary Thromboembolic Disease
CARDIOVASCULAR/MEDIASTINUM
Carlos S. Restrepo, MD and Helen T. Winer-Muram, MD 840 Pneumomediastinum
776 Sickle Cell Disease John P. Lichtenberger, III, MD
Aletta Ann Frazier, MD 844 Traumatic Aortic Injury
780 Fat Embolism Allen Heeger, DO
Brett W. Carter, MD, CPPS 848 Esophageal Perforation
782 Hepatopulmonary Syndrome John P. Lichtenberger, III, MD and Diane C. Strollo, MD,
John P. Lichtenberger, III, MD FACR
784 Illicit Drug Use, Pulmonary Manifestations 852 Thoracic Duct Tear
Tyler H. Ternes, MD and Carol C. Wu, MD Allen Heeger, DO
DISEASES OF THE HEART AND PERICARDIUM PLEURA, CHEST WALL, AND DIAPHRAGM
786 Valve and Annular Calcification 854 Traumatic Pneumothorax
Brett W. Carter, MD, CPPS Allen Heeger, DO
790 Aortic Valve Disease 856 Traumatic Hemothorax
794 Mitral Valve Disease 858 Thoracic Splenosis
Claudio Silva, MD, MSc, MBA and John P. Lichtenberger, Allen Heeger, DO
III, MD 860 Rib Fractures and Flail Chest
798 Left Atrial Calcification Cristina Fuss, MD and Jonathan Hero Chung, MD
Claudio Silva, MD, MSc, MBA 864 Spinal Fracture
800 Ventricular Calcification John P. Lichtenberger, III, MD
Claudio Silva, MD, MSc, MBA and Brett W. Carter, MD, 866 Sternal Fracture
CPPS John P. Lichtenberger, III, MD
802 Coronary Artery Calcification 868 Diaphragmatic Rupture
Claudio Silva, MD, MSc, MBA and Brett W. Carter, MD, Cristina Fuss, MD and Jonathan Hero Chung, MD
CPPS
806 Post Cardiac Injury Syndrome SECTION 11: POST-TREATMENT CHEST
Claudio Silva, MD, MSc, MBA
808 Pericardial Effusion
Cristina Fuss, MD 874 Approach to Post-Treatment Chest
814 Constrictive Pericarditis Santiago Martínez-Jiménez, MD
LIFE SUPPORT DEVICES
CARDIOVASCULAR NEOPLASMS 876 Endotracheal and Enteric Tubes
816 Cardiac and Pericardial Metastases Cristina Fuss, MD
xx
TABLE OF CONTENTS
880 Chest Tubes and Drains 958 Chylothorax
Cristina Fuss, MD Claudio Silva, MD, MSc, MBA
884 Vascular Catheters 960 Empyema
Cristina Fuss, MD Julia Alegría, MD and Jonathan Hero Chung, MD
890 Cardiac Conduction Devices
Cristina Fuss, MD PNEUMOTHORAX
964 Iatrogenic Pneumothorax
SURGICAL PROCEDURES AND Cristina Fuss, MD
COMPLICATIONS 966 Primary Spontaneous Pneumothorax
894 Pleurodesis Cristina Fuss, MD
John P. Lichtenberger, III, MD and Florian J. Fintelmann, 970 Secondary Spontaneous Pneumothorax
MD, FRCPC Cristina Fuss, MD
896 Sublobar Resection
Allen Heeger, DO PLEURAL THICKENING
898 Lung Volume Reduction Surgery 974 Apical Cap
John P. Lichtenberger, III, MD and Carol C. Wu, MD John P. Lichtenberger, III, MD
900 Lobectomy 976 Pleural Plaques
904 Lobar Torsion 980 Pleural Fibrosis and Fibrothorax
Cristina Fuss, MD and Jeffrey P. Kanne, MD Allen Heeger, DO
906 Pneumonectomy
Allen Heeger, DO NEOPLASIA
912 Thoracoplasty and Apicolysis 982 Malignant Pleural Effusion
Julia Alegría, MD and Jeffrey P. Kanne, MD Allen Heeger, DO
914 Lung Herniation 984 Solid Pleural Metastases
Cristina Fuss, MD and Jeffrey P. Kanne, MD Melissa L. Rosado de Christenson, MD, FACR
916 Sternotomy 986 Malignant Pleural Mesothelioma
John P. Lichtenberger, III, MD and Diane C. Strollo, MD, Brett W. Carter, MD, CPPS
FACR 990 Localized Fibrous Tumor of the Pleura
920 Heart Transplantation Melissa L. Rosado de Christenson, MD, FACR
924 Lung Transplantation SECTION 13: CHEST WALL AND
Cristina Fuss, MD and Jeffrey P. Kanne, MD DIAPHRAGM
928 Esophageal Resection
Julia Alegría, MD and Tomás Franquet, MD, PhD INTRODUCTION AND OVERVIEW
RADIATION, CHEMOTHERAPY, ABLATION 996 Approach to Chest Wall and Diaphragm
930 Radiation-Induced Lung Disease
Sonia L. Betancourt-Cuellar, MD CHEST WALL
936 Drug Reaction, Intrathoracic 998 Chest Wall Infections
Sonia L. Betancourt-Cuellar, MD John P. Lichtenberger, III, MD
940 Ablation Procedures 1000 Discitis
Sonia L. Betancourt-Cuellar, MD Julia Alegría, MD
1002 Chest Wall Lipoma and Liposarcoma
SECTION 12: PLEURAL DISEASES Brett W. Carter, MD, CPPS
INTRODUCTION AND OVERVIEW 1006 Elastofibroma and Fibromatosis
946 Approach to Pleural Diseases 1010 Chest Wall Metastases
Melissa L. Rosado de Christenson, MD, FACR Claudio Silva, MD, MSc, MBA
1014 Chondrosarcoma
EFFUSION
948 Transudative Pleural Effusion 1016 Plasmacytoma and Multiple Myeloma
Claudio Silva, MD, MSc, MBA Brett W. Carter, MD, CPPS
952 Exudative Pleural Effusion
Claudio Silva, MD, MSc, MBA DIAPHRAGM
956 Hemothorax 1018 Diaphragmatic Eventration
Claudio Silva, MD, MSc, MBA Santiago Martínez-Jiménez, MD
1020 Diaphragmatic Paralysis
xxi
THIRD EDITION
Martínez-Jiménez
Restrepo | Betancourt-Cuellar
Carter | Lichtenberger
Heeger | Ternes
Carrillo-Bayona | Frazier
Silva | Garrana
Alegría | Fuss
SECTION 1
Introduction and Overview

Approach to Chest Imaging 4
Illustrated Terminology
Approach to Illustrated Terminology 6
Acinar Nodules 8
Air Bronchogram 9
Air-Trapping 10
Airspace 11
Architectural Distortion 12
Bulla/Bleb 13
Cavity 14
Centrilobular 15
Consolidation 16
Cyst 17
Ground-Glass Opacity 18
Honeycombing 19
Interlobular Septal Thickening 20
Intralobular Lines 21
Mass 22
Miliary Pattern 23
Mosaic Attenuation 24
Nodule 25
Peribronchovascular 26
Perilobular Pattern 27
Perilymphatic 28
Pneumatocele 29
Reticular Pattern 30
Secondary Pulmonary Lobule 31
Traction Bronchiectasis 32
Tree-in-Bud Opacities 33
Chest Radiographic and CT Signs

Approach to Chest Radiographic and CT Signs 34
Air Crescent Sign 40
Cervicothoracic Sign 41
Comet Tail Sign 42
CT Halo Sign 43
Deep Sulcus Sign 44
Fat Pad Sign 45
Finger-in-Glove Sign 46
Hilum Convergence Sign 47
Hilum Overlay Sign 48
Incomplete Border Sign 49
Luftsichel Sign 50
Reversed Halo Sign 51
Rigler and Cupola Signs 52
S-Sign of Golden 53
Signet Ring Sign 54
Silhouette Sign 55
Atelectasis and Volume Loss

Approach to Atelectasis and Volume Loss 56
Atelectasis 60
Cicatricial Atelectasis 64
Rounded Atelectasis 65
Approach to Chest Imaging
Introduction dyspnea, or inability to understand or follow technologist's

instructions.
Chest diseases are prevalent worldwide, and heart disease,
malignant neoplasms, and chronic lower respiratory disease PA and lateral chest radiography: Ambulatory patients are
are among the top four causes of death in the United States. imaged with orthogonal posteroanterior (PA) and lateral chest
Chest diseases can be categorized based on anatomic location radiographs, which allow identification and anatomic
as affecting the airways, lungs, pleura, mediastinum, chest localization of abnormalities. Optimal imaging is obtained in
wall, or diaphragm. Each of these regions may be involved by the upright position, at full inspiration, without motion or
developmental abnormalities, neoplasms, or infections. rotation, and with minimal superimposition of upper
Additionally, idiopathic, inflammatory, connective tissue, extremities, head, neck, or scapulae. PA refers to the
autoimmune, and lymphoproliferative disorders may also posteroanterior direction of the x-ray beam as it traverses the
affect the chest. The ventilatory and respiratory functions of patient to expose the image receptor. Source-image distance
the lungs and airways provide a portal for exposure to a (SID) is 72 in., and a high kilovoltage technique (120-150 kVp) is
variety of inhalational diseases, some of which are related to used. Lateral radiography is obtained with the patient's left
the patient's environment and occupation. Thoracic diseases side closest to the image receptor.
may also be categorized based on their physiological effects Bedside (portable) chest radiography: Neonates and infants,
as obstructive or restrictive abnormalities. Finally, the various debilitated and unstable patients, and those who have
organs and anatomic regions of the chest may be affected by sustained major trauma or are seriously ill or bed-ridden
traumatic or iatrogenic conditions. undergo portable anteroposterior (AP) chest radiography, in
Clinical Presentation which the x-ray beam traverses the patient anteroposteriorly
Patients with chest disease often present with chest pain, using a SID of 40 in. and relatively low kilovoltage techniques
dyspnea, &/or cough, which may arise acutely or be chronic. with resultant magnification of anterior structures and
Systemic complaints may include malaise, fatigue, and weight decreased image sharpness. Portable chest radiography plays
loss. Patients with thoracic malignancy may present because an important role in the evaluation of medical life support
of systemic effects of the neoplasm unrelated to metastatic devices and the identification of complications of their use.
disease or with symptoms related to systemic metastases. Decubitus radiography is occasionally used to evaluate pleural
Assessment of Chest Disease effusion or pneumothorax. Apical lordotic radiography
An understanding of the patient's chief complaint and past (formerly used to evaluate the lung apices) is rarely used
medical and surgical history is of foremost importance, today. Inspiratory and expiratory chest radiography for
including relevant habits, such as cigarette smoking, use of identification of pneumothorax is also rarely used, as it has
prescription or illicit drugs, and environmental or occupational been shown that it does not improve pneumothorax
exposures. It is important to determine the patient's immune visualization while effectively doubling radiation dose.
status, as altered immunity may result in a variety of Computed Tomography
infectious, inflammatory, and neoplastic conditions. The Computed tomography (CT) is easily and expeditiously
physical exam may provide important clues to the diagnosis performed. It allows accurate anatomic localization and
and is complemented by laboratory and pulmonary function characterization of radiographic abnormalities and may help
tests. detect additional abnormalities that may enable a diagnosis
Imaging plays a pivotal role in the assessment of patients with and a management course.
thoracic complaints and is frequently obtained during the As the growth of multidetector CT utilization has resulted in a
initial evaluation. Thus, radiologists often impact patient substantially increased radiation dose to the population,
management by identifying abnormalities and providing a radiologists and vendors continue to implement dose
focused differential diagnosis and management reduction measures. It is postulated that up to 2% of future
recommendations. In selected cases, the radiologist may cancers will be linked to the increased utilization of medical
perform image-guided tissue sampling of specific lesions or imaging. Thus, radiologists should actively communicate with
provide definitive treatment with various thoracic and educate referring physicians and work with them toward
interventions (e.g., drainage of fluid collections, ablation reducing the number of unnecessary studies. Electronic
procedures). decision support systems that use evidence-based guidelines
Thoracic Imaging and appropriateness criteria have helped reduce the number
of inappropriate studies.
Chest Radiography
The chest radiograph is frequently the initial imaging study Radiologists can take additional measures to reduce dose with
obtained on patients with chest complaints but may also be the use of shielding, tube current modulation, and adaptive
obtained in asymptomatic subjects as part of a physical exam statistical iterative reconstruction techniques. As it has been
or a preoperative evaluation. It allows assessment of the shown that the radiation dose during CT imaging is directly
airways, lungs, cardiovascular system, pleura, diaphragm, and proportional to tube current, the reduction of tube current-
chest wall osseous structures and soft tissues. Chest time product (mAs) can achieve low-dose chest CT studies that
radiographic interpretation is challenging because of the preserve satisfactory image quality. Low-dose CT imaging
broad range of densities produced by the superimposition of techniques should be used routinely in small patients and in
the various thoracic organs and tissues and the subtlety of those who will receive serial CT examinations, such as young
many abnormalities. Thus, accurate interpretation requires an patients imaged for restaging of malignancy and those
in-depth knowledge of imaging anatomy, impeccable imaging imaged for the evaluation of indeterminate lung nodules or
technique, and optimal viewing and working conditions. diffuse infiltrative pulmonary diseases.
Additional challenges relate to the population referred for
imaging, including patients with large body habitus, severe
4

Unenhanced chest CT: Evaluation of the lungs and airways noninvasive evaluation of the abnormal thymus and allows the
does not require the use of intravenous contrast. Unenhanced distinction of thymic hyperplasia from thymic neoplasia.
chest CT is ideally suited for lung cancer screening, identifying Positron Emission Tomography
intralesional calcifications, and assessing indeterminate Positron emission tomography (PET) and combined PET/CT
nodules, diffuse infiltrative lung diseases, and airways are invaluable in the staging of patients with malignancy. PET
diseases. and CT images obtained in a single imaging session are fused
Contrast-enhanced chest CT: Administration of intravenous into a co-registered image that allows correlation of abnormal
contrast is mandatory for vascular imaging and the metabolic activity with CT abnormalities. It is the imaging
assessment of hilar lymphadenopathy. Contrast is also modality of choice for staging and restaging lymphoma and
valuable in the assessment of thoracic malignancy, as it may other malignancies. Areas of abnormal metabolic activity
help identify and characterize tumors surrounded by following treatment can be localized and targeted for tissue
atelectasis or consolidation. CT aortography is mandatory for sampling. Normal increased metabolic activity may be seen in
excluding traumatic vascular injury and pulmonary certain anatomic regions (e.g., the interatrial septum
thromboembolism. Acute aortic syndromes are evaluated corresponding to brown fat deposition). False-positive PET/CT
with both unenhanced and enhanced aortic CT in order to studies may occur in infectious or inflammatory processes,
diagnose intramural hematoma. and false-negative studies may occur in indolent malignancies.
Post processing: Image reformation in various planes Ventilation-Perfusion Scintigraphy
(coronal, sagittal, oblique) helps determine the distribution of Ventilation-perfusion (V/Q) scintigraphy has been largely
lung disease. Because some diseases involve the lung replaced by CT pulmonary angiography (CTPA) in the
diffusely, while others exhibit a predilection for the upper evaluation of pulmonary thromboembolism, although CTPA
lung zones or lung bases, recognizing the pattern of and V/Q scintigraphy have similar positive predictive values.
distribution allows the radiologist to provide a reasonable CTPA is superior in the evaluation of patients with evidence of
differential diagnosis. For example, lung disease on radiography and has the advantage of
lymphangioleiomyomatosis (LAM) and pulmonary Langerhans demonstrating alternate etiologies for the patient's
cell histiocytosis (PLCH) both manifest with pulmonary cysts. symptoms.
However, LAM affects the lung diffusely, while PLCH However, a growing body of literature supports performing
characteristically spares the lung bases. In addition, since perfusion scintigraphy instead of CTPA in the setting of
neoplasms may grow in all directions, multiplanar imaging pregnancy, provided that chest radiographs are normal, and in
may allow documentation of craniocaudad growth of a tumor cases in which an alternative diagnosis is not suspected. CTPA
that appears stable on axial imaging. may yield indeterminate results in pregnant patients due to
Maximum-intensity projection (MIP) and minimum- physiologic hemodilution of contrast and interruption of
intensity projection (minIP) images: MIP images retain the contrast by unopacified blood from the inferior vena cava. It
relative maximum value along each ray path, preferentially should be noted that CTPA delivers a higher radiation dose to
display contrast-filled and higher attenuation structures, and the maternal breast when compared to V/Q scintigraphy.
allow detection of subtle lung nodules and evaluation of Appropriate measures (e.g., hydration) must be taken to
vascular structures. minIP images display the minimum value decrease the radiation dose to the fetus in pregnant patients
along the ray paths and are useful in the assessment of the undergoing V/Q scintigraphy.
airways, emphysema, and air-trapping.
Volume and surface rendering: These techniques do not
Chest radiographs are the most frequent imaging studies
always add value to diagnostic interpretation but are often
performed in most practices and possibly the most
greatly appreciated by referring physicians. Volume-rendering
challenging to interpret. Identification of a radiographic
techniques can provide a 3D image display of vascular
abnormality must be correlated with its localization to a
anatomy. Surface-rendered displays are ideally suited for
specific anatomic compartment in order to provide a
depiction of tubular structures, such as the airways, and are
differential diagnosis. Identification of associated findings,
employed in performing virtual bronchoscopy, which mimics
such as lesion calcification or cavitation, lymphadenopathy,
the airway luminal visualization achieved on bronchoscopy.
&/or pleural effusion, enables the formulation of a focused
High-resolution CT (HRCT): HRCT is the modality of choice differential diagnosis. Comparison to prior studies is of
for evaluating diffuse infiltrative lung disease. It uses a narrow paramount importance as documentation of stability
slice width (1-2 mm) and a high spatial resolution image generally supports a benign diagnosis.
reconstruction algorithm. The ability to analyze diffuse lung
Communication of imaging findings to the referring physician
involvement in relation to the anatomy of the secondary
is typically accomplished via the radiologic report. Radiologists
pulmonary lobule allows accurate and reproducible disease
must strive to produce concise, clear, and unambiguous
characterization and the formulation of an appropriate
reports that "answer the question" and include a description
differential diagnosis.
of the abnormality, the differential diagnosis, the most likely
Magnetic Resonance Imaging diagnosis, and management recommendations that may
Magnetic resonance (MR) imaging is routinely employed in the include advanced imaging (e.g., CT, HRCT, MR, scintigraphy,
evaluation of the cardiovascular system and is the modality of etc.), a course of treatment, tissue sampling, or emergent
choice for the assessment of myocardial perfusion and medical/surgical intervention. Critical and unexpected findings
ventricular and valve function. MR helps evaluate locally must be promptly communicated to the appropriate member
invasive thoracic tumors, particularly to identify invasion of of the healthcare team.
cardiovascular structures and to evaluate the brachial plexus
in cases of Pancoast tumor. MR is particularly valuable in the
5
Approach to Illustrated Terminology
Introduction Terminology of Thoracic Imaging

Advancements in diagnostic imaging are not limited to In recent years, thoracic imaging has undergone immense
evolving technology or the introduction of novel state-of-the- growth and technological advancement. Thoracic CT and high-
art imaging equipment but have also impacted the way resolution computed tomography (HRCT) allow identification
radiologists view and interpret images and the manner of and characterization of subtle abnormalities that were
completing radiologic reports. Picture archiving and previously seen only by anatomists and pathologists. Today,
communication systems (PACS) permit inexpensive storage of the radiologist can thoroughly analyze pulmonary
large image data sets, which are easily accessed by radiologists abnormalities with respect to the underlying units of lung
and referring physicians for interpretation and consultation. structure, such as the secondary pulmonary lobule and the
Radiologists readily access comparison images and prior pulmonary acinus. The ability to correlate imaging
reports in order to document change or stability of imaging abnormalities with the anatomic portion of the lung affected
abnormalities. Speech recognition technology allows the allows the radiologist to make confident diagnoses of
expeditious generation of radiologic reports that can be diseases, such as pulmonary fibrosis, sarcoidosis, interstitial
reviewed for accuracy prior to their release. The availability of edema, and emphysema. In fact, thoracic imagers play an
electronic medical records provides access to timely relevant integral role in the multidisciplinary diagnosis of interstitial
clinical and laboratory data that enhances interpretation and lung disease and adenocarcinoma of the lung. In addition, the
the formulation of a focused differential diagnosis. growing field of quantitative lung imaging may allow
The wide availability of viewing stations has also impacted radiologists to contribute to the noninvasive assessment of
the entire lung in the setting of diffuse lung diseases and
communication between radiologists and clinicians, an
correlate those findings with abnormalities of pulmonary
interchange that frequently occurs via secure electronic mail
or by telephone. In fact, face-to-face communication between function.
clinicians and radiologists has greatly diminished with the Thoracic imagers are able to evaluate a series of complex
unfortunate consequence of lessening the opportunity to ask imaging abnormalities affecting the thorax and to work in
for additional medical history that may not be available on the conjunction with clinical colleagues toward an expeditious
requisition or electronic medical record. diagnosis and course of management. The protean and
In today's practice, the radiologic report is the principal complex findings identified on chest CT and HRCT, along with
advances in our understanding of lung diseases, mandate the
method used by radiologists to communicate diagnostic
consistent use of correct terminology for the description of
imaging findings. Although unexpected critical abnormalities
abnormalities. In 2008, the Fleischner Society published the
should always be verbally communicated to a member of the
glossary of terms recommended for thoracic imaging
healthcare team, most abnormal findings are communicated
reporting, a lexicon that reflects the emergence of new terms
via the radiology report. In addition, increased transparency in
healthcare has made imaging reports accessible to patients, and the obsolescence of others.
which generates additional challenges for radiologists as they The Fleischner glossary is not only a list of proper terminology
strive to simplify and clarify the report language and in thoracic imaging but also includes definitions and
impression. Thus, radiologists must strive to generate concise, illustrations of anatomic locations in the thorax, signs in
clear, and unambiguous reports that not only contain relevant thoracic imaging, specific disease processes (such as
findings but also include focused differential diagnoses and emphysema and rounded atelectasis), and the many
specific recommendations for further imaging &/or future interstitial pneumonias.
management. Pneumonia is defined as inflammation of the airspaces and
The Proper Language interstitium. The term is predominantly used to denote an
infectious process of the lung. The diagnosis may be made
As imaging specialists, we must strive to use proper and
clinically or may be proposed by the radiologist based on the
correct language in both verbal communications and in our
correlation of imaging findings with the clinical history.
reports. For example, the phrase "chest x-ray" may be forever
However, the term "pneumonia" is also used for a number of
ingrained in colloquial communications in spite of the fact that
noninfectious pulmonary disorders related to inflammation
it is an incorrect descriptor of the imaging study. As x-rays are
and fibrosis (e.g., the idiopathic interstitial pneumonias).
invisible, a radiologist does not interpret a chest x-ray but
rather a chest radiograph. Likewise, modern radiologists rarely Summary
review or interpret films or analog images given the The use of clear and concise terminology facilitates
ubiquitous nature and broad utilization of PACS that allow
communication with other radiologists, clinicians, and
interpretation of soft copy images. increasingly with patients. Interpretation of thoracic imaging
Infiltrate is a term formerly used to describe any pulmonary studies requires knowledge of imaging anatomy and the
opacity produced by airspace &/or interstitial disease on chest utilization of correct descriptors of imaging abnormalities. In
radiography or computed tomography (CT). In medicine, the many instances, the description of an abnormality allows the
word "infiltrate" is used to describe the accumulation in tissue radiologist to suggest the correct diagnosis and formulate the
of either abnormal or excess normal substances. The use of appropriate next step in patient management.
this term is controversial, has various meanings, is imprecise in
its implications, and is no longer recommended for the
Selected References
description of chest imaging abnormalities. Instead, the term 1. Lourenco AP et al: Optimizing radiology reports for patients and referring
physicians: mitigating the curse of knowledge. Acad Radiol. 27(3):436-9,
"opacity" with the addition of appropriate descriptors 2020
(airspace, reticular, nodular) is preferred. 2. Hansell DM et al: Fleischner Society: glossary of terms for thoracic imaging.
Radiology. 246(3):697-722, 2008
6
Approach to Illustrated Terminology

Bacterial Pneumonia Bacterial Pneumonia
(Left) PA chest radiograph of a
54-year-old man with cough,
fever, and leukocytosis shows
a right upper lobe
consolidation located above
the horizontal fissure and,
therefore, involving the
anterior segment of the right
upper lobe. (Right) Lateral
chest radiograph of the same
patient shows consolidation in
the right upper lobe anterior
and posterior segments. Based
on the radiographic and
clinical findings, the final
impression was right upper
lobe pneumonia. In this case,
the term pneumonia refers to
bacterial pulmonary infection.
Usual Interstitial Pneumonia Nonspecific Interstitial Pneumonia

(Left) Axial HRCT of an 83-
year-old woman with
idiopathic pulmonary fibrosis
shows a usual interstitial
pneumonia (UIP) pattern of
fibrosis characterized by
basilar predominant
subpleural honeycomb cysts
arrayed in layers. (Right) Axial
NECT of a patient with
nonspecific interstitial
pneumonia (NSIP) shows
patchy, basilar, ground-glass
opacities and mild traction
bronchiectasis ﬅ.
Noninfectious diffuse fibrotic
lung diseases form part of the
spectrum of idiopathic
interstitial pneumonias.
Chronic Eosinophilic Pneumonia Lipoid Pneumonia

(Left) Axial NECT of a patient
with chronic eosinophilic
pneumonia shows peripheral
subpleural ground-glass
opacities ﬅ. This description
is preferred over the term
"infiltrate," although this
noninfectious disease is
characterized by alveolar and
interstitial eosinophilic
infiltration. (Right) Composite
image with axial CECT in lung
(left) and soft tissue (right)
window shows multifocal
consolidations with intrinsic
fat attenuation ﬅ,
representing exogenous lipoid
pneumonia secondary to
mineral oil aspiration.
7
Acinar Nodules
KEY FACTS
TERMINOLOGY • CT/HRCT
• Acinar nodule (accumulation of pathologic material in ○ Multifocal ground-glass or part-solid nodular opacities
pulmonary acinus) ○ 5-8 mm in size
○ Clustered, rounded, poorly-defined opacities PATHOLOGY
○ Typically multifocal
• Etiology
○ Size: 5-8 mm in diameter
○ Infection
• Acinus
○ Aspiration
○ Largest lung unit in which all airways participate in gas
○ Edema
exchange
○ Hemorrhage
– Structural lung unit distal to terminal bronchiole
○ Pulmonary vasculitis
– Supplied by 1st-order respiratory bronchioles
○ Pulmonary contusion
– Contains alveolar ducts and alveoli
○ Lung cancer: Invasive mucinous adenocarcinoma
○ Size: 6-10 mm in diameter
• Secondary pulmonary lobule DIAGNOSTIC CHECKLIST
○ Contains 3-25 acini • Sputum analysis for diagnosis of infection
IMAGING • Diagnosis of vasculitis or malignancy may require
bronchoscopic or open lung biopsy
• Radiography
• History of blunt trauma in pulmonary contusion
○ Multifocal, ill-defined, small, rounded opacities

who presented with fever and
cough shows
bronchopneumonia
characterized by acinar
nodules ﬉ manifesting as
multifocal, rounded, ill-
defined, ground-glass and
part-solid right upper lobe
nodules. (Right) Axial NECT of
a patient with a moderate
hiatus hernia (not shown) and
aspiration bronchiolitis shows
left lower lobe acinar nodules
manifesting as rounded
nodular consolidations ﬉
surrounded by ground-glass
opacity halos ﬈.
(Left) Axial CECT of a patient

with hemoptysis and
pulmonary hemorrhage shows
multifocal ground-glass acinar
opacities ﬈ adjacent to
medial nodular opacities that
exhibit the crazy-paving sign
﬉. The former correspond to
alveolar hemorrhage within
pulmonary acini. (Right)
Coronal CECT of a patient
with multicentric invasive
mucinous adenocarcinoma
shows multifocal, bilateral
lower lobe consolidations and
right upper lobe
heterogeneous, part-solid
acinar nodules with intrinsic
lucencies ﬈.
8
Air Bronchogram
KEY FACTS

TERMINOLOGY TOP DIFFERENTIAL DIAGNOSES
• Air bronchogram • Pulmonary interstitial emphysema
○ Definition: Visualization of air-filled bronchi within
PATHOLOGY
background of opacified lung parenchyma
○ Implies patency of proximal airways • Alveolar filling with pus, edema fluid, blood, tumor
○ Central obstruction is unlikely • Etiologies
○ May occur in confluent interstitial disease ○ Pneumonia: Infectious, lipoid, aspiration
• Bronchi not normally visible in outer 1/3 of lung ○ Neoplasms
– Lung cancer; particularly lepidic adenocarcinoma
IMAGING – Lymphoma
• Radiography ○ Alveolar edema
○ Air-filled branching lucencies representing patent ○ Alveolar hemorrhage
bronchi ○ Fibrosis: Radiation, sarcoidosis
○ Surrounding airspace disease
DIAGNOSTIC CHECKLIST
○ Indicates intrapulmonary location of abnormality
• CT • Consolidation with air bronchograms in a febrile patient is
○ Air-filled branching tapering bronchi consistent with pneumonia
○ Surrounding consolidated lung parenchyma • Consolidations in adults should be followed to radiographic
resolution to exclude underlying malignancy

patient with right upper lobe
pneumonia shows a dense
consolidation with an intrinsic
air bronchogram ﬅ, the
presence of which excludes a
central obstructing lesion.
Nevertheless, consolidations in
adults should be followed to
complete resolution to exclude
underlying malignancy. (Right)
Coronal CECT of a patient
with pneumonia shows a
dense right upper lobe
consolidation with an intrinsic
air bronchogram ﬈ that
manifests as branching
lucencies within the
consolidated lung.

with pneumonia shows a
lingular consolidation with an
intrinsic air bronchogram ﬈
manifesting as branching air-
filled tubular lucencies within
surrounding airspace disease.
(Right) Axial NECT of a patient
with chronic cough and
exogenous lipoid pneumonia
shows heterogeneous
consolidations in the middle
and right lower lobes and a
middle lobe air bronchogram
﬈. A variety of alveolar filling
disease processes may produce
air bronchograms on imaging.
9
Air-Trapping
KEY FACTS
TERMINOLOGY PATHOLOGY
• Air-trapping • Etiologies
○ Air retention in lung distal to airway obstruction shown ○ Constrictive bronchiolitis: Peribronchiolar fibrosis of
on expiratory CT membranous and respiratory bronchioles
– Infection, chronic rejection in transplantation,
IMAGING
connective tissue disease, inhalational lung disease,
• Radiography: Lung hyperlucency on expiration hypersensitivity pneumonitis, diffuse idiopathic
• CT pulmonary neuroendocrine cell hyperplasia
○ Inspiration ○ Cellular bronchiolitis: Tree-in-bud nodules +
– Normal lung is homogeneously lucent mosaic attenuation
– Mosaic attenuation: Patchwork of regions of different – Infection, aspiration, respiratory bronchiolitis, follicular
attenuation bronchiolitis, panbronchiolitis
○ Expiration ○ Asthma
– Increased attenuation of normal lung ○ Endoluminal foreign body or neoplasm
– Air-trapping: Sharply-defined geographic foci of lower
attenuation; follow outlines of secondary pulmonary
lobules; affects > 25% of lung volume; not limited to • Consider expiratory HRCT in patients with mosaic
lower lobe superior segments or lingular tip attenuation or suspected constrictive bronchiolitis
– Lobular air-trapping in < 3 adjacent lobules is normal
(Left) Composite image with

axial HRCT of a patient with
constrictive bronchiolitis
obtained in inspiration (top)
and expiration (bottom) shows
areas of expiratory air-
trapping that manifest as
geographic areas of
hyperlucent lung ﬅ. (Right)
Composite image with axial
HRCT on inspiration (left) and
expiration (right) of a patient
with constrictive bronchiolitis
shows inspiratory mosaic
attenuation and expiratory
air-trapping with decreased
vascularity. Suspected air-
trapping is confirmed on
expiratory CT imaging.

with hypersensitivity
pneumonitis shows multiple
foci of hyperlucent lung ﬅ
due to expiratory air-trapping.
In patients with
hypersensitivity pneumonitis,
areas of air-trapping may be
accentuated by surrounding
normal lung and ground-glass
opacity foci. (Right) Axial
NECT of a patient with a
central partially obstructing
carcinoid tumor shows
hyperlucency ﬅ of the
visualized left lower lobe
secondary to obstruction by
the tumor and resultant air-
trapping.
10
Airspace
KEY FACTS

• Airspace • Etiologies
○ Gas-containing portions of lung: Respiratory bronchioles, ○ Pneumonia
alveolar ducts, alveolar sacs, and alveoli – Bacterial, viral, fungal
○ Excludes purely conducting airways – Aspiration
• Airspace disease: Increased airspace opacity ○ Alveolar edema
○ Air loss (atelectasis); air replaced by fluid, pus, blood, ○ Alveolar hemorrhage
cells, fat, and other substances ○ Alveolar proteinosis
IMAGING ○ Neoplastic: Lung cancer, lymphoma, metastasis
○ Inflammation/fibrosis
• Radiography
– Sarcoidosis, eosinophilic pneumonia, organizing
○ Consolidation, mass, nodule; focal or multifocal, may be
pneumonia, lipoid pneumonia, vasculitis, interstitial
heterogeneous
lung disease, drug toxicity, radiation
• CT
pneumonitis/fibrosis
○ Airspace consolidation: Increased lung attenuation,
obscuration of normal structures DIAGNOSTIC CHECKLIST
○ Mass • Consider myriad etiologies of airspace filling in differential
○ Nodule diagnosis of airspace disease in patient without signs or
– Solid or subsolid symptoms of infection
(Left) Graphic demonstrates

the airspaces of the lung,
which are composed of the
small airways that participate
in gas exchange (respiratory
bronchiole ﬇, alveolar duct
ﬅ, and alveolar sac) and the
alveoli ﬆ and excludes purely
conductive airways. (Right) PA
chest radiograph of a patient
with interstitial edema shows
interlobular septal thickening,
perihilar haze, and focal
airspace opacity ﬅ in the
right lower lobe due to
alveolar filling with edema
fluid.

patient with fever and cough
demonstrates pneumonia
manifesting with extensive
airspace consolidation in the
left upper and lower lobes
with intrinsic air
bronchograms ﬈. Pulmonary
infection is a common etiology
of airspace disease. (Right)
Axial NECT of a patient with
subacute (nonfibrotic)
hypersensitivity pneumonitis
shows innumerable small
subsolid airspace nodules ﬇
in a centrilobular distribution.
This nodular form of airspace
disease is also referred to as
acinar nodules.
11
Architectural Distortion
KEY FACTS
• Architectural distortion • Interstitial fibrosis, honeycombing
○ Abnormal displacement of bronchi, vessels, fissures, or • Etiologies
septa secondary to diffuse or localized retractile fibrosis ○ Fibrosing interstitial lung disease (e.g., idiopathic
○ Characteristically related to interstitial fibrosis pulmonary fibrosis, fibrotic nonspecific interstitial
pneumonia)
IMAGING
○ End-stage sarcoidosis
• Radiography ○ Radiation-induced fibrosis
○ Reticular opacities; nodular and mass-like opacities ○ Pneumoconiosis
○ Volume loss ○ Chronic (fibrotic) hypersensitivity pneumonitis
○ Hilar displacement related to volume loss ○ Sequela of infection (e.g., tuberculosis, COVID-19)
○ Bronchiectasis related to volume loss ○ Sequela of acute respiratory distress syndrome
• CT
○ Abnormal displacement of pulmonary vessels and DIAGNOSTIC CHECKLIST
bronchi associated with pulmonary fibrosis • Architectural distortion is an irreversible process that
○ Reticular opacities with interlobular septal thickening denotes fibrosis
and intralobular lines ○ Usually associated with volume loss, reticulation, traction
○ Traction bronchiectasis, honeycombing bronchiectasis/bronchiolectasis, and honeycombing
○ Cicatricial atelectasis; may be nodular or mass-like
(Left) Coronal NECT of an 87-

year-old man with idiopathic
pulmonary fibrosis shows
basilar and subpleural
reticulation, architectural
distortion and honeycombing,
and a CT pattern consistent
with usual interstitial
pneumonia (UIP). (Right)
Composite image with PA
chest radiograph (left) and
coronal CECT (right) of a 66-
year-old woman with chronic
sarcoidosis shows upper lobe
volume loss and upper lung
zone predominant
peribronchovascular fibrosis
and architectural distortion
typical of end-stage disease.

78-year-old woman with a
history of prior tuberculosis
shows architectural distortion
of the entire left lung with
severe volume loss and
intrinsic bronchiectasis. Note
shift of the mediastinum to
the left. (Right) Axial CECT of
a 62-year-old man with right
upper lobe lung cancer treated
with stereotactic body
radiation shows marked right
upper lobe volume loss with
intrinsic vascular crowding and
bronchiectasis. The resultant
architectural distortion can be
characterized as cicatricial
atelectasis.
12
Bulla/Bleb
KEY FACTS

TERMINOLOGY • CT
• Bulla ○ Peripheral subpleural air-filled space
○ Definition: Air-containing space > 1 cm ○ Thin smooth walls
○ Surrounded by thin wall < 1 mm thick ○ Typically multifocal
○ Subpleural location; largest at lung apex ○ Thick walls, intrinsic fluid, air-fluid levels, or soft tissue
○ Associated with emphysema: Typically paraseptal but should suggest secondary infection but may also relate
also centrilobular to hemorrhage or neoplasm
• Bleb PATHOLOGY
○ Definition: Small gas-containing space within visceral • Paraseptal/centrilobular emphysema
pleura or subpleural lung measuring < 1 cm • Acute respiratory distress syndrome with interstitial
○ Difficult distinction between bleb and bulla, as both are emphysema and secondary subpleural bullae
peripherally located
○ Term has also been used to describe air-containing space DIAGNOSTIC CHECKLIST
< 1 cm • Pulmonary bullae are typically manifestations of paraseptal
emphysema
IMAGING
• Bullae are recognized cause of secondary spontaneous
• Radiography pneumothorax
○ Thin-walled lucency (typically apical) • Some authors use terms bulla/bleb interchangeably;
○ May mimic solid lesion when fluid-filled indistinguishable on imaging

patient who presented with
acute left chest pain and a
spontaneous left
pneumothorax shows a visible
pleural line ﬅ and a large
bulla ﬇ in the left lung apex,
likely responsible for the
pneumothorax. (Right)
Coronal CECT of the same
patient shows the left
pneumothorax ﬅ and a
cluster of large left apical
bullae ﬊. Paraseptal
emphysema with giant bullous
disease is one of the causes of
secondary spontaneous
pneumothorax.

with benign metastasizing
leiomyoma and left upper lobe
giant bullous disease shows a
large left apical air-filled
space with internal septations.
(Right) Composite image with
axial CECT of a patient with a
left upper lobe bulla, which
became secondarily infected,
shows a thin-walled
retrosternal bulla ﬈
completely filled with air.
Subsequent studies show an
internal air-fluid level ﬆ
within the bulla that
progressed to a completely
fluid-filled bulla ﬊
secondary to infection.
13
Cavity
KEY FACTS
TERMINOLOGY TOP DIFFERENTIAL DIAGNOSES

• Cavity • Infection
○ Gas-containing space; lucency or air attenuation within ○ Necrotizing pneumonia, abscess, septic emboli
nodule, mass, or consolidation ○ Organisms: Bacteria, mycobacteria, fungi, protozoa,
○ Implies lung necrosis and expulsion of necrotic material viruses
via tracheobronchial communication • Malignancy: Lung cancer, metastatic disease
IMAGING • Autoimmune diseases
○ Vasculitis: Granulomatosis with polyangiitis
• Radiography
○ Rheumatoid arthritis
○ Lucency within nodule, mass, or consolidation
• Pulmonary infarct secondary to pulmonary
○ May exhibit air-fluid level
thromboembolism
○ Smooth or nodular cavity wall; thickness > 4 mm
• CT DIAGNOSTIC CHECKLIST
○ Identification &/or assessment of extent of cavitation • Cavitation with associated centrilobular nodules should
○ Exclusion of pseudocavities: Cysts, bullae, blebs suggest active tuberculosis
○ Evaluation of cavity wall • Multifocal cavitary nodules in setting of infection should
○ Malignancy: Identification of other lesions, staging suggest septic emboli
○ Infection: Associated centrilobular nodules imply • Progression of consolidation to mass-like lesion with
bronchogenic dissemination cavitation should suggest abscess formation

58-year-old man who
presented with cough and
weight loss shows a left upper
lobe mass-like consolidation
with multiple intrinsic cavities
﬉ of variable size secondary
to primary squamous cell lung
cancer. (Right) Axial NECT of a
64-year-old man with a right
upper lobe squamous cell lung
cancer shows a spiculated soft
tissue mass with intrinsic
cavitation manifesting with
low-attenuation areas ﬅ and
intrinsic gas ﬆ. Squamous cell
carcinoma is the most
common cell type of lung
cancer to exhibit cavitation.
(Left) Coronal NECT of a 49-

year-old IV drug user who
presented with fever and
dyspnea shows multifocal
bilateral peripheral nodules
ﬅ and consolidations ﬆ,
some of which exhibit intrinsic
cavitation characteristic of
septic emboli. (Right) Axial
NECT of a 40-year-old woman
who presented with cough and
night sweats shows a right
upper lobe cavitary nodule ﬈
with nodular cavity walls and
surrounding centrilobular
nodules and tree-in-bud
opacities typical of
tuberculosis diagnosed on
sputum culture.
14
Centrilobular
KEY FACTS

• Abnormalities centered in bronchiolovascular core of • Etiologies
secondary pulmonary lobules ○ Bronchiolitis
IMAGING – Infectious bronchiolitis
– Aspiration bronchiolitis
• Radiography: May appear normal
– Respiratory bronchiolitis
• CT: Bronchiolitis and vascular nodules
– Hypersensitivity pneumonitis
○ Centrilobular micronodules
– Follicular bronchiolitis
– Solid or ground-glass
○ Vascular: Excipient lung disease, tumor emboli
– Tree-in-bud opacities
○ Other: Cholesterol granulomas, pulmonary capillary
– Subpleural sparing
hemangiomatosis
○ Bronchiolitis ancillary findings: Mosaic attenuation, air-
• Histology
trapping, bronchial wall thickening, bronchiectasis
○ Bronchiolitis: Luminal or submucosal cellular infiltration,
○ Vascular nodules ancillary findings: Dilated pulmonary
bronchiolar narrowing
trunk, right heart strain
○ Excipient lung disease: Birefringent crystals in
○ Multiplanar reformatted images for optimal
centrilobular arterioles
characterization of relationship of nodules to interlobar
○ Cholesterol granulomas: Stellate lesions, cholesterol
fissures
clefts, multinucleated giant cells, lymphocytes
– Absence of pleural or fissural involvement
(Left) Graphic shows the

anatomic distribution of
centrilobular nodules ﬊ at
the center of the secondary
pulmonary lobule that may
involve the lobular bronchiole
﬈ or artery ﬉. There is no
involvement of the periphery
of the secondary pulmonary
lobule, interlobar fissures, or
interlobular septa. (Right)
Axial NECT of a patient with
aspiration bronchiolitis after
laryngectomy shows basilar
centrilobular micronodules ﬉,
tree-in-bud opacities ﬈, and
consolidations ﬊ with
subpleural and fissural
sparing.
(Left) Coronal HRCT of a

patient with acute infectious
bronchiolitis secondary to
respiratory syncytial virus
shows diffuse tree-in-bud
nodules ﬈ and upper lobe
ground-glass opacities ﬉.
(Right) Composite image with
axial CECT (left) and MIP
reformatted image (right) of a
patient with respiratory
bronchiolitis shows subtle
centrilobular ground-glass
nodules ﬉, more conspicuous
on the MIP reformation. The
nodules spare the subpleural
lung, indicating their
centrilobular location.
15
Consolidation
KEY FACTS
TERMINOLOGY • CT
• Replacement of alveolar air by edema fluid, pus, blood, ○ Increased lung attenuation; obscures underlying lung
neoplastic cells, or other material (e.g., lipoprotein) architecture
○ Often implies infection (pneumonia) ○ May exhibit intrinsic air bronchograms &/or adjacent
• Synonyms: Airspace/alveolar consolidation acinar or centrilobular nodules
• Focal, patchy, multifocal, or diffuse PATHOLOGY
• Focal consolidation • Etiology
○ Nonsegmental, segmental, lobar ○ Infection: Bacterial, mycobacterial, viral, fungal
○ Mass-like or tumor-like ○ Pulmonary alveolar edema or hemorrhage
IMAGING ○ Neoplastic: Lung cancer, pulmonary lymphoma
• Radiography ○ Inflammatory: Organizing pneumonia, alveolar
sarcoidosis, eosinophilic pneumonia, alveolar
○ Increased parenchymal density
lipoproteinosis, lipoid pneumonia
○ Obscures underlying normal structures (e.g., bronchi,
○ Post treatment: Radiation or drug-induced pneumonitis
vessels)
○ Obscures adjacent structures DIAGNOSTIC CHECKLIST
– Sign of silhouette • Consolidations in adults should be followed to complete
○ May exhibit intrinsic air bronchograms radiographic resolution to exclude underlying malignancy
○ May be spherical, sublobar, or lobar

patient with fever and
leukocytosis shows a large
right lung mass-like
consolidation. (Right) Axial
NECT of the same patient
shows a dense right upper
lobe consolidation with
intrinsic air bronchograms ﬈
and adjacent ground-glass
opacity on a background of
interlobular septal thickening
and intralobular lines ﬉ (that
produce the so-called crazy-
paving pattern). Community
acquired pneumonia was
diagnosed and resolved on
follow-up imaging after
treatment.
(Left) Axial CECT shows a

round pneumonia manifesting
as a mass-like consolidation
with adjacent ground-glass
opacity ﬆ, which resolved
with medical therapy.
Consolidations in adults
should be followed to
resolution to exclude
underlying malignancy. (Right)
Axial CECT of a 71-year-old
man with the batwing pattern
of pulmonary edema shows
bilateral consolidations ﬆ
that represent alveolar edema
and adjacent bilateral
ﬅ, consistent with coexistent
interstitial edema.
16
Cyst
KEY FACTS

TERMINOLOGY • CT
• Cyst: Circumscribed spherical space lined by thin fibrous or ○ Optimal assessment of size, shape, number, wall
epithelial wall, usually < 2 mm thick characteristics, and distribution of lung cysts
• Lung cyst: Pulmonary thin-walled space that contains air ○ Contrast-enhanced CT for assessment of mediastinal
but may contain fluid, air/fluid level, or solid material cysts; assessment of cyst wall, cyst content, and presence
○ Cystic lung disease: Series of conditions characterized by or absence of soft tissue septa &/or mural nodules
thin-walled air-filled spherical spaces PATHOLOGY
• Mediastinal cyst: Congenital anomaly of foregut budding, • Etiology
thymic, or pericardial origin; acquired cyst vs. cystic
○ Cystic lung diseases: Lymphangioleiomyomatosis,
neoplasm
Langerhans cell histiocytosis, lymphoid interstitial
○ Unilocular or multilocular pneumonia, Birt-Hogg-Dubé, light chain deposition
IMAGING disease, Pneumocystis pneumonia, metastases
• Radiography ○ Congenital lung cysts: Intrapulmonary bronchogenic cyst,
pulmonary airway malformation
○ Lung cysts: May not be visible or may manifest as linear
opacities; larger cysts may manifest as thin-walled ○ Mediastinal congenital cysts: Bronchogenic cyst,
spherical lucencies enteric/neurenteric cyst, pericardial cyst, thymic cyst
○ Mediastinal cyst: Mediastinal contour abnormality ○ Mediastinal cystic lesions: Mature teratoma,
typically in middle mediastinum or cardiophrenic angle lymphangioma, cystic thymic neoplasms
(Left) Axial CECT shows

lymphangioleiomyomatosis
manifesting with multifocal
pulmonary cysts of varying
size with intervening normal
lung parenchyma. The cysts
are distributed diffusely
throughout both lungs, the
cyst walls are thin but
perceptible, and there are no
associated pulmonary nodules.
(Right) Axial NECT of a smoker
with pulmonary Langerhans
cell histiocytosis shows upper
lobe predominant pulmonary
nodules ﬈ and pulmonary
cysts ﬉; the latter exhibit
thick nodular walls and bizarre
shapes.
(Left) Axial CECT of a patient

with lymphoid interstitial
pneumonia shows thin-walled
pulmonary cysts in the left
lung. The differential
diagnosis for this case of cystic
lung disease should also
include Birt-Hogg-Dubé
syndrome, light-chain
deposition disease, and cystic
metastases. (Right) Axial CECT
of a 31-year-old man with
chest pain shows a water
attenuation mass ﬅ in the
visceral mediastinum with a
thin enhancing wall. The
findings are characteristic of
bronchogenic cyst. Note trace
bilateral pleural effusions ﬇.
17
Ground-Glass Opacity
KEY FACTS
• Ground-glass opacity: Increased lung density or attenuation • Etiology
that does not obscure underlying lung architecture (i.e., ○ Acute
bronchi, vessels) – Pneumonia (including Pneumocystis jirovecii, viral,
• Mechanisms mycoplasma), hemorrhage, edema, acute interstitial
○ Alveolar filling &/or collapse pneumonia (AIP), acute respiratory distress syndrome
○ Interstitial thickening (ARDS), eosinophilic lung disease, radiation
○ Increased blood volume pneumonitis, drug toxicity, E-cigarette or vaping
○ Combination of above mechanisms product use-associated lung injury (EVALI)
○ Chronic
IMAGING – Interstitial pneumonias: Nonspecific interstitial
• Radiography pneumonia, desquamative interstitial pneumonia,
○ Hazy increased lung density that does not obscure respiratory bronchiolitis, respiratory bronchiolitis-
underlying structures associated interstitial lung disease
○ Although term may be used to describe radiographic – Hypersensitivity pneumonitis, drug toxicity, radiation
finding, it is typically reserved to describe CT findings pneumonitis, eosinophilic lung disease, vasculitis (with
• CT associated pulmonary hemorrhage or eosinophilic
○ Increased lung attenuation that does not obscure lung disease), lipoid pneumonia, adenocarcinoma
underlying bronchovascular structures (preinvasive, minimally invasive, invasive)

with acquired immune
deficiency syndrome who
presented with several days of
dyspnea and fever shows
patchy bilateral ground-glass
opacities secondary to
Pneumocystis jirovecii
pneumonia. (Right) Coronal
NECT of a patient with mitral
valve disease who presented
with acute dyspnea shows
bilateral ground-glass
opacities and acinar ground-
glass nodules ﬅ due to
pulmonary edema. Infection,
hemorrhage, and edema may
all manifest with ground-glass
opacity.

who presented with chronic
dyspnea shows bilateral lower
lobe ground-glass opacities.
Biopsy demonstrated
pneumonia. (Right) Axial NECT
of a smoker who presented
with chronic dyspnea and
cough shows patchy bilateral
ground-glass opacities and
cystic changes secondary to
desquamative interstitial
pneumonia. Chronic lung
diseases that may manifest
with ground-glass opacity
include idiopathic interstitial
pneumonias and chronic
eosinophilic pneumonia.
18
Honeycombing
KEY FACTS

• Definition: Destroyed lung with fibrosis and cysts with • Etiologies
fibrous walls ○ Fibrosing interstitial lung diseases: Basilar, subpleural
• Term used to describe both CT and pathologic features – UIP
IMAGING – Nonspecific interstitial pneumonia
○ Other: Sarcoidosis (peribronchovascular); chronic
• Radiography
(fibrotic) hypersensitivity pneumonitis (upper lung);
○ Closely approximated ring shadows acute respiratory distress syndrome (anterior,
– Cysts 3-10 mm subpleural)
– Walls 1-3 mm thick • Histologic findings: Remodeled fibrotic lung with cystic
○ Subpleural reticular opacities airspaces and loss of normal lung architecture
• CT ○ Cysts: Few mm to several cm; variable cyst wall thickness;
○ Clustered lung cysts that share their walls lined by metaplastic bronchiolar epithelium
○ Cysts: Subpleural and multilayered/stacked
○ Comparable cyst diameter
– Average size: 3-10 mm • Subpleural honeycombing may mimic paraseptal
– May be as large as 25 mm emphysema on CT
○ Finding specific for fibrosis; diagnostic criterion for usual ○ Honeycombing: Stacked layers of subpleural cysts
interstitial pneumonia (UIP) ○ Paraseptal emphysema: Single layer of subpleural cysts

patient with usual interstitial
pneumonia shows low lung
volume and extensive coarse
bilateral reticular opacities
and the suggestion of round
cystic spaces with visible walls.
(Right) Axial prone HRCT of a
patient with usual interstitial
pneumonia shows stacked
layers of cysts of similar sizes
that share walls and exhibit a
typical lower lobe and
subpleural distribution. If not
associated with other
diseases, the pattern indicates
idiopathic pulmonary fibrosis
with such certainty that lung
biopsy is not required.
(Left) Low-power
photomicrograph (H&E stain)
of a specimen of usual
interstitial pneumonia shows
dense fibrosis ﬈ and
honeycomb cysts ﬉, which
correlate with the layered
cystic spaces seen on CT.
(Right) Axial HRCT of a patient
with end-stage sarcoidosis
shows extensive
honeycombing ﬈ with
peribronchovascular
distribution. This distribution
may occur in both end-stage
sarcoidosis and fibrotic
hypersensitivity pneumonitis.
19
Interlobular Septal Thickening
KEY FACTS
• Thickening of interlobular septa, which outline secondary • Etiology
pulmonary lobule ○ Smooth interlobular septal thickening
• Normal interlobular septa are not visible on imaging – Interstitial edema
IMAGING – Lymphangitic carcinomatosis
– Alveolar lipoproteinosis
• Radiography
– Other interstitial lung diseases
○ Thick interlobular septa manifest as Kerley lines
○ Nodular interlobular septal thickening
○ Kerley B lines: Short horizontal lines perpendicular to
– Lymphangitic carcinomatosis
pleura (1.5-2 cm long)
– Lymphoproliferative disorder
○ Kerley A lines: Lines 2-6 cm long, upper lung zones,
course obliquely from hilum toward lung periphery – Sarcoidosis, silicosis, and coal workers pneumoconiosis
○ Kerley C lines: Net-like branching linear opacities at lung ○ Irregular interlobular septal thickening
bases; Kerley B lines seen en face – Pulmonary fibrosis, end-stage sarcoidosis
• CT/HRCT DIAGNOSTIC CHECKLIST
○ Thick interlobular septa • Interstitial edema is most common cause of interlobular
○ Surround and delineate secondary pulmonary lobule septal thickening
○ Smooth or nodular thickening • Nodular interlobular septal thickening should suggest
○ Irregular septal thickening in pulmonary fibrosis malignancy
(Left) Coned-down AP chest

radiograph shows asymmetric
alveolar and interstitial
edema, manifesting as ill-
defined airspace disease ﬈
and as Kerley B lines ﬈,
respectively. Perihilar haze,
peribronchial thickening, and
right pleural effusion are
additional features of edema.
(Right) PA chest radiograph of
a 57-year-old man with
advanced malignancy shows
lymphangitic carcinomatosis
that manifests as asymmetric
bilateral interstitial opacities
with interlobular septal
thickening and Kerley A and C
lines.
(Left) Axial NECT of a 43-year-

old man with pulmonary
alveolar lipoproteinosis shows
diffuse smooth interlobular
septal thickening and
intralobular lines on a
background of ground-glass
opacity, producing the
characteristic crazy-paving
pattern. (Right) Axial NECT of
a 52-year-old woman with
chronic or fibrotic
shows subpleural reticulation,
scattered thick interlobular
septa ﬅ, and mosaic
attenuation ﬇, consistent
with fibrosing interstitial lung
disease.
20
Intralobular Lines
KEY FACTS

TERMINOLOGY ○ Connective tissue disease-associated interstitial lung
• Fine linear opacities identified within confines of secondary disease
pulmonary lobule ○ Chronic (fibrotic) hypersensitivity pneumonitis
• There are no intralobular septa: Term "intralobular septal ○ Asbestosis
thickening" is erroneous ○ Other diffuse fibrotic interstitial lung diseases
○ Alveolar lipoproteinosis
IMAGING • Parenchymal (intralobular) interstitium: Interstitial network
• Radiography of thin connective tissue fibers in alveolar walls; supports
○ Intralobular lines not visible secondary pulmonary lobule
• CT/HRCT • Intralobular lines: Thick intralobular interstitium, typically
○ Fine irregular reticular opacities separated by few mm due to fibrosis
○ Located within secondary pulmonary lobule
○ When numerous: Fine reticular pattern
• Intralobular lines should suggest interstitial fibrosis
PATHOLOGY • Combined interlobular septal thickening and intralobular
• Etiology lines: Reticular opacities
○ Idiopathic pulmonary fibrosis • Identification of intralobular lines on thin-section CT: Low
○ Nonspecific interstitial pneumonia interobserver agreement
○ End-stage sarcoidosis
(Left) Graphic shows the

parenchymal and peripheral
interstitium of the secondary
pulmonary lobule. The
peripheral interstitium
extends along the interlobular
septa ﬅ and subpleural
regions while the parenchymal
interstitium ﬆ forms a
meshwork around alveoli and
alveolar sacs within the
secondary pulmonary lobule.
(Right) Axial HRCT of a patient
with scleroderma and fibrotic
pneumonia shows profuse
﬈, intralobular lines ﬉, and
traction bronchiectasis ﬆ.
(Left) Axial HRCT of a patient

with idiopathic pulmonary
fibrosis shows fine linear and
ground-glass opacities within
the confines of the secondary
pulmonary lobule demarcated
by thickened interlobular
septa ﬈. Note bilateral
subpleural honeycomb cysts.
(Right) Axial NECT of a 43-
year-old man with alveolar
proteinosis shows the
characteristic crazy-paving CT
pattern produced by diffuse
bilateral patchy ground-glass
attenuation on a background
of interlobular septal
thickening ﬈ and fine
intralobular lines ﬈.
21
Mass
KEY FACTS
TERMINOLOGY • CT
• Thoracic lesion > 3 cm in maximal diameter ○ Lung mass: Morphologic features and clinical staging
○ Typically solid, but may exhibit necrosis &/or cavitation (local invasion, lymphadenopathy, metastases)
• May be located in any thoracic anatomic compartment ○ Pleural mass: Focal vs. multifocal; evaluation of local
invasion, lymphadenopathy, pleural effusion
○ Lung, pleura, mediastinum, chest wall, diaphragm
○ Mediastinal mass: Assessment of lesion morphology and
IMAGING attenuation, identification of lymphadenopathy,
• Radiography evaluation of local invasion
○ Lesion identification and localization to specific thoracic ○ Chest wall mass: Assessment and characterization of
anatomic compartment degree of skeletal &/or soft tissue involvement
○ Lung mass: Surrounded by lung, well- or ill-defined, PATHOLOGY
spiculated or lobular borders
• Etiology
○ Pleural mass: May exhibit obtuse angles with adjacent
○ Lung: Lung cancer, lung abscess, metastasis
pleura and incomplete border sign
○ Pleura: Localized fibrous tumor of pleura, metastasis
○ Mediastinal mass: Alteration of mediastinal contours;
focal vs. diffuse; lateral radiography allows localization to ○ Mediastinum: Thymic neoplasm, neurogenic neoplasm,
specific mediastinal compartment lymphadenopathy, congenital cyst, vascular lesion
○ Chest wall mass: Incomplete border sign; may exhibit ○ Chest wall: Metastasis, chondrosarcoma, myeloma
skeletal erosion/destruction &/or soft tissue involvement

65-year-old man who
presented with cough and
weight loss shows a large
lobulated right upper lobe
lung mass. (Right) Axial CECT
of the same patient shows a
large right upper lobe soft
tissue mass that invades the
adjacent mediastinum and
produces mass effect on the
right upper lobe bronchus with
obliteration of the lumen of
the posterior segmental
bronchus ﬈. Lung masses
usually represent malignant
neoplasms, most commonly
primary lung cancer.

24-year-old woman with facial
swelling and malaise shows a
large lobulated mediastinal
mass that extends to both
sides of the midline and was
located in the anterior
mediastinum on lateral
radiography (not shown).
(Right) Axial CECT of a 30-
year-old woman with a
metastatic gynecologic
malignancy shows a large left
anterior chest wall mass ﬈
with rib destruction.
Additional sternal ﬊ and
vertebral ﬉ lesions with bone
destruction are consistent
with chest wall metastases.
22
Miliary Pattern
KEY FACTS

TERMINOLOGY • CT/HRCT
• Miliary pattern ○ Profuse, bilateral, discrete, well-defined pulmonary
○ Pulmonary micronodules of uniform size; ≤ 3 mm micronodules
○ Discrete, round, well defined ○ Random (diffuse, uniform) distribution; no specific
relationship to secondary pulmonary lobule structures
○ Profuse, bilateral
• Synonym TOP DIFFERENTIAL DIAGNOSES
○ Miliary nodules • Perilymphatic nodules (e.g., sarcoidosis) occasionally
• Term "miliary" difficult to differentiate from miliary micronodules
○ Derived from "millet" seeds • Centrilobular nodules (e.g., cellular bronchiolitis) do not
○ Lung nodules with size and appearance reminiscent of involve pleura/fissures
millet seeds
PATHOLOGY
IMAGING • Etiology
• Radiography ○ Hematogenous metastases: Thyroid and renal cell
○ Bilateral, tiny, discrete, often profuse pulmonary cancers, melanoma, lung adenocarcinoma
micronodules ○ Hematogenous infection: Tuberculosis, fungal infection
○ Diffusely distributed ○ Lung adenocarcinoma, with EGFR mutation/exon 19
○ May be subtle deletions
○ Lung mass may be visible in cases of lung cancer
(Left) Axial NECT of an

immunocompromised patient
with miliary tuberculosis
shows profuse pulmonary
micronodules that exhibit a
miliary pattern and a random
distribution. The miliary
pattern is consistent with
hematogenous dissemination
of disease, in this case,
infection. (Right) PA chest
radiograph of an
immunocompromised patient
with disseminated
coccidioidomycosis shows
bilateral, profuse, miliary
micronodules, consistent with
hematogenous dissemination
of fungal infection.

patient with advanced lung
adenocarcinoma shows a
dominant right upper lobe
mass ﬅ and multifocal
bilateral pulmonary
micronodules that exhibit a
miliary pattern of metastatic
disease. (Right) Axial CECT of
the same patient shows a right
upper lobe lobulated mass ﬉
(primary lung cancer) that
encases the right upper lobe
bronchus ﬈. Bilateral
pulmonary miliary metastases
are consistent with
adenocarcinoma with EGFR
mutation and exon 19
deletions.
23
Mosaic Attenuation
KEY FACTS
• Mosaic attenuation • Etiology
○ Heterogeneous lung attenuation with alternating areas ○ Patchy interstitial lung disease: Hypersensitivity
of low and high attenuation on CT pneumonitis, bronchiectasis
• Synonyms: Mosaic perfusion, mosaic oligemia ○ Constrictive bronchiolitis
• Mosaic attenuation is more inclusive preferred term – Idiopathic
– Complication of transplantation
IMAGING
– Autoimmunity: Rheumatoid arthritis, Sjögren
• Radiography syndrome
○ Typically normal chest radiography – Toxic inhalational injury
○ ± associated findings, such as bronchiectasis – Other: Drug-induced lung disease, recurrent
• CT/HRCT infection/aspiration, Swyer-James-MacLeod, diffuse
○ Heterogeneous patchwork-like lung attenuation idiopathic pulmonary neuroendocrine cell hyperplasia
○ Alternating areas of low and higher attenuation (DIPNECH), inflammatory bowel disease,
○ ± reduced vessel caliber in areas of lung hyperlucency paraneoplastic pemphigus
○ Bronchiectasis, bronchial wall thickening, and mucus ○ Occlusive vascular disease: Chronic pulmonary
plugs should suggest airways disease thromboembolism, pulmonary hypertension
○ Expiratory thin-section CT: Identification of air-trapping
secondary to bronchiolar obstruction

with subacute (nonfibrotic)
shows mild diffuse mosaic
attenuation of the lung
parenchyma. This pattern of
mosaic attenuation may be
accentuated by expiratory
imaging. (Right) Axial NECT of
a patient with subacute
(nonfibrotic) hypersensitivity
pneumonitis shows
heterogeneous lung
attenuation with a patchwork
of lower and higher
attenuation areas. In this case,
heterogeneity may be
accentuated by patchy
ground-glass opacity.

with cystic fibrosis shows
bilateral mosaic
attenuation/perfusion with
areas of low attenuation ﬉
alternating with areas of
higher attenuation ﬈. Note
bronchiectasis, bronchial wall
thickening, and mucus plugs
ﬅ. (Right) Coronal CECT of a
patient with chronic
pulmonary thromboembolic
disease shows mosaic
attenuation/perfusion. Note
enlarged blood vessel caliber
ﬅ in high-attenuation areas.
Mosaic attenuation may occur
with small airways or occlusive
vascular diseases.
24
Nodule
KEY FACTS

• Nodule • Etiology
○ Rounded opacity with variable border characteristics ○ Solitary pulmonary nodule
○ Size: ≤ 3 cm – Granuloma
• Micronodule – Lung cancer, preinvasive lesion
○ Rounded opacity that measures < 3 mm – Carcinoid
– Hamartoma
IMAGING
○ Multiple diffuse micronodules
• Radiography
– Characterized by distribution: Centrilobular,
○ Rounded opacity (≤ 3 cm) surrounded by lung perilymphatic, or random
○ May exhibit calcification or cavitation
• CT DIAGNOSTIC CHECKLIST
○ Rounded opacity (≤ 3 cm) with variable borders • Solitary nodules characterized as likely benign, possibly
○ Nodules characterized as solid or subsolid malignant, or indeterminate
– Solid nodules are of soft tissue attenuation ○ Indeterminate nodules require further evaluation with
– Subsolid nodules follow-up imaging &/or tissue sampling
□ Ground-glass (nonsolid) attenuation • Follow-up of solid and subsolid nodules based on Fleischner
□ Part-solid with both ground-glass and solid Society guidelines according to risk factors and size
attenuation components (including size of solid and nonsolid components)
(Left) PA chest radiograph of

an asymptomatic 72-year-old
woman demonstrates a subtle
incidentally discovered
spiculated left upper lobe
solitary pulmonary nodule ﬈.
There are no other
radiographic abnormalities.
(Right) Axial NECT of the same
patient shows a left upper
lobe spiculated solid nodule
﬈ with pleural tags and a
small eccentric focus of
cavitation anteriorly. These
findings are highly suspicious
for primary lung cancer. This
nodule is amenable to image-
guided percutaneous biopsy.
(Left) Axial CECT of an

asymptomatic 80-year-old
woman shows an incidentally
discovered right upper lobe
part-solid nodule ﬈ with
spiculated borders, pleural
tags, and a dominant solid
component. Invasive
adenocarcinoma was
diagnosed at surgical excision.
(Right) Axial NECT of a 40-
year-old asymptomatic
woman shows an incidentally
discovered left lower lobe
subsolid ground-glass nodule
﬈, which persisted on follow-
up imaging. Atypical
adenomatous hyperplasia was
diagnosed at surgical excision.
25
Peribronchovascular
KEY FACTS
• Diseases that characteristically involve the • Peribronchovascular infiltration
peribronchovascular interstitium ○ Extravascular water, blood
• Peribronchovascular and perilymphatic distributions often ○ Infection, granulation tissue
coexist given anatomic continuum of lymphatic channels ○ Tumor
IMAGING ○ Air
• Etiologies
• Radiography
○ Hydrostatic pulmonary edema
○ Central pulmonary opacities
○ Organizing pneumonia
○ Peribronchial cuffing
○ Bronchopneumonia
• CT
○ Kaposi sarcoma
○ Bronchial wall thickening, nodularity
○ Mucosa-associated lymphoid tissue lymphoma
○ Perivascular thickening (optimally characterized with IV
(MALToma)
contrast)
○ Pulmonary interstitial emphysema
○ Perivascular nodularity
○ Interstitial pulmonary arterial hemorrhage
○ Peribronchovascular consolidation
○ Peribronchial/perivascular lucency DIAGNOSTIC CHECKLIST
○ Perilymphatic findings often coexist: Septal and fissural • Recognition of peribronchovascular pattern requires
thickening &/or nodularity knowledge of anatomy of secondary pulmonary lobule

with cardiogenic pulmonary
edema shows bilateral
peribronchovascular
consolidations with subpleural
sparing. The process is
typically peribronchovascular
with later progression to
involvement of the peripheral
interstitium. (Right) Axial
NECT of a patient with S.
aureus bronchopneumonia
shows patchy bilateral
peribronchovascular
consolidations ﬈ bilaterally.
These abnormalities may later
progress to involve the
bilateral lungs more
extensively.
(Left) Axial HRCT of a patient

with cryptogenic organizing
pneumonia shows multifocal
irregular peribronchovascular
nodules ﬈ in the left lung. A
frequent imaging pattern of
organizing pneumonia is the
presence of
peribronchovascular nodules,
as shown in this case. (Right)
Axial CECT of a patient with
AIDS-related Kaposi sarcoma
shows multifocal bilateral ill-
defined spiculated
peribronchovascular nodules
that exhibit a characteristic
flame-shaped morphology ﬉
and spare the subpleural lung
parenchyma.
26
Another random document with
no related content on Scribd:
which many have of shuffling cards, so that when dealing at whist or
écarté, &c., he could put into his own hand or that of others the cards
he pleased. He added that, though possessing this extraordinary
faculty from boyhood, he had never taken advantage of it in a
dishonest or unworthy manner except when, as quite a youth, he
desired to go to Paris to make his way in the world as a conjurer, and
his father, a poor gentleman, had not been able to give him more
than a few gold pieces wherewith to defray the expenses of his
journey. He described how he had started with his knapsack from
some town in Austria, occasionally travelling by diligence, and
passing the nights at inns on the road. During the journey, Bosco
said, he frequently had a gold piece changed, and whilst the change
was being delivered he managed to recover the gold coin, and thus
arrived at Paris with sufficient means to enable him to live until he
found employment. ‘Since then,’ he added, ‘I have been an honest
man.’
Other recollections of those days follow.
Lord and Lady Londonderry arrived at Constantinople and called
on the Ambassador, and Lady Londonderry requested his Excellency
to present her to the Sultan.
As the presentation of a European lady to H.I.M. had never been
heard of in those days, Lord Ponsonby declined to take steps to
meet the wishes of the fair lady, on the plea that such an
unprecedented request might give annoyance to the Sultan. Lady
Londonderry was, however, determined to gain her point, and also to
show Lord Ponsonby that if he had not sufficient influence to obtain
such a special favour from the Sultan, another Representative might
be found who would pay more attention to her wishes.
Lady Londonderry had made the acquaintance at Vienna of Baron
Stummer, the Austrian Ambassador at Constantinople, who, though
he had not the powerful influence which Lord Ponsonby then
enjoyed, was regarded by the Sultan and his Ministers as a very
important personage to whose wishes it was politic and advisable to
attend.
Lady Londonderry made known her request to the Baron, who at
first demurred for the same reason as Lord Ponsonby; but pressed
by the fair dame—who pleaded that she only asked for a private
interview with the Sultan—and knowing that Lord Londonderry held a
high position in his own country, he promised to mention her wishes
to Reshid Pasha, who was at that time Minister for Foreign Affairs
and spoke French fluently, to ascertain whether it was possible that
such an extraordinary favour could be granted by H.I.M.
Reshid Pasha raised many objections; but being most desirous to
please the Austrian Ambassador, he informed him that there was
one possible way by which the lady could be brought very privately
into the presence of His Majesty. He had heard, he said, that the
noble lady travelled with untold wealth in diamonds, &c.: the Sultan
was passionately fond of jewelry, of which he made frequent
purchases; and possibly His Majesty might consent, on learning that
there was a person in Constantinople who had a large assortment of
jewels, that she should be allowed to bring them herself to the
Palace. Should His Majesty consent, the Pasha informed the Baron,
no one but himself (Reshid) and Lady Londonderry would be present
at the interview with the Sultan, and in such case he would act as
interpreter.
Reshid Pasha having made known to the Sultan that a person
had arrived at Constantinople with a wonderful collection of most
valuable jewelry, asked whether His Majesty would like to see them.
The following conversation is said to have taken place:—
Sultan. ‘Let the jewelry be brought and prices stated.’
Reshid. ‘This individual never trusts the jewelry to any one, and
would have to come in person.’
Sultan. ‘Bring the jeweller.’
Reshid (in a hesitating manner). ‘I beg your Majesty’s pardon for
indelicacy, but it is—it is—a female[4], and she always carries the
jewels on her person when she wishes to dispose of them for sale,
and never puts them in a case.’
Sultan. ‘Bring her, and let her put them all on. You come also, to
interpret.’
Reshid returned and told the Baron he might inform Lady
Londonderry that she would be presented at a private audience by
him, but that the Sultan, having heard of the fame of her jewelry, had
particularly requested she would put it all on, and he, the Pasha,
hoped therefore she would raise no objection to such a strange
request.
Lady Londonderry was very good-natured, and being much
amused at the condition made by the Sultan, consented to put on all
her most valuable jewelry.
On arrival at the Palace, Reshid Pasha conducted Lady
Londonderry into the presence of the Sultan. Her dress glittered with
diamonds, pearls, turquoises, and other precious stones.
‘Pekkei—good,’ said the Sultan (as Lady Londonderry curtseyed),
‘she has brought magnificent jewels.’
Reshid (turning to the lady). ‘His Majesty graciously bids you
welcome.’
Lady Londonderry bowed and expressed her thanks in French.
Reshid (interpreting). ‘She says she has other jewelry, but could
not put on all.’
Sultan. ‘Ask her what is the price of that diamond necklace.’
Reshid. ‘His Majesty inquires whether this is your first visit to
Constantinople.’
Lady Londonderry. ‘It is my first visit, and I am delighted with all I
have seen.’
Reshid (to Sultan). ‘She asks a million of piastres.’
Sultan. ‘That is too much.’
Reshid (to Lady Londonderry). ‘His Majesty asks whether you
have seen the Mosques. If not, offers you a firman.’
Lady Londonderry expresses her thanks.
Sultan. ‘What price does she put on that set of turquoises?’
Reshid (to Lady Londonderry). ‘His Majesty says that perhaps you
would like to take a walk in the garden.’
Lady Londonderry expresses her thanks, and would like to see
the garden.
Reshid (to Sultan). ‘She says 400,000 piastres.’
Sultan. ‘Take her away, I shall not give such prices.’
Reshid (to Lady Londonderry). ‘His Majesty graciously expresses
satisfaction at having made your acquaintance.’
Lady Londonderry curtseys low and withdraws from His Majesty’s
presence to visit the garden with the amiable and courteous Reshid
Pasha.
* * * * *
In the summer months at Constantinople, Turkish ladies and their

children were wont to drive in ‘arabas’ to the ‘Sweet Waters.’ Groups
of Mohammedan women of the better class, with their families and
slaves, were to be seen in picturesque dresses reclining on carpets
and cushions, enjoying coffee, sweetmeats, &c., under the shade of
the fine old trees on this beautiful spot. Men were not allowed to
approach the ground where the women were seated. Kavasses
warned off intruders; but the members of Embassies, especially
when accompanied by a kavass, were not interfered with, even if
they walked near the groups of women.
Turkish ladies in those days wore the ‘yashmak’ or veil, supposed
to cover their faces, but worn so low as frequently to expose even
the mouth, and at the ‘Sweet Waters’ yashmaks were thrown aside
still more, thus displaying embroidered jackets, bright-coloured belts,
and silk or cotton ‘shalvas.’ Turkish women, even the far-famed
Circassians, are not in general pretty, but they have fine eyes and a
piquant expression.
When passing these groups of ladies, I have often heard
humorous remarks, evidently intended to reach the ears of the
unabashed ‘Frank’ who had ventured to intrude amongst them.
One evening, when taking a walk, I had wandered to a secluded
spot, when I suddenly came upon two Turkish ladies and a slave
taking coffee. One of the ladies looked up and smiled, making some
remark to her companion, evidently about myself, the purport of
which I did not quite understand. I merely returned the smile and
walked hurriedly away, for the dinner-hour at the Embassy was
approaching. I had gone but a short distance when I heard some one
running up behind me. On turning round I was accosted by an old
black woman, who, in a breathless voice, said, ‘Khanem’ (my
mistress), ‘whom you have just passed, requests that you will give
her a pin for her dress.’
As I happened to have a pin, I was about to hand it to the slave,
when she said, ‘Khanem wishes you to bring it to her;’ adding, in a
whisper, ‘there is no one near, and she has something to say to you.’
Looking at my watch, I replied it was late, and requested her to tell
her mistress that I was sorry I could not comply with her request,
adding, ‘Tell me, who is your beautiful khanem?’
The slave replied, ‘She is the wife of the late Sultan Mahmud’s
dwarf.’
I had already heard something about this lady, but having a vivid
recollection of a late adventure of Baron B., a member of a foreign
Legation and a particular friend of mine, whom I had helped out of a
serious scrape where his life had been in great danger, and who had
been obliged to quit Constantinople suddenly (having been given to
understand that unless he left the country his recall would be
required by the Turkish Government), I made up my mind not to
satisfy my curiosity by seeking for an interview with the fair
Circassian.
The next day, I requested a Turkish police officer of high rank,
who had aided me in helping Baron B. out of the scrape to which I
have alluded, to tell me what he knew about the wife of the dwarf,
not mentioning, however, the incident which had occurred at the
‘Sweet Waters.’
The officer then related the following tale:—
‘Sultan Mahmud had a humpbacked dwarf, with a hideous
countenance, but who was renowned for wit and humour. This
monster was frequently admitted by the Sultan into the harem when
H.M. was seated with his odalisques enjoying the “chebúk.”
‘To please the ladies, the dwarf was made a constant butt, both by
H.I.M. and the odalisques, and he answered them by his gibes and
ready repartee: having full permission to say what he pleased, even
should he cast reflections on H.I.M.’s sacred person.
‘Amongst the odalisques who happened to be present one
evening, was a tall Circassian of great beauty, with a graceful figure.
She was very lively, and in order to amuse the Sultan, had made pert
remarks about the admirable figure and handsome countenance of
the dwarf, thus giving rise to much merriment, in which the Sultan
Mahmud joined. Turning to the dwarf, H.I.M. said, “Now if you can
kiss Leila (the tall Circassian) she shall be your wife.”
‘The dwarf replied, “Can a dog reach the moon? Can a bramble
entwine the top of the lofty cypress?”
‘The Circassian continued to make fun of the dwarf, who
appeared to take no further thought of the Sultan’s words, though it
was observed he kept his eye on her tall figure.
‘Later in the evening, when the pipe which the Sultan was
smoking had to be renewed, Leila bent down for that purpose. In a
moment the dwarf, watching his opportunity, sprang up and kissed
her as she stooped. She struck him, and, in a volley of violent and
passionate language, implored the Sultan to punish him for his
insolence and outrage.
‘The dwarf exclaimed, “The Commander of the Faithful, the Sultan
of Sultans, has spoken. His word cannot be broken. I claim Leila for
my wife.”
‘The Sultan looked displeased; and, after a pause, with a severe
expression on his countenance, ordered the dwarf to leave the room;
then, turning to Leila, said, “Retire. Henceforth consider yourself the
wife of the dwarf. A dowry shall be given you, and the wedding shall
forthwith take place. Depart from my presence. I see you no more.”
‘The Circassian, as she left the room, turned towards the dwarf,
who was also about to withdraw, and cursed him, saying, “Monster!
The day will come when you will rue and bitterly repent your cruel
treachery.”
‘Leila duly became the wife of the dwarf. She drove about in her
“araba” through the streets of Pera, and, wearing a transparent
“yashmak” lowered to the chin, even entered the shops, and
conversed—when not observed—with Europeans. She visited the
studio of a French artist, by whom her portrait was painted in water-
colours, and of which she allowed copies to be taken to present to
favourite Franks with whom she became acquainted. Her conduct
became a source of great scandal, and was brought under the notice
of the Sultan.
‘H.I.M. said, “Let her be free to do what she pleases. I committed
a great injustice in giving her to the dwarf; but my word could not be
set aside.”’
The police officer having thus concluded his story, I inquired
where the French artist lived, and, calling on him, offered to
purchase a copy of the portrait. He told me he could not give it
without the consent of the wife of the dwarf. I then requested him to
let her know that the ‘Frank,’ one of the British Secretaries, of whom
she had requested the gift of a pin at the ‘Sweet Waters,’ begged for
her portrait. Her consent was thereupon given, on condition that I
should not show it to any one in Constantinople.
I paid a round sum for the water-colour, and on my return to
England, after Lord Ponsonby had resigned the post of Ambassador,
I gave the portrait of the beautiful Circassian to Lady Ponsonby—
from whom I had received great kindness—as a souvenir of
Constantinople.
* * * * *
Very extraordinary hours were kept at the Embassy: we rarely sat

down to dinner before 9.30, and frequently not till ten p.m. At eleven
o’clock Lord and Lady Ponsonby had a rubber of whist in which I
was always required to take a hand, it being thought I knew more
about the game than the other members of the Embassy. As his
Excellency required that Lady Ponsonby should be his partner, and
as that charming lady knew very little about the game, they almost
invariably lost.
After whist, Lord Ponsonby was wont to request one of the
attachés to remain and converse, and his Excellency would then
hold forth for hours upon events present and future, both in Turkey
and Egypt; foretelling much that has since happened to the ‘Sick
Man.’ One night, when it was my watch, and I had listened to his
Lordship until I nearly fell asleep and was conscious that dawn was
approaching, he rose, opened one of the blinds and said, ‘The sun is
rising. I think it is time, Mr. Hay, to go to bed. Have you followed and
understood my views upon the Eastern Question?’ I answered, I
had, to the best of my ability. ‘Then,’ said he, ‘have the goodness to
embody to-morrow in a memorandum all that you may have
retained.’ Observing that I looked aghast at having such a task
imposed upon me, he patted me on the shoulder and added, ‘Well,
well, don’t trouble yourself. Eat, drink, and sleep; the rest’s a joke.’
There was great charm in the manner of both Lord and Lady
Ponsonby, and they showed much kindness to all the members of
the Embassy. There was not one of us who would not have been
ready to make any sacrifice of time and pleasure to meet their
wishes.
Lord Ponsonby was not a wealthy peer, but his expenditure was
lavish as far as the table was concerned. Briant, a Frenchman, was
steward and head cook, and his wife was maid to Lady Ponsonby.
They received £400 a year between them for their services, but it
was well known by the members of the Embassy that Briant, during
the few years he had been at Constantinople, had been enabled to
deposit several thousand pounds in one of the banks at Pera,
levying a heavy percentage on everything that he purchased, wine
included, and some of which it was discovered he was in the habit of
selling to an hotel in Pera; so when any member of the Embassy
passed a night in the town and dined at the said hotel, he always
called for ‘Chateau Briant’! An old friend of Lord Ponsonby’s, who
remained for some months on a visit at the Embassy, hearing of the
scandalous manner in which Briant was accumulating money at the
bank, thought it would be a friendly act to make known to his
Lordship that which was in the mouth of every one—Briant’s system
of peculation. He did so. Lord Ponsonby thanked him for the
information and observed, ‘How much do you think Briant robs
annually and deposits in the bank?’
‘At least £1000 a year,’ his friend replied.
‘Pray,’ said Lord Ponsonby, ‘pray keep what has passed between
us most secret; I had thought Briant’s pilferings far exceeded that
sum. I would not, for double that amount, lose such an excellent
chef. Keep it secret, Mr. ———, keep it secret!’
Though he may not have possessed the brilliant talents of his
successor, the great ‘Elchi,’ Lord Ponsonby acted with much energy,
decision, and success in carrying out the views which he knew were
entertained by that most admirable of statesmen, Lord Palmerston,
regarding the Turkish Empire at the time when Mehemet Ali, backed
by France, was seeking to declare his independence, and to place
Egypt under the aegis of the latter power; to attain which object has
been, and is, the aim of France even up to the present day.
The Sultan, Abdul Mijid, and his Minister, Reshid Pasha, accepted
thankfully and unreservedly the dictum of Lord Ponsonby in all
questions—and as long as Palmerston was at the head of foreign
affairs, Lord Ponsonby carried out his views in the East without a
check, notwithstanding the vigorous opposition made by the French
Ambassador, Monsieur Pontet, and the constant threat that extreme
measures would be adopted by France under certain contingencies;
but when Lord Aberdeen came into power and sought to pursue a
conciliatory policy towards France, Lord Ponsonby received
dispatches, couched in a spirit which pointed out distinctly that he
should moderate his action in support of the Sultan against Mehemet
Ali’s pretensions. From private letters that Lord Ponsonby received
from friends at home, he knew more or less what was the tenor of
the instructions contained in those dispatches, so he did not break
the seals but continued to follow up vigorously the same policy as
before, until the object he had in view, viz., Mehemet Ali’s
submission to the Porte, was achieved, and then Lord Ponsonby
retired, or was required to retire.
It happened one day that I was standing near the Ambassador at
his writing-table whilst he was giving me directions to convey a
message to an Armenian banker of the Porte, upon a monetary
question affecting the interests of the Turkish Government. He pulled
open the drawer of the table at which he was seated to get out a
paper, and I caught a glimpse of several sealed dispatches,
addressed to his Excellency, from the Foreign Office. Lord
Ponsonby, whilst closing the drawer, perceiving, as I suppose, an
expression of surprise on my face, looked up with a smile, and re-
opening the drawer, said, ‘You are astonished, Mr. Hay, at seeing
such a number of Foreign Office dispatches lying here unopened: so
am I!—for though I had certainly left in this drawer a few sealed
letters, they have since been breeding;’ adding, whilst he re-closed
the drawer, ‘Let them breed!’
Those were days when an Ambassador possessed extraordinary
powers, and could carry out a policy which he considered best for
the interests of his country, without allowing himself to be fettered by
the vacillating views of Government and be moved—as now
happens—like a puppet, by telegraph wires or other rapid means of
communication.
In pursuance of instructions received from Lord Ponsonby, I called
on the Armenian banker, before mentioned, at his private dwelling.
This was a beautiful house, fitted up in the same manner as was
then usual with Turks, for the Armenians of Constantinople at that
time adopted the Turkish mode of living. The Armenian women
veiled their faces and wore costumes similar to those of the
Mohammedans, except that their slippers were red, whereas those
used by Turkish females were yellow.
After making known to the porter who I was, and that I had come
upon an errand from the Ambassador, the old banker came to meet
me, led me to a room set apart for receiving his guests, and seated
me on a luxurious divan. He was attired in a handsome Armenian
costume, wearing a black head-dress much like an inverted iron
cauldron.
A few moments after my arrival, a damsel of about seventeen—
daughter of the banker—set before me a ‘narghileh,’ and adroitly
placed between my lips the amber mouthpiece. I had never used a
‘narghileh’ or smoked ‘tumbaki,’ which is the form of tobacco
employed in that kind of pipe, and was glad to have an opportunity of
trying it, as presented to me by the Armenian maiden.
She was a pretty girl, with brilliant dark eyes, and features much
resembling those of a Jewess of Morocco. The Turkish costume,
with its yellow satin ‘shalvas’ or trousers, and the graceful shawl
which girded her waist, looked most picturesque and charming, and I
sank back on the cushions and gurgled my hubble-bubble with
satisfaction; whilst another pretty damsel, a younger sister, brought
in coffee, which she presented with a graceful bow.
The banker and I talked and puffed, drank coffee and sherbet,
and eat sweetmeats of all kinds which were brought to us in
succession. I felt happy, as if I had reached the seventh heaven of
the Mohammedan. Time slipped by very quickly. I had finished the
business of my mission when the old banker looked at his watch, put
aside his ‘narghileh’ and fidgeted a little, thus giving me clearly to
understand it would be convenient that I should leave. Much as I was
enjoying myself, I was also of the same opinion, and made an effort
to rise and get my feet to the ground—for I was seated cross-legged
on the divan—but could not move them; they seemed to be
paralysed. The banker, not knowing my state, and fancying perhaps
that my admiration for his pretty daughters had checked my
departure, told them rather roughly, when they again appeared
smiling and bringing more Turkish sweetmeats, that their presence
was no longer required, and then, looking once more at his watch,
he said most politely, and with profuse apologies, ‘I see the hour is
past at which I ought to present myself to the Porte.’
I made many excuses for not having taken my leave and told him,
with a nervous laugh, that I felt very strange sensations, but did not
know the cause; that on attempting to rise I found I had no control
over my legs, and could not remove them from the divan, feeling as
if my body did not belong to me. I added, ‘You can see however I am
not deprived of my senses.’ Could it be the effect of the narghileh—
which I had never smoked before—and that the tumbaki had
produced this extraordinary languor in my limbs, as it possibly
contained opium?
The Armenian appeared much amused on hearing of my helpless
state. He assisted me from the divan, supporting me while I tried to
walk, and finding that I could not do so, a daughter was summoned
to fetch some cordial, which the maiden, with an expression of mirth,
brought and administered. Having taken this and rested awhile, I
regained the use of my legs. The banker, on my taking leave,
expressed repeatedly his regret that I should have suffered any
inconvenience from the effects of the narghileh, and added that were
not his presence required at the Porte he would have insisted on my
remaining at his house to rest for that night at least.
About a year or more after this incident, when Sir Stratford
Canning had replaced Lord Ponsonby as Ambassador, a fancy ball
was given by Lady Canning at the Embassy at Pera, and I was
requested by her Ladyship to take the lead and the direction of the
dancing. I was dressed in Highland costume, and had selected for
my partner in the cotillon the daughter of the Armenian banker
mentioned in this story. In those days Armenian ladies rarely mixed
in European society, but she had been permitted on this special
occasion to appear at the ball at the Embassy, accompanied by her
father. She was beautifully dressed in the ancient Armenian
costume, was certainly the belle of the evening, and waltzed like a
sylph, so made a perfect partner for one who loved dancing as I did,
and we led the various figures in the cotillon with great spirit. Our
conversation was carried on in Turkish, which I spoke fluently.
Whilst we danced I observed that one of the Turkish Ministers,
who was present at the ball, took every opportunity of coming close
to where I happened to halt with my partner; gazing at her rudely, as
I thought, especially as she was a shy and modest girl.
At last, when the cotillon was drawing to a close, the Pasha came
up to us smiling and said, ‘Pekkei, pekkei’ (very good). ‘You are
suited to each other. She is “chok ghazal” (very pretty), and you are
a well-favoured youth. You must marry her: she will have money; you
have position. My friend the banker will consent; I am pleased.’ And
so the old fellow rattled on, much to my dismay and to the confusion
of the pretty Armenian maiden.
I remonstrated courteously with the old Minister, saying, ‘My
partner is very beautiful, but we have not thought of love or marriage,
for we are of different nations and creeds. Moreover, she would not
accept me as a candidate for wedlock, even if I offered myself; but I
shall always look back with pleasure to this evening when I have
been honoured by having such a lovely partner for this dance.’
‘Ah,’ said the Pasha, ‘she is, I know, the daughter of the banker. I
will speak to him and arrange matters, for I should like to make you
both happy.’
Luckily the time had come for me to bring the cotillon to a close;
so, bowing to the meddling old gentleman, I carried off my partner to
her father, telling her how vexed I felt; for she must have suffered
great annoyance from the foolish language held by the Pasha. The
fair Armenian replied, very shyly and prettily, that she did not think he
had said anything from malice, so she hoped I would forgive, as she
had done, his remarks. To this I readily agreed, and leading her back
to where her father the banker was standing I took my leave, and
never met again the pretty Armenian.
CHAPTER V.
CONSTANTINOPLE WITH SIR STRATFORD CANNING. 1841.
Sir Stratford Canning succeeded Lord Ponsonby as

Ambassador in 1841. He arrived at Constantinople on board a
Government steamer, and all the members of the Embassy
presented themselves on the arrival of his Excellency. These were
Charles Bankhead, Secretary of Embassy, Percy Doyle, Charles
Alison, and myself; Lord Napier and Ettrick, William Maule,
Mactavish, and Count Pisani, keeper of the archives, besides the
elder Pisani (Etienne). Robert Curzon, afterwards Lord Zouche,
accompanied his Excellency as private secretary.
The fame of Sir Stratford for severity towards his subordinates
had preceded him, and we all felt sad at the loss of our late chief, the
kind and courteous Lord Ponsonby, and at the prospect of being
ruled with an iron hand.
Sir Stratford inquired of Doyle as to the method employed in the
conduct of business at the Chancery. He replied that office hours
were from eleven till half-past three, but that Lord Ponsonby allowed
the gentlemen of the Embassy to attend at, or leave, the Chancery
when they pleased, so long as the work was done efficiently. Sir
Stratford said that such an irregular way of conducting business
would not suit him and that he should appoint one of the gentlemen
to hold the key of the archives, to receive the dispatches and letters
and come to him for orders every morning. Then, turning towards us,
he added, ‘I am not acquainted personally with any one of you, and
therefore have no ground for selection, but I choose Mr. Hay.’
Gladness flashed across the faces of the other attachés, and,
when out of hearing of the great Elchi, they chaffed me by saying,
‘You are the smallest, so his Excellency thinks he can get the better
of you if there is a row!’
When we arrived at the Embassy, which was at that time at
Buyukdere, I was summoned, and was directed by the Ambassador
to take possession of the key of the archives and not to allow any
one to have access to, or to see, the dispatches which might be
received from, or written to, the Secretary of State on political
subjects, and that I should be held responsible if anything of
importance transpired. Sir Stratford told me his reason for making
this arrangement was that an attaché, at one of the Missions he had
held, had by foolish indiscretion betrayed the contents of an
important dispatch to a member of a foreign Legation. He directed
that I should myself copy all dispatches of importance to the
Secretary of State and give out the rest of the work to the other
attachés.
I made known to the Secretary of Embassy, Bankhead, and to the
attachés, the instructions I had received. They were indignant—it
appeared to me with good reason—that they were not to be trusted;
especially Bankhead, who remonstrated and said he considered he
had a right to see all the dispatches to and from the Foreign Office,
and therefore should pay no attention to the Ambassador’s
directions. I replied that, having told them the orders I had received,
they were free to act as they thought fit and that I was not going to
be a Cerberus, but suggested that they should remonstrate with Sir
Stratford and not with me.
Sir Stratford seems to have been satisfied with his selection of Mr.
Hay as his confidential attaché, for shortly after he writes in a note
dated from Buyukdere to Mr. Hay at the Embassy, ‘I have welcomed
your first communication to me in writing. All quite clear. Everything
necessary, nothing superfluous.’
In 1843, the British Consul at Broussa laid before the Ambassador

complaints against the Pasha of the district where he resided, and
the latter had also brought under the notice of the Porte grievances
of a serious character, alleged to have been suffered from the
proceedings of the Consul. Attempts were made by both the Porte
and the Ambassador to bring about a settlement of the differences
but without success. British subjects, Ionians, and Turks whose
interests were affected by this state of affairs, appealed to the
Embassy and to the Porte, urging that steps should be taken to
secure the ends of justice.
Sir Stratford Canning proposed to the Porte that an officer of the
Embassy should be sent to Broussa to make an inquiry into the
conduct of the two functionaries, and that he should be empowered
both by the Porte and the Ambassador to bring about a settlement of
these differences, which had been a constant source of vexatious
correspondence.
Sir Stratford selected me for this duty, and delivered to me letters
from the Porte to the Pasha and from himself to the Consul,
acquainting them respectively that I had been authorised to inquire
into the various questions at issue, and to endeavour to bring about
a settlement.
Accompanied by a Greek servant, who knew the country and
could act as guide, I embarked in a steamer which took us to a port
where we hired horses and proceeded to Broussa.
Both the Consul and Pasha, on my arrival, offered me hospitality,
which I declined under the peculiar circumstances in which I was
placed by my mission.
The day after my arrival the Pasha summoned a Divan of several
local notables, who were to give evidence, and the Consul was also
requested to attend.
When I entered the Divan, being then a youth of about twenty-six,
I was much shocked at seeing that the Pasha, Consul, and other
notables—upon whom I had, as it were, to sit in judgment—were
men with white and hoary beards and of a venerable appearance.
After pipes and coffee, the hearing of the various subjects in
dispute commenced. Though I refer to this scene, as it affects the
end of my tale, it is needless to relate what passed, further than to
mention that I found both Pasha and Consul were in the wrong, but
that neither had acted in a manner to require any severe censure on
the part of the Porte or Ambassador, and I drew up a report in that
sense. On my return journey to the port, having heard that game was
plentiful, I gave my horse to the Greek to lead and wandered over
the country. I had good sport; and the Greek frequently warned me
that unless we kept to the beaten path and rode on quickly, we
should not be able to reach the port before dark.
Continuing however to shoot, I wandered after game many miles
from the road, or rather track, until it became so dark that I could no
longer see the birds rise. On remounting, I told the Greek to lead the
way, but he declined; he knew not where we were, nor even what
direction to take. It was a bright clear night, and at a distance of
about two miles I espied a light; thither I decided to direct our steps
and to ask for shelter for the night, or for a guide.

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Diagnostic Imaging: Chest 3rd Edition

Melissa L. Rosado-de-Christenson, MD, FACR

DIAGNOSTIC IMAGING: CHEST, THIRD EDITION ISBN: 978-0-323-79663-7

Previous edition copyrighted 2012.

Library of Congress Control Number: 2021944546

Printed in Canada by Friesens, Altona, Manitoba, Canada

Last digit is the print number: 9 8 7 6 5 4 3 2 1

Allen Heeger, DO Julia Alegría, MD

We were fortunate to recruit a world-class team of authors who delivered

ART DIRECTION AND DESIGN

INTRODUCTION AND OVERVIEW CARDIAC, PERICARDIAL, AND VALVULAR

EMPHYSEMA AND SMALL AIRWAY DISEASES VIRUSES

LUNG CANCER IDIOPATHIC INTERSTITIAL LUNG DISEASES

EOSINOPHILIC LUNG DISEASE THORACIC COMPLICATIONS IN

Overview of Chest Imaging

Introduction and Overview

Chest Radiographic and CT Signs

Atelectasis and Volume Loss

Introduction dyspnea, or inability to understand or follow technologist's

Overview of Chest Imaging

Introduction Terminology of Thoracic Imaging

Overview of Chest Imaging

Usual Interstitial Pneumonia Nonspecific Interstitial Pneumonia

Chronic Eosinophilic Pneumonia Lipoid Pneumonia

(Left) Axial NECT of a patient

(Left) Axial CECT of a patient

Overview of Chest Imaging

(Left) PA chest radiograph of a

(Left) Axial NECT of a patient

(Left) Composite image with

(Left) Axial NECT of a patient

Overview of Chest Imaging

(Left) Graphic demonstrates

(Left) PA chest radiograph of a

(Left) Coronal NECT of an 87-

(Left) PA chest radiograph of a

Overview of Chest Imaging

(Left) PA chest radiograph of a

(Left) Axial NECT of a patient

TERMINOLOGY TOP DIFFERENTIAL DIAGNOSES

(Left) PA chest radiograph of a

(Left) Coronal NECT of a 49-

Overview of Chest Imaging

(Left) Graphic shows the

(Left) Coronal HRCT of a

(Left) PA chest radiograph of a

(Left) Axial CECT shows a

Overview of Chest Imaging

(Left) Axial CECT shows

(Left) Axial CECT of a patient

(Left) Axial NECT of a patient

(Left) Axial NECT of a patient

Overview of Chest Imaging

(Left) PA chest radiograph of a

(Left) Coned-down AP chest

(Left) Axial NECT of a 43-year-

Overview of Chest Imaging

(Left) Graphic shows the

(Left) Axial HRCT of a patient

(Left) PA chest radiograph of a

(Left) PA chest radiograph of a

Overview of Chest Imaging

(Left) Axial NECT of an