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DIAGNOSTIC IMAGING: CHEST 3rd
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Santiago Rosado-De-Christenson
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THIRD EDITION
Rosado-de-Christenson
Martínez-Jiménez
Restrepo | Betancourt-Cuellar
Carter | Lichtenberger
Heeger | Ternes
Carrillo-Bayona | Frazier
Silva | Garrana
Alegría | Fuss
ii
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.
No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical,
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This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as
may be noted herein).
Notices
Practitioners and researchers must always rely on their own experience and knowledge in
evaluating and using any information, methods, compounds or experiments described herein.
Because of rapid advances in the medical sciences, in particular, independent verification of
diagnoses and drug dosages should be made. To the fullest extent of the law, no responsibility is
assumed by Elsevier, authors, editors or contributors for any injury and/or damage to persons or
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any methods, products, instructions, or ideas contained in the material herein.
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
x
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
xii
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
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THIRD EDITION
Rosado-de-Christenson
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
hypersensitivity pneumonitis
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
Another random document with
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[20] Well employed.
[21] Sir Francis Burdett.
Hd. Quarters, Fornos D’Algodres, May 23, 1810.

My Dear Ellen,
As you desire to hear from me immediately I will not lose a
moment in thanking you for your dear letter of the 15th and 24th
April, and for your affectionate kind wishes on my birthday....
We have been in this Quarter near a month and most heartily tired
of it. It is a miserable little village on the side of a very high mountain,
opposite to the famous mountains of the Estrella, and about a mile
from the river Mondego, and 8 from Celorico the Hd. Qrs. of Lord
Wellington.
I have lately changed my abode, as in the last the rain ran in upon
my bed, and we were three in a very small room with one window
without a pane of glass. Indeed in the whole of the Marshal’s
Quarters there are but 6 in one window. We only had one bason and
one jug, and you may imagine the squabbling as to who was to wash
first. I have deposed some silkworms from my present room, and
have at least the luxury of being alone, and having a broken pewter
bason, none of the cleanest, to myself. There’s luxury for you! The
rain however, which has been incessant for the last 3 months or
more, has found its way in, and runs in tolerable streams in four
parts of my dismal abode. My bed escapes, and my bason and some
broken jars catch water. Therefore I am rather well off.
At the General’s, my last Quarter, we had 7 or 8 grown up young
ladies, des grands du Village, the most affected stupid misses I ever
met with in any barbarous country. They never were three miles from
home, and ape notwithstanding from hearsay what they fancy great
people should do. They think me I believe very proud, and the young
ladies are mighty shy. I am not, however, quite safe from the attacks
of a maiden aunt of 30 to 40 with little cat’s eyes and bad teeth. I
think she will find I am bomb-proof to her kind looks and sighs. She
has already begun to try what disdain will do, to my great joy and
amusement. You would be much entertained to see us assemble at
breakfast and dinner, near 20 people. We have succeeded at last in
making them wash their hands and faces, and if we remain long
enough no doubt will also attain the desideratum of combing their
hair, even for breakfast, or rather before breakfast, and once or twice
a week, oftener than on Sunday morning.
Public news I have none to tell you, except the arrival of Masséna
to command the army of Portugal, which is between Ciudad Rodrigo
and Salamanca. He is a very clever enterprising Officer, and will
soon give us something to do, I have no doubt, but we are not at all
afraid of him, as our troops both English and Portuguese are in the
highest spirits, and the latter so much improved that they hardly
know themselves again. I have no doubt they will do their duty, but
should wish to break them in by degrees....
Ever yr. most affectionate Brother,
Wm. W.
Extract from a Letter of Thomas Warre

London, June 20, 1810.
My Dear Father,
I write these few lines to inform you I this morning received a long
letter from William, from Fornos d’Algodres, June 6th, the same
place they were in before. He is very well and writes in very good
spirits. They have had dreadful bad weather by continual rains.
The French have invested Ciudad Rodrigo closer, but William
thinks before they attack that place, they will drive in our advance
corps, General Crawfurd’s Division, which overlooks their operations,
and should they succeed in driving them in, Beresford’s forces must
retire to concentrate. But William does not expect they will succeed,
not being in sufficient force. He still speaks favourably of the native
troops, who are kept a good deal on the alert. They have lately had
great feasting. Ld. Wellington on the 4th inst. gave a dinner to
Beresford, which was returned by him, and all went off remarkably
well.
William has again written to poor Clara, but fears nothing he can
urge will induce her to move at present. I lament it exceedingly....
On getting to Throgmorton St. I found a few lines from Capt.
Hardy. The date is 28th of May off Fernesen in the Gt. Belt. He
merely says that he is quite well, and that they are proceeding on to
the Baltic, that is the St George, Formidable, Stately and Resolution,
and that nothing had occurred worth noticing.
Extract from a Letter of Thomas Warre

Hendon Place, July 8, 1810.
[I deferred writing to you as I expected to find letters in town from
Wm., which we did of 13th June.]
He wrote as usual in great spirits, but the crisis of their fate
approaches. The French had completed their bridges across the
Agueda, so Cd. Rodrigo was invested, but their heavy artillery had
stuck in the mud near Tamames, somewhere between Salamanca
and C. Rodrigo. They have three Corps d’Armée, viz.: Junot, Ney,
and Regnier’s, which is opposed to Genl. Hill to the Southward. Their
force he supposes to be 60 to 70,000, very sick and discontented.
Much will depend on their first sweep, but if the Portuguese troops
fulfil the promise they give at present, he has no doubt they shall
give them a good licking. Ld. Wellington’s Hd. Qrs. were at Celorico.
The front of the allied army extended from Pinhel to Guarda. Adv. gd.
at Gallegos, 2 leagues from C. Rodrigo and the advanced Picket at
Marialva, close to the French outposts. I saw Col. Ross yesterday.
He has exchanged into the 48th; both Batts. of which are in Portugal
in Genl. Hill’s Division. He had seen a letter from Ld. Wellington to
one of Mrs Ross’s Brothers. He writes in great spirits. My Father
likewise saw a letter yesterday from General Off. of high rank, who
said that their position was an excellent one, and that the C. in. C.
has made the most judicious arrangements. All this is very good as
far as it goes, but I shall look for the next arrivals with much anxious
impatience.
Hd. Qrs., Fornos D’Algodres, June 20, 1810.

My Dear Father,
I am sorry to tell you that the Marshal has not yet received any
answer from the Government respecting the admission of Rice and
Grain free of duty; and I begin to fear that their usual narrow and
absurd policy opposes more obstacles to this very desirable object
than was at first expected. Indeed, if so, nothing can be more
absurd, as although the harvest promises very well, particularly Rice
and Barley, owing to the uncommon lateness of the season, the
Indian corn is in most places but just sown, and in many not yet.
Much must therefore depend upon the dryness of the latter end of
the Autumn, and before that I think the scarcity will be so great, that
they will be forced, though late, to open their ports, and give every
encouragement to importation, or starve. The men and oxen have
been kept away from their agricultural pursuits, to attend the armies
with their carts, and this has delayed and impeded very much the
ploughing, and hoeing, and reaping, as has also in some degree the
very great consumption of cattle. The moment the Marshal gets an
answer I will write to you, and to Porto to Pedro Alvez, which I have
not done hitherto, because in the first place I could tell him nothing
decisive, and in the next, it appeared to me prudent that it should be
kept quite a secret that such an allowance in point of duties was in
agitation.
The weather has at last set in very hot, which I hope will increase
the great sickness of the French, who have been mostly exposed to
the continued rains we have had till now. Our people, both English
and Portuguese, are getting into the most satisfactory state of health,
having been under cover and quiet.
The Enemy continues almost in statu quo. They have completed
their bridges over the Agueda at Val d’Espino, and covered them by
a small tête de pont. By their means the investment of Ciudad
Rodrigo is completed. Their heavy Artillery and Mortars are, I
believe, still fast in the mud half-way to Salamanca, but this hot
weather will now soon enable them to bring them up. After which I
have no idea that Ciudad Rodrigo can hold out a fortnight, from its
construction, which is completely irregular and very defective,
besides being in some degree commanded at about 800 yards. This
will probably be the prelude to our play, and then we shall all become
actors. They seem very shy of us, and I do not believe have as yet
completed their preparations, or collected a sufficient force to attack
us. Their foreigners continue to desert in considerable numbers, and
more would I am sure come over, but for the steps the French have
taken to prevent them. Our advanced Picquets have frequent
skirmishes with them, which lead to nothing but wounding a few men
and horses on each side.
We went over two days ago to Francozo to inspect a Portuguese
Brigade with Lord Wellington, and afterwards to Minucal (?) to see
the 16th Lt. Dgns., who are in very fine order, and made a most
excellent review. At Francozo we visited the Nuns. The Porteress
gave Lord Wellington, etc., etc., leave to enter, and some of us
rambled all over the Convent. I never saw more poverty, misery, and
dirt, except indeed some of the cells which were tolerably neat. Most
of the Nuns were in the Choro at prayers, and not a little astonished
at seeing a large party of men appear at the door from the inside.
There were some pretty girls enough, but they were so long at
Prayers, that we could not stop to speak with them, and had the full
and free range of their abode. This visit of the great people will
furnish conversation, I dare say, for years!
The price of Indian Corn at Montemor Velho, which regulates for
Coimbra and all that neighbourhood, was last week at 11
Testoons[22] the Alqueire. It had been at 12 T. the fortnight before.
Believe me ever, my dear Father, Your most sincerely affectionate
son,
Wm. Warre.
[22] Testoon = about 5d. Alqueire = about 3 Imp. gallons.
To His Brother
Hd. Qrs., P.A. Francoso, Nr. Pinhel, June 27, 1810.
My Dear Tom,
We removed our Hd. Qrs. here two days ago and the English Hd.
Qrs. to Almeida, on account of the very interesting situation of
Ciudad Rodrigo, and to be within reach of immediate information
respecting any movements of the French Army, which becomes
every day more interesting. Their heavy Artillery being arrived, they
on the evening of the 24th commenced a brisk fire on the place,
which was returned with great vivacity by the besieged, and
continued until 10 o’clock on the 25th in the morning, when a most
tremendous explosion took place in the French lines from their
Powder Magazine blowing up, (N.B. has since been ascertained to
have been in the town), and immediately after two lesser explosions
(which were in the French lines). The quantity of Powder must have
been very great, as it was seen at this place by several of our
officers, nearly 40 miles off, and at Almeida, half-way between this
and the Ciudad Rodrigo, the shock was very strongly felt, and
Governor Cox writes that it shook the whole place. Certain it is that
the French batteries ceased firing and the Spaniards continued for
two hours after.
If their loss is what we suppose from these circumstances, it will
be a most serious loss to them, as I know not how soon they can
replace it in Spain, and will probably delay their attack upon us for 6
weeks or 2 months, a great point gained for us, whose object is by
gaining time to complete the discipline of our Army, etc., and who are
getting very healthy. These, however, are the effects we wish for,
and, like other people, we are very apt to fancy the probability of
what we wish for, though at the same time you must not imagine that
we are the least afraid of them even now. We know that their army is
very sickly. They average deaths 46 to 50 a day, are in want of
everything, and their intercepted letters show that they are very
much disgusted. The Spaniards carry on a desultory and most
destructive warfare. They scarcely dare move out of their Quarters
without risking to be assassinated, and their losses in this way and
by desertion are very great in every part of Spain.
They drive in our Picquets now and then. They have a great
superiority of Cavalry, but nothing of any consequence has taken
place. But if the greatest part of their powder is not destroyed, we
may expect something every day. I cannot think they will let
Crawfurd with the advance Guard remain so near them. Their and
our vedettes are 400 to 500 paces from each other and we overlook
their camp, which is very extensive, I suspect more so than they
have any occasion for, considering the number of men they have.
They are quite up to all this sort of humbug. If our Portuguese do as
we expect, we are not uneasy as to the result, and if we lick them
what a glorious day for Old England! I like this place better than
Fornos, though we are not very well off either, and have a large
Brigade of Infantry with us in the town. I am very well, the only
annoyance is my face, which as well as my lips always peel and are
very sore. By the end of the campaign I daresay we may pass
ourselves off for Portuguese Indians, or any other tawny gentry you
please. Adieu, etc.
Francoso, July 9, 1810.

July 2.—Hardinge and myself left Francoso about 6 in the evening
to visit the advanced guard and outposts of the Army under Br. Genl.
Crawfurd stationed in front of Gallegos, in New Castile, with his Hd.
Qrs. at Almeida, about 4 miles in the rear. We arrived late in the
evening at Pinhel, where we remained the night. Next morning set
out after breakfasting with our friend Major Murphy of the 88th, (the
Bishop of Pinhel being absent from Pinhel,) having dined at
Francoso the day we left it for Almeida, the direct road to which we
missed, and proceeded by an almost impassable path down to the
Coa, which here on either side presents a most formidable position,
totally impracticable for cavalry and artillery except over the bridge
and high road leading to Almeida from Freixedas, Guarda, Pinhel,
etc. According to the reports of its whole course from its confluence
into the Douro to near Alfaiates, with the exception of two leagues
beyond Almeida towards its source, it presents, from the very great
steepness and rocky soil of its banks, a most formidable barrier to
any army attempting to advance towards Vizeu, Celorico, Guarda, or
Francozo, from the neighbourhood of Ciudad Rodrigo. It is, however,
liable to be turned by Sabugal, or Castello Branco, and opposed to a
superior army its great extent is a very serious inconvenience, as
any part of the line being forced must oblige the rest to retire.
While Almeida, which is about a mile and a half from the river on
the Spanish side, holds out, I consider any attack by that road as not
to be feared. Though the greatest part of the descent to the bridge is
out of sight of the town, the enemy’s movements would be very
much impeded in attempting to advance. Considering all
circumstances, the great superiority of the enemy and nature of a
great part of our troops, I have much doubt in my own mind of any
position being attempted to be defended on the Coa, as a general
one for the Army, but this a few days must show, and I am no way in
the secret.
We crossed the Coa at a very bad ford called Veia, about a mile
below the bridge, and arrived at Almeida, waited on Governor Cox;
and, after walking round the works (which from their nature I do not
at all envy him the defence of, considering the troops he has, mostly
Militia,) continued our march to Fort Conception to see our friend Lt.
Col. Sutton, who had been appointed Governor, when there was an
intention to defend it. But since the great superiority of the enemy
rendered it impossible to attempt to relieve the brave Spaniards in
Ciudad Rodrigo, it has been resolved to blow it up, and it has for that
purpose been mined all round. When the enemy seriously advance
this beautiful Fort will be entirely destroyed. It is a thousand pities. I
never saw a more complete or perfect fortification with every part
bomb-proof, even stabling for 200 horses. Its outworks are admirably
adapted to defend the approaches, which are all round a perfect
natural glacis to several hundred yards. Of the necessity of the
measure I am no judge, but fear it will much vex the Spaniards.
We arrived about 3 o’clock at Almeida, and dined with Genl.
Crawfurd, with whom after dinner we rode out to look at the French
posts beyond the little river Azara, over which there is a bridge of
stone leading to the village of Marialva, and about a mile beyond
Gallegos. Along this line were about 3 squadrons of the German 1st
Hussars doing the outpost duty, their reserves in Gallegos. I went
down to the bridge and endeavoured to persuade two French
Officers to come down and speak to me. They were, however, very
shy, and only came near enough for me to tell them that some
friends of theirs, who were taken prisoners near Chaves a year and
a half ago, were well. I observed they were constructing a wooden
bridge a short distance to the left of the former, and from the
exhausted appearance of the Forage on the other side, their having
removed the cars from blocking up the stone bridge, and certain
reports of deserters, it appeared very probable they would drive in
our posts next morning, the 4th July. They had there and near Carpio
about 5 or 6 Regts. of Cavalry and some Infantry, 4 to 5000 men I
should guess in all. Our Infantry, consisting of the 43rd, 52nd, Rifle
Corps, and two Portuguese Caçadores Battns., one very good and
the other very bad, were stationed in the woods in front of Alumeda,
about 3 or 4 miles in our rear.
At daybreak they crossed the little river Azara over their two
bridges, and drove in our Picquets. They had 12 squadrons and 2
Brigades of Infantry, but our three squadrons were supported by a
troop of Horse Artillery, which kept them in check and enabled our
little body to retreat in safety on the Infantry though close pressed
and skirmishing very sharply the whole way. It was the prettiest
thing, en fait de guerre, I ever saw. The retreat was very well
conducted. Their Artillery could not come up till near the end of the
affair, and ours killed a great many of their men and horses, while
our Cavalry were in comparative safety. Their numbers enabled
them constantly to turn our flanks, and the superiority of our horses
as often to get out of the scrape.
A party of the German Hussars under Capt. Kranckenberg
behaved particularly well, charging at the passage of a small bridge
a very superior number of the enemy, though supported by four
Squadrons within pistol shot on the other side. It was very well done.
Two French Officers were severely wounded and some men, and
one prisoner was taken, though, poor devil, he was covered with
wounds, 6 in the head, and his arm nearly cut off, also run through
the body, and wonderful to say, he is expected to recover. The
French seemed much irritated at this check, and kept up a very brisk
fire up the road we retreated by, within about 50 yards from us. Nor
were they sparing in abuse, and confident of still cutting us off, when
we arrived at our Infantry which checked them, and a Squadron of
their 3rd Hussars coming unexpectedly on the 3rd P. Caçadores (an
excellent Corps commanded by Lt.-Col. Elder) received a very warm
salutation which dispersed them. The Battalion behaved very
steadily and well, and give us hopes of the Portuguese troops, on
whose conduct the issue of this Campaign must in a great measure
depend.
The Division commenced its retreat towards Fort Conception
covered by the Cavalry, whom I here quitted, having offered myself
to act as aide-de-camp to Genl. Crawfurd. The Infantry returned in
very good order through Alumeda towards Fort Conception, and
General Carrera with his Spaniards, who were in our rear, by the
fords of Algardon to a very strong position covering the roads that
way. These Spaniards are remarkably fine men, about 3000 well
clothed, though not uniformly, and armed. I did not, however, think
much of their discipline or regularity. Hardinge placed them, and
seemed to be much pleased with General Carrera’s appearance and
manner.
The French gave up the pursuit about half a league from Fort
Conception, and retired again to Gallegos, on this side of which
place they established their vedettes, having attained, what I
suppose was their intention, a new ground to forage on, and having
reconnoitred our force, to ascertain whether or not Lord Wellington
had come up with the army. Our loss was about 4 or 5 men wounded
and as many horses. That of the French, so far as we could see, and
have since heard from deserters, several Officers and about 30 or 40
men killed and wounded. After halting about two hours near the Fort,
our advanced guard took up a position at Val de la Mula, on the
Portuguese frontier, with the Cavalry about a league in front, leaving
a space of about a league between their vedettes and ours. And this
ended this little affair which Hardinge and myself had so much
wished to see, and which was certainly very instructive. Au reste a
great deal of firing to very little purpose. A strong proof of how
ineffectual the skirmishing of Cavalry is, except to cover the retreat
of larger bodies, and prevent the columns being fired into. Our
people and theirs were constantly within 30 yards of one another
firing with no effect, though neither party had any idea of fear. When
it can possibly be avoided the less powder wasted this way the
better. The best arm for Cavalry is the sword or sabre, a well broken
horse and firm presence of mind, reserving the pistol or carbine
merely for the purpose of vedettes, or covering some movement.
At Val de la Mula Col. Pakenham asked us to breakfast and
afterwards to dinner, and during the whole of our stay we are much
indebted to his civility, as also to Capt. Rowan and Wm. Campbell,
brother to Augustus, who prevented our ever wanting a meal or
forage for our horses during our stay. General Crawfurd was also
very civil to us. While retreating he sent me with some letters to
Governor Cox at Almeida, whom, however, I was fortunate enough
to meet at Val de la Mula, which saved me a very tiresome ride, and
enabled me to return immediately, but everything was over, and I
was so tired that I was very glad to lay down in the guard-room of the
Fort, which was evacuated, to take a nap, which was not of long
duration, as I had taken possession of the mattress of a Spanish
shepherdess of no very gentle nature, who was so clamorous and
violent in claiming her property, that I was forced to yield it up for fear
I might not escape so well from her gentle paws, as I had from the
French. Besides, poor things, I could not but pity them. It was most
distressing to see them abandoning their habitations, and flying
away from the miscreants, loaded with what little property they could
carry away, crying and lamenting, followed by their helpless children,
while the men drove away their cattle, and all uncertain where they
might find a place of safety. In Portugal the natural animosity which
exists so violently on the frontiers, and which even the similarity of
their misfortunes and distress cannot do away, they had but a dismal
prospect of meeting with a friendly reception. I pitied them from my
heart, to relieve was not in my power. How little does the
independent happy English Peasant know how to value the peace
and security in which he lives! And how would those miscreants who
preach discontent and faction through the country, giving them ideas
of wants and liberties which are incompatible with society and
government, how would they blush if they were to witness the
sufferings and oppression which these poor people undergo! They
would see that in England alone the peasantry are now happy and
free, and would see their own infamy in sowing the seeds of discord
and civil dissension among that happy people, when every mind
should be united and heart joined to resist the oppressor of mankind!
If reform is necessary let us wait for moments of peace with foreign
enemies, when we do not risk, by dividing amongst ourselves, the
entire ruin of the most perfect fabric of government that ever existed,
even with all its faults, and give every advantage to our enemies by
exposing as some of our Senators do, by way of opposition to
Ministers, or to get themselves in, our forces, intentions, weakness,
faults, etc., etc., in fact, for the sake of a popular speech in the
House, tell the enemy everything they ought most to conceal, even
the stations and exact numbers of the troops, of ourselves, or of our
allies. This conduct leads us half way to our ruin, and we shall repent
it when it is too late.
On the 5th, early in the morning, Hardinge and myself rode out
beyond Alumeda, towards Gallegos, till near the enemies posts, to
see what damage we had done them the day before and what they
were about. We found in the road two of their dead and some
horses, evidently from the effects of our Artillery, as they were much
mangled, and we also saw some more to the right and left of the
road at a distance. A very large flight of vultures of very large size
were flying about them, and on the ground, which added much to the
disgust of the scene, and after ascertaining the positions of their
vedettes, we hastened to return. Being but indifferently mounted,
and at a great distance from our outposts, we were very much afraid
of being cut off by some of their patrols, and, returning through
Alumeda, I was just observing to Hardinge that we should look very
foolish if we were to be taken, when I turned my head and saw a
French Hussar close to us. Hardinge had not even his sabre, having
broken it the day before, and I saw nothing was to be done but to
charge him, for which purpose I drew my pistol and galloped at him,
when he surrendered, a no very glorious prize, as his horse was so
tired that he could not move out of a very slow pace, and it was with
difficulty and anxiety we got him into one of our picquets. He was a
French lad, and told me he had deserted that morning, owing to the
ill-treatment of his chief, and the want of everything they experienced
in their Camp, and said he intended to go to England and work at his
trade, a cabinet maker, as he had a cousin there, whom he intended
to enquire for at the Commune (police office), though he had not
heard of him for 4 years. I have great doubts of his being a deserter
at all, and rather think he was as much surprised to see us, as we
were to see him. He is quite a Frenchman, and contradicted himself
twenty times!
We arrived at our quarters at 8 o’clock, and breakfasted with Col.
Pakenham. After which we set out, 5 in number, well armed and
mounted, to reconnoitre the enemy on our left, and proceeded
without meeting any as far as Villa de Porco and Barcilha, from the
heights above which we distinctly saw with our glasses Ciudad
Rodrigo, which was keeping up a very heavy fire, and defending
itself as if it were manned by heroes. Let them now surrender when
they may. They have done their duty, and it is heartbreaking to think
we can in no way assist them.
At Barcilha our party divided. Hardinge, Col. Pakenham, and Capt.
Cotton went by the right, and Capt. Shaw, A.D.C. to Genl. Crawfurd,
and myself agreed to go and visit Villar de Ciervo, and all that line,
and ascertain whether the French had occupied all those places, or
Villar de la Egoa, where there are some excellent fords over the
Agueda, and which, being in rear considerably of our left on the 4th,
gave Genl. Crawfurd no small anxiety. We met nothing, and returned
about 4 to dinner, having suffered only from the extreme heat, which
fagged me a good deal, being rather bilious, and prevented my
accompanying them in the evening, instead of which I paid a visit to
my friends in the 52nd, whom I was very glad to see looking as well
as ever I saw them at Shorncliff, though perhaps with less pipeclay.
Next day was spent nearly in the same way. In the morning we
rode out reconnoitring to Alumeda, dined afterwards with General
Crawfurd, and set off on our return to Pinhel, 4 leagues, where we
arrived late at night and slept, and next day came home, after a most
delightful trip, and having just seen what we wished and expected.
The retreat of the advanced guard had for some days appeared
inevitable, and it was to see how it would be conducted that we went
over.
The desertion continues from the French in great numbers, 8 to 12
of a day while we remained with the advance guard, and they all
agree in stating that their Army is badly off for provisions, and the
foreigners much disgusted, and would desert in greater numbers but
for the vigilant means that are taken to prevent. Junot and Ney with
their Corps are before C. Rodrigo, and I believe also Masséna, as
are also the traitors Alorna, Pampeluna, Sancos Mezeude, against
whom no measures are taken by this Government, and we know
they are supplied with money, etc., from their estates in this country,
which are not sequestered or disturbed. So much for weakness and
infatuation! The count Doidga(?) has been declared infamous and
his offspring for three generations, and his property sequestered. He
is a poor wretch and can do no harm, though not less a traitor, while
these scoundrels, with arms in their hands, known traitors before the
Prince embarked, and treated by him with great lenity, are suffered to
attack their native country with impunity. It is most disgusting.
I do not think the French will attempt anything till C. Rodrigo falls,
which, notwithstanding their heroic conduct, cannot be long delayed.
It will enable the French to establish their magazines and hospital.
What the plans for the Campaign are I know not. Everything
promises a very warm one, and I confess I look with some anxiety to
the conduct of the Portuguese troops, on whom much, nay
everything, must depend. They promise well, it is true, in every
respect, but still they are very young troops and never tried. The
force against us is very superior. But on the other hand the greater
must be the difficulty of supplying them and means of transport. We
retire on our supplies while they advance from them. And everybody
has great confidence both in Lord Wellington and Marshal Beresford,
and if the native troops fight like men, I have not a doubt we shall
succeed, though the loss must be inevitably great on both sides.
My own idea of their attack is that they will keep their principal
Corps in our front, leave Regnier with his Corps, and keep Hill in
check in the Alemtejo, while with a strong column they endeavour to
force the passes near Castello Branco, or by Sabugal, endeavouring
to unite near Thomar. By this means if Hill retires and crosses the
Tagus, either at Villa Velha or Abrantes, the Alemtejo is left open,
and we cannot but feel some anxiety for the Capital, or rather for the
opposite side of the river, which would occasion great confusion. Hill
must then defend the passage of the Tagus, which abounds in fords
as low as Salvaterra, and also endeavour to check the enemy’s
advance by the passes of Salhadas, etc., from Castello Branco or
Abrantes, and if either of these movements of the enemy succeed, I
should imagine the whole Army must fall back from the Upper Beira
upon our works round Lisbon, that is Torres Vedras, Bucellas, etc.,
etc., for fear of its communications with Lisbon and our stores. Or if
they do not attempt Alemtejo, I think they will attempt advancing in
three columns by Castello Branco from Coria and Placencia, and
from Guinaldo, etc., by Sabugal, and in our front by Celorico or
Guarda, endeavouring to unite beyond the Sierra de Estrella. In this
case we shall come into play immediately. Almeida, I think, they will
merely mask by a strong Corps, and leave in their rear. If they
succeed, the place must fall of course. If not, there is not force
enough in it to annoy them. These are my own private opinions, and,
from the very little means I have of information, must be considered
as mere speculations, and as such, if erroneous, I may be excused,
as I really know not how far they may agree with any others.
Hd. Qrs., Francoso, July 10, 1810.
My Dear Father,
I received your letters of 13th, 15th June, on the 1st of this month,
and my having been absent at the outposts alone prevented me
writing by last packet to thank you for the very interesting information
you give me about Ferguson in particular, and the other occurrences
of the day, as also for the affectionate friendship and solicitude on
my account, which would be a sufficient reward in themselves for
anything I can ever do.
I send you, annexed, a sort of journal of my proceedings during
my little excursion to the outposts, which was very interesting. It was
written in considerable hurry and just as the things occurred to me.
The opinions also merely speculative, as I have but little means of
positive information. I should therefore wish you to consider it as
merely for your amusement and confidential, and for those few who
can feel any interest in such trifles because they concern me.
Our situation becomes every day more interesting. The heroic
defence of Ciudad Rodrigo has delayed the operations against this
country, but I consider that it is impossible the place can hold out
much longer.
What the issue of this contest may be, it is very difficult to guess.
The enemy have certainly from 70 to 80,000 men, and we as
certainly Troops of the Line not so many, though we have other
advantages which they cannot have, particularly the people and the
country in our favor. Lord Wellington and the Marshal appear very
confident and in high spirits, and so does the whole army, who are in
excellent order. Our Chiefs know best the real situation in which they
stand, and the confidence every one feels in them will make the
Army do wonders. Much must depend upon the Portuguese troops.
At all events I think prudence would dictate the removal of all
property from this country, and leaving as little to chance of war in
point of business as possible, and although I by no means wish to
croak, when I consider the great superiority of the enemy in
numbers, and the nature of our Troops, with many other
circumstances, I confess I do not feel quite so confident of our
ultimate success. But I shall not form any decided opinion till I see
our people tried.
Pray thank my dear mother for her kind letter of the 30th May from
Hendon, and Tom for his of the 19th June, and for Greenwood and
Cox’s abstract of my account. I am a good deal surprised they have
not received my claim for losses. By the account I see they have
received no part of them and suspect they do not much exert
themselves, as I know other Officers have received theirs. By Tom’s
letter I observe a warrant has been issued for £36, 15s., I suppose
for my horse shot at Vimiero.
I hope you have had a pleasant trip to Woburn and Holkham. I am
always happy when I hear of your amusing yourself in a way I know
to be so much to your satisfaction.
I have got at Lisbon two Merino Rams and 3 Ewes. They tell me
they are very fine, and my difficulty now is how to send them to you. I
write by to-day’s post to Messrs Bulkeley to beg them to take charge
of them for you, and send them by the first ship to London, and shall
inform you of their answer. If you had no place to keep them
yourself, and nobody else you wish to give them to, pray present
them to my uncle Greg with my kind love. I am, however, a good
deal bothered about getting them home, being myself at such a
distance from Lisbon.
Adieu; pray give my kindest love to my dearest mother, and
believe me ever your most truely Affectionate and Dutiful Son,
Wm. Warre.
I will tell Ld. W. about the pipe of wine when I see him, and am
much obliged by your attention about it.
July 11th.—A very heavy firing and cannonade was heard
yesterday morning at Ciudad Rodrigo, which is a proof that the place
still holds out. Poor fellows, I fear they will pay dear for their heroic
gallantry, since we cannot assist them.
I have been able to hear nothing further about the free importation
of rice and grain, and I fear it will not be allowed from the delay.
Hd. Qrs., Francoso, July 25, 1810.
My Dear Father,
I have but just time to write you a few lines that neither you nor my
mother may be anxious about me, when you hear of the unfortunate
affair of our Advanced Guard yesterday, at which, however, I was not
even present. The French attacked Br. Genl. Crawfurd’s Division,
consisting of 43, 52, 95, and 1st and 3rd Portuguese Caçadores,
about 3000 men, and some squadrons of Cavalry, with 23 squadrons
and about 10 to 12,000 Infantry. I fear there was some delay in
retiring across the Coa, and, being very close prest in their retreat,
our brave fellows suffered very considerable loss, about 300 killed
and wounded and 30 Officers. The 43rd I hear have suffered most,
and have 14 Officers killed and wounded, as also the 95th, of whose
loss I am ignorant, except of the death of poor Capt. Creagh. Col.
Nutt of 43rd is killed and Capt. Hull wounded. They had arrived from
England the evening before. The 52nd also lost some men and
Officers, but I have not been able to hear any names, except that of
Lt.-Col. Barclay being slightly wounded in the head. The 3rd
Caçadores under Col. Elder behaved very well, and suffered some
loss.
I am sorry I cannot add as much for the 1st, who did not behave
so, and ran off at the very beginning, though their Col. d’Arilez, a
very fine young man, behaved very well, as also some of the
Officers. So much for want of discipline and confidence. I had before
expressed my fears about them. I am just about setting off to enquire
into the business, and I hope a most severe example may be made
to prevent the recurrence of such a horrid disgraceful business. If
they will not fight from feelings of patriotism or honour, they must be
made to do so from fear of a more infamous death, and a more
certain one, if they deserve it. It is a measure of peremptory
necessity; though I have much pleasure in being able to add that in
an attack which Regnier made on Salvaterra away to our right, the
1st Portuguese Cavalry commanded by Col. Pays of Mangoalde
behaved most nobly, charged three times, and as often repulsed the
enemy, and at last completely drove them back, and I believe the
French had the superiority in numbers. Our advance guard having
effected its retreat at all before so very great a superiority is most
fortunate, that is across the Coa, whose banks are tremendously
steep, and the road narrow. The French three times attempted to
force the bridge after them but were repulsed, and lost a good many
men on it. The tremendously heavy rains and storm we have had
these last two days had fortunately spoiled the Fords of the River
entirely. Otherwise I much fear our little Corps would have been
entirely cut off and taken.
The English kept possession of the bank till early this morning,
when the whole line was abandoned and our advance established at
Carvalhos or Carvalhal. The French vedettes are on this side the
river, and Almeida is consequently in some degree invested. I scarce
believe they will besiege it, but rather content themselves with
blockading and starving it, which will not be easy, as they have 4
months’ provisions complete. Pray send Augustus Campbell word
that I hear both John and William are well, the former I am not sure
was engaged. Wm. was of course with Crawfurd. I fear you will be
scarce able to read this very hasty scrawl, but I have at this moment
so many things to do in order to get away before late in the evening
to reach Freixedas to-night, that they must serve as my excuse. You
shall hear from me every opportunity. Adieu. Pray give my kindest
love, etc. Yr. ever dutiful and affectionate Son,
Wm. Warre.
Lagiosa, August 8, 1810.

My Dearest Father,
Many many thanks for your very kind letter from Eastley End of the
16th July, and for the excellent account you give me of all my friends.
We continue here very quietly, and except the taking of a few
prisoners at the outposts in front, and the peasantry having risen and
killed a good many of the enemy, who straggle into the villages to
plunder or seek for food, nothing of any consequence has occurred
since my last.
The French appear to be preparing for the siege of Almeida, but
have not yet established any batteries. From the accounts of all
deserters and prisoners they are much distressed for provisions,
particularly bread, which as the Peasantry all fly from their ill-
treatment, they are forced to thrash out, carry to the mills, and grind
and bake themselves. In some places the Officers alone have bread,
in others they sometimes receive 3 lb. between 8 men. They are also
much in want of shoes. A very intelligent Italian sergeant, who was
brought in yesterday, assured me that their 66th Regt. lost on the
24th Ultmo., in the attack near Almeida, 500 killed and wounded, and
the other two Regiments also a very large proportion. They therefore
must have lost upwards of 1000 men in all, which is more than we
supposed. They continue to desert in great numbers whenever they
have the opportunity.
Our Portuguese troops are behaving very well. The 1st Regt. of
Dns. at Atalaya towards Castello Branco attacked 80 French who
were in the town, killed 25, and took 20 men and horses. Yesterday
evening an account arrived from Bragança that a squadron of the
12th Dns. had been attacked by a French squadron, which they
defeated, took 40 men and horses Prisoners, and killed all the rest,
except 2 Officers and a soldier who escaped. Many of these
Prisoners are badly wounded. The Portuguese squadron must have
behaved very well to have done the business so effectually, and
although these small affairs are of no great consequence (in
themselves), yet they give us very pleasant hopes of what the
Portuguese [troops] will do when more seriously engaged.
I have this instant been to see three French Cavalry, who deserted
yesterday evening. They say they did so because they are starved,
and that 25 of the 3rd Hussars and 8 more of their men had deserted
the day before. These men, who are native French, come over
mounted and completely armed. They say that nothing but
desperation could make the Infantry go leagues from the Army to get
food at the risk they run from the Peasantry, and that their Regt. of

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DIAGNOSTIC IMAGING: CHEST 3rd

Edition Melissa L Martinez Jimenez

Diagnostic Imaging: Chest 3rd Edition Melissa L.

Diagnostic Imaging: Gynecology 3rd Edition Akram M.

Diagnostic Imaging: Pediatric Neuroradiology 3rd

Diagnostic Imaging: Interventional Radiology 3rd

Diagnostic Imaging: Head and Neck 4th Edition

Chest, abdomen, pelvis 2nd Edition Federle

Muller’s Imaging of the Chest 2nd Edition Christopher

Diagnostic Imaging: Musculoskeletal Non-Traumatic

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