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Chest Radiology: Plain Film Patterns and Differential Diagnoses, 6th Edition, by James C Reed, MD, provides expert guidance on interpretation of the most often seen radiologic patterns of chest disease. The new edition continues to emphasize pattern recognition on plain film -- with correlative CT, MR and other important modalities included where appropriate. Each pattern is introduced with radiographs followed by a series of questions, tables of differential diagnosis, and discussions of the most likely diseases to present with such a pattern. The discussion sections emphasize the importance of clinical correlation to narrow down the differential diagnosis, and what follow-up tests are indicated to definitively confirm a diagnosis. New high-quality digital images and updated questions enhance the latest edition of this trusted reference.

  • Get all you need to know about the fundamentals of plain film chest radiology as well as CT, MR, and other important modalities.
  • Overcome clinical challenges with guidance about the pitfalls of plain film radiography, and indications for CT, HRCT, biopsy, and other procedures.
  • Use comparative image study to master pattern recognition and improve your understanding of the correlation between findings on plain film, CT, MR, and more.
  • See imaging findings as they appear in practice and discern subtle nuances found in new, high-quality digital images.
  • Test your knowledge with illustrated case studies and quizzes featuring newly written questions that address the challenges seen in practice today.

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Chest Radiology
Plain Film Patterns and Differential Diagnoses
Sixth Edition
James C. Reed, M.D.
Professor of Radiology, University of Louisville, Louisville,
Kentucky
M o s b yFront Matter
6th EDITION
Chest Radiology: Plain Film Patterns and Differential Diagnoses
James C. Reed, M.D.
Professor of Radiology
University of Louisville
Louisville, Kentucky
with 548 illustrations?
?
Copyright
1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899
CHEST RADIOLOGY, SIXTH EDITION ISBN: 978-1-4377-2345-8
Copyright © 2011, 2003, 1997, 1991, 1987, 1981 by Mosby, Inc., an
affiliate of Elsevier Inc.
No part of this publication may be reproduced or transmitted in any form or
by any means, electronic or mechanical, including photocopying, recording, or
any information storage and retrieval system, without permission in writing from
the publisher. Details on how to seek permission, further information about the
Publisher’s permissions policies and our arrangements with organizations such as
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at our website: www.elsevier.com/permissions.
This book and the individual contributions contained in it are protected under
copyright by the Publisher (other than as may be noted herein).
Notices
Knowledge and best practice in this eld are constantly changing. As new
research and experience broaden our understanding, changes in research
methods, professional practices, or medical treatment may become necessary.
Practitioners and researchers must always rely on their own experience and
knowledge in evaluating and using any information, methods, compounds, or
experiments described herein. In using such information or methods they should
be mindful of their own safety and the safety of others, including parties for
whom they have a professional responsibility.
With respect to any drug or pharmaceutical products identi ed, readers are
advised to check the most current information provided (i) on procedures
featured or (ii) by the manufacturer of each product to be administered, to verify
the recommended dose or formula, the method and duration of administration,
and contraindications. It is the responsibility of practitioners, relying on their
own experience and knowledge of their patients, to make diagnoses, to determine
dosages and the best treatment for each individual patient, and to take all
appropriate safety precautions.?
To the fullest extent of the law, neither the Publisher nor the authors,
contributors, or editors, assume any liability for any injury and/or damage to
persons or property as a matter of products liability, negligence or otherwise, or
from any use or operation of any methods, products, instructions, or ideas
contained in the material herein.
Library of Congress Cataloging-in-Publication Data
Reed, James Croft, 1942-
Chest radiology : plain lm patterns and diCerential diagnoses / James C.
Reed.—6th ed.
p. ; cm.
Includes bibliographical references and index.
ISBN 978-1-4377-2345-8 (hardcover : alk. paper)
1. Chest—Radiography. 2. Diagnosis, Radioscopic. I. Title.
[DNLM: 1. Radiography, Thoracic. 2. Diagnosis, DiCerential. 3. Respiratory
Tract Diseases—radiography. WF 975 R324c 2011]
RC941R4 2011
617.5′407572—dc22
2010022429
Senior Acquisitions Editor: Rebecca Gaertner
Editorial Assistant: David Mack
Publishing Services Manager: Patricia Tannian
Team Manager: Radhika Pallamparthy
Senior Project Manager: Kristine Feeherty
Project Manager: Antony Prince
Design Direction: Lou Forgione
Printed in the United States of America
Last digit is the print number: 9 8 7 6 5 4 3 2 1D e d i c a t i o n
To my wife, Sharon, whose continuing support and encouragement made it
possible for this book to reach the Sixth Edition.Preface to the Sixth Edition
Chest radiology continues to be a large part of medical imaging, and advances
in technology have resulted in a number of important changes. This could have
impacted the title of this book. Most radiology practices have converted to digital
imaging, and the title Plain Film Patterns may seem quaint, but I choose not to call
it chest x-ray, radiographic, or image patterns.
Chest radiology procedure volume continues to be high, making it an important
part of most radiology practices. The primary problems in plain lm interpretation
fall into the two broad categories of perception and interpretation challenges. It is
always the goal of the radiologist to make a speci c diagnosis, and many exams
permit a precise radiographic diagnosis but many more require additional studies.
CT, MR, ultrasound, and image-guided interventional procedures may all be
used to make precise diagnoses, but CT has had the greatest impact on diagnostic
chest imaging. This edition has expanded the number of CT images, which are
correlated with the plain lm to better explain the basic patterns of chest
radiology.
TOP 5 DIAGNOSES is a new feature of this edition. This is intended to
emphasize the importance of o- ering short, clinically relevant di- erential
diagnoses, but remember that a speci c diagnosis is always preferred to a
differential list.
James C. Reed, M.D.
#


#
#


Preface to the Fifth Edition
The practice of chest radiology continues to evolve with rapid changes in
technology and our understanding of diseases. I have continued to refer to the
chest radiographic image as a plain lm for simplicity. As a result of digital
radiography, the techniques for creating and viewing the chest radiograph are
more variable than ever, but the basic principles requiring a high-quality image
and careful interpretation still apply. The impact of CT on chest radiology has
continued to expand with the technical advances of spiral and multi-detector CT,
which have made CT angiography a reality. HRCT has also continued to have a
greater impact on the diagnosis and management of di use lung diseases. The
improved imaging of the di use diseases, combined with changes in the
pathologic and clinical understanding of these diseases, has resulted in signi cant
changes in the classi cation of di use lung diseases. Lung cancer detection is a
continuing problem, but there are signi cant changes in the way lung cancer is
detected, staged, and followed. Infectious diseases also remain a cause of more
life-threatening complications. Since September 11, 2001, there are new threats in
the form of biologic terror that have even impacted chest radiology. Anthrax
previously has not been considered a likely human disease, but it is now included
as an important cause of acute onset of mediastinal adenopathy and mediastinal
widening. Continued study leads to ongoing improvements in the diagnosis and
management of chest diseases. Chest radiology is a discipline that requires the
mind of a detective and the ability to nd answers to the unknown by careful
review of the shadows.
James C. Reed, M.D.




Preface to the Fourth Edition
Progress in the diagnosis and treatment of chest diseases continues to expand
the scope of chest radiology. In an e ort to avoid confusing terminology, I have
reconsidered an old semantic concern for description of basic observations: The
term d e n s i t y is correctly used to describe the mass of a substance per unit volume.
The radiologist recognizes that an increase in tissue may cast a shadow or opacity
that appears white on the lm. Such a shadow is frequently described as a density,
but density has an opposite meaning when it is used to describe lm blackening or
optical density. The term d e n s i t y has therefore been a recurring source of
confusion. While density is still often used to describe a white abnormality on
exams such as mammograms, the glossary of terms published by the Fleischner
Society has shown a strong preference for the term o p a c i t y. New advances in our
understanding of di use pulmonary diseases have also led to some updates in
pathologic and radiologic descriptive terminology.
Our advancing knowledge of diseases such as AIDS continues to expand our
understanding of the diversity of patterns of chest disease. Many common diseases
including lung cancer, tuberculosis, and AIDS-related diseases produce a variety of
plain lm patterns. AIDS-related diseases are considered causes of mediastinal
adenopathy, di use air-space disease, multifocal opacities, and hyperlucent
abnormalities. The major technical advances to a ect chest disease are in CT.
High-resolution thin section CT has replaced bronchography for the diagnosis of
bronchiectasis and has advanced our understanding of the patterns and
distributions of di use pulmonary diseases. Single-breath hold spiral CT has
reduced artifacts and provides a new area for further research. The plain lm,
however, continues to be the most frequently performed of all radiologic
procedures, and while it appears to be simple to perform, it is often the most
challenging of radiologic exams to interpret.
James C. Reed, M.D.








Preface to the Third Edition
In the last decade, we have seen the emergence of exciting new techniques and
the appearance of new diseases. AIDS has profoundly a ected many aspects of our
society and the practice of medicine, including interpretation of the plain chest
lm. Computer technologies are changing the way we examine patients, and they
o er a host of new imaging options. Computed radiography is addressing some old
technical problems and should provide better quality bedside plain lms.
Highresolution CT is very sensitive for con rming abnormalities that are only suspected
from plain lm or the clinical information, particularly ne reticular or nodular
interstitial diseases and early emphysema. To optimize our use of these new
technologies, we still need a thorough understanding of the diseases and their
plain lm patterns. This edition continues to emphasize plain lm interpretation
and uses radionuclide scans, ultrasound, CT, MR, and angiography to provide
clarification of the patterns and to confirm specific diagnoses.
James C. Reed, M.D.



%
%


Preface to the Second Edition
This book utilizes a unique format in order to walk the reader through the
differential diagnoses of 23 common plain film patterns of chest disease.
Each chapter opens with one or more unidenti ed radiographs. A series of
questions follow, all designed to help identify the pattern of disease presented on
the lm. For those desiring immediate answers, the legends for the introductory
radiographs are at the end of each chapter. So, too, are the answers to the multiple
choice, yes-no, and true-false questions.
Sandwiched between the presentation of the case at each chapter’s beginning
and the answers at the end are a tabular listing of di erential considerations and a
discussion o£ the problem case. The discussion follows a step-by-step approach to
eliminating inappropriate diagnoses and arriving at the correct one or by
suggesting that other radiology procedures and laboratory tests be performed,
concluding with a summary. This section makes reference to several additional
radiographs, all of which are fully identi ed and grouped after the discussion and
summary.
It has been my intention to simulate within the con nes of a book the
radiologist’s decision-making process of going from lm to diagnosis. Although
limitations of the format make it impossible to realistically reenact the process, it
is hoped that your trip through these pages is both instructive and enjoyable.
The second edition of this book has expanded some of the di erentials, and
emphasized the impact of the newer modalities, particularly CT scanning, on the
diagnosis of chest disease. While the role of MR appears to be limited mainly to
the evaluation of the mediastinum, CT has impacted almost all of the patterns in
chest radiology. While a number of cases have been added to demonstrate the use
of CT, the emphasis of this text continues to be the plain lm patterns and their
differential diagnoses.
The reference list is also substantially expanded because of the continued rapid
growth of the medical literature related to chest radiology. Because this is
intended to be an introductory text, a large number of topics are considered in a
simplistic manner. The reference list is intended to be used as a suggested reading
list. This will provide the reader with a more comprehensive work on a particular
entity.James C. Reed, M.D.



Preface to the First Edition
This manual is designed to provide a comprehensive di erential diagnosis for 23
of the most common radiologic patterns of chest disease. Each chapter is
introduced with problem cases and a set of questions, followed by a tabular listing
of the appropriate di erential considerations. The discussion centers on the
problem case and demonstrates how the radiologist can use additional radiologic
procedures along with correlative clinical and laboratory data to narrow the
differential diagnosis or to suggest a specific diagnosis.
The book aims to provide a thorough background in the di erential diagnosis of
chest disease for residents in radiology, internal medicine, pulmonary medicine,
family medicine, and emergency medicine. It also o ers the practicing radiologist
an updated review of the radiologic patterns of chest disease and a concise
reference on differential diagnosis.
Acknowledgments
It is impossible to acknowledge adequately all of the sources of inspiration,
background, and support for this text. It began when Captain Q.E. Crews, Jr.,
M.C., U.S.N., and Dr. Elias G. Theros appointed me to the faculty at the Armed
Forces Institute of Pathology. Dr. Theros created a stimulating environment and
inspired early interest in chest radiology. Many of the ideas in this text were
developed in the rich and dynamic atmosphere of the AFIP where my interaction
with Drs. Theros, Madewell, Allman, Olmsted, and Korsower in radiology and Drs.
Johnson, Hockholzer, Sobonya, Kagan-Hallet, and Daroca in pathology provided
the framework on which this text has been built.
Preparation of the text and illustrations was accomplished during my tenure on
the radiology faculty at Duke University. Special mention must be given to Dr.
Charles E. Putman, who arranged for photographic support; David Page, who
prepared the illustrations; Brenda Peele and Susan Morrison, who typed the text;
and Dr. Lawrence Hedlund, whose editorial suggestions and proofreading were
invaluable.
The list of friends providing support for a text cannot be complete, nor would
enumeration express my gratitude adequately.
Finally, the completion of the text is due in no small measure to the untiringsupport and encouragement of my wife, Sharon.
James C. Reed, M.D.A c k n o w l e d g m e n t s
A special thank you to the following individuals:
Dr. Gregory Postel, Chair of the Department of Radiology, for providing a great
work environment.
Mr. Danny McGrath for technical assistance and help with the production of the
digital illustrations.
Dr. Edward DeAngelo for his suggestion of a TOP 5 list for each of the patterns.Table of Contents
Front Matter
Copyright
Dedication
Preface to the Sixth Edition
Preface to the Fifth Edition
Preface to the Fourth Edition
Preface to the Third Edition
Preface to the Second Edition
Preface to the First Edition
Acknowledgments
Part 1: Chest Wall, Pleura, and Mediastinum
Chapter 1: Introduction
Chapter 2: Chest Wall Lesions
Chapter 3: Pleural and Subpleural Opacities
Chapter 4: Pleural Effusions
Chapter 5: Pleural Thickening and Pleural Calcification
Chapter 6: Elevated Diaphragm
Chapter 7: Shift of the Mediastinum
Chapter 8: Widening of the Mediastinum
Chapter 9: Anterior Mediastinal Mass
Chapter 10: Middle Mediastinal Mass
Chapter 11: Hilar Enlargement
Chapter 12: Posterior Mediastinal Mass
Part 2: Pulmonary Opacities
Chapter 13: AtelectasisChapter 14: Segmental and Lobar Opacities
Chapter 15: Diffuse Air-Space Opacities
Chapter 16: Multifocal Ill-Defined Opacities
Chapter 17: Diffuse Fine Nodular Opacities
Chapter 18: Fine Reticular Opacities
Chapter 19: Coarse Reticular Opacities (Honeycomb Lung)
Chapter 20: Solitary Pulmonary Nodule
Chapter 21: Multiple Nodules and Masses
Part 3: Hyperlucent Abnormalities
Chapter 22: Hyperlucent Thorax
Chapter 23: Solitary Lucent Defect
Chapter 24: Multiple Lucent Lesions
Bibliography
IndexPart 1
Chest Wall, Pleura, and
Mediastinum

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1
Introduction
The simplicity of performing a chest radiograph often leads to the mistaken
impression that interpretation of a chest plain lm should also be a simple task.
Despite the fact that the chest radiograph was one of the rst radiologic procedures
available to the physician, the problems of interpreting chest plain lms continue
to be perplexing as well as challenging. The volume of literature on the subject
indicates the magnitude of the problem and documents the many advances that
have been made in this subspecialty of radiology. A casual review of the literature
quickly reveals the frustrations a radiologist encounters in evaluating the numerous
patterns of chest disease. There are as many e orts to de ne the patterns identi ed
on chest radiographs as there are critics of the pattern approach. Because
radiologists basically view the shadows of gross pathology, it is not surprising that
the patterns are frequently nonspeci c and that those who expect to nd a
one-toone histologic correlation of the radiographic appearances with the microscopic
diagnosis will be frustrated. It is much more important to develop an
understanding of gross pathology to predict which patterns are likely in a given
pulmonary disease. With this type of understanding of pulmonary diseases, we are
better quali ed to use nonspeci c patterns in developing a di erential diagnosis
and planning the procedures required to make a definitive diagnosis.
Colonel William LeRoy Thompson of the Armed Forces Institute of Pathology rst
adumbrated the concept of radiologic di erential diagnosis. Later, Reeder and
Felson ampli ed and popularized the approach in their book Gamuts in Radiology
by providing an extensive list of the various patterns and the corresponding
differential diagnoses.
This manual illustrates the common patterns of chest disease to facilitate
recognition. After recognition, the second step in evaluating a pattern is to develop
an appropriate di erential diagnosis. The complete di erential diagnosis must
include all of the major categories of disease (Chart 1-1) that might lead to the
identi ed pattern. Next, the di erential must be signi cantly narrowed by (1)
careful analysis of the lm for additional radiologic ndings, (2) consideration of
the evolving patterns of the disease by review of serial examinations, and (3)
correlation of patterns with clinical and laboratory data (Chart 1-2). With this
narrowed di erential, we will be able to function as consultants, suggesting further
procedures that may lead to a precise diagnosis. These procedures vary from simple
radiographic examinations, such as those taken with the patient in oblique
positions, to percutaneous biopsy under 2uoroscopic, computed tomography (CT),






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or ultrasound guidance.
Chart 1-1 Categories of Diseases
I Inflammatory
II Vascular
A Thromboembolic
B Cardiovascular
C Collagen-vascular
III Neoplastic
IV Traumatic
V Developmental
VI Idiopathic
Chart 1-2 Algorithmic Application of Chest Patterns
A radiologist should have a thorough understanding of the radiologic di erential
diagnosis to determine appropriate procedures for investigating diseases of the
chest. It should be obvious that the rst step in evaluating many abnormalities
identi ed on the standard posteroanterior (PA) and lateral chest x-ray lm is to
con rm that the abnormality is real. A newcomer to radiology frequently forgets
the value of simple techniques such as reviewing examinations taken in oblique
positions, repeated PA chest lms with nipple markers, 2uoroscopy, full chest
lordotic views, and, most important, old lms. These simple procedures should be
used to con rm the presence of an abnormality before considering more
complicated procedures such as radionuclide scanning, arteriography, CT scanning,
magnetic resonance imaging (MRI), or biopsy. In fact, the later procedures are
special procedures that should be undertaken to answer specific questions.
After deciding that an opacity is a true abnormality, one of the most important!
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radiologic decisions to be made is to localize the abnormality. Localization to soft
tissues, the chest wall, pleura, diaphragm, mediastinum, hilum, peripheral vessels,
or the lung parenchyma is absolutely necessary before a logical di erential
diagnosis can be developed. Once the abnormal opacity is localized to a speci c
anatomic site, it is necessary to classify or describe the pattern. Some of the
patterns of parenchymal lung disease considered in this text are nodules, masses,
di use opacities, cavities, calci cations, and atelectasis. If the pattern is
nonspeci c, a moderately long di erential must be o ered. As mentioned earlier,
one of the objectives of this manual is to further re ne pattern analysis and develop
methods of improving diagnostic speci city. For example, in the analysis of
parenchymal lung disease, assessment of the distribution—deciding whether the
process is localized or di use, peripheral or central, in the upper vs. lower lobes, or
alveolar vs. interstitial—is extremely helpful. In correlating these features, we are
able to eliminate a number of possible diagnoses from initial consideration. Once
the di erential has been narrowed on the basis of identi cation of the disease
pattern and distribution, examination of old lms is valuable. Unfortunately, a
common mistake is oversight of the very dynamic changes in the patterns of chest
disease. A typical case history may be as follows:
This is the rst admission for this patient, and therefore the rst chest x-ray
examination. The knowledge that a solitary nodule was present on a film taken 2 years
earlier at another hospital, or even 5 or 10 years earlier at still other hospitals, could
completely resolve the problem of how to manage the patient.
It is not always necessary to make a precise diagnosis, particularly in a case such
as the one just described. The diagnosis of old granuloma, whether secondary to
tuberculosis or histoplasmosis, is almost always adequate for the clinical
management of the patient. Without old lms, the solitary nodule is a frustrating
problem because the di erential is long and, more important, cancer cannot be
260,601ruled out, whereas with the old film, the diagnosis may be obvious.
Careful clinical correlation is also important in understanding the evolution of a
pulmonary disease. For example, in evaluating a patient with a solitary
pleuralbased nodule on admission, a history of pleuritic chest pains 6 weeks earlier
drastically changes the probable diagnosis. An additional history of
thrombophlebitis and multiple episodes of pleuritic chest pain makes the diagnosis
794of pulmonary embolism with a resolving infarct almost certain.
It is hoped that the 23 problems in di erential diagnosis that follow this
introductory chapter will be instructive as to how the radiologist can interpret the
pattern on a single chest x-ray lm, develop a moderately long di erential
diagnosis, narrow the di erential diagnosis to a reasonable number of possibilities,
and make recommendations for further procedures, leading to a single diagnosis.2
Chest Wall Lesions
Questions
1 The most likely diagnosis in the afebrile patient in Figure 2-1 is:
a Neurofibroma.
b Lipoma.
c Multiple myeloma.
d Osteosarcoma.
e Chondrosarcoma.
2 The most likely diagnosis in Figure 2-2 is:
a Ewing’s sarcoma.
b Osteosarcoma.
c Chondrosarcoma.
d Metastatic lung cancer.
e Plasmacytoma.Figure 2-1
Figure 2-2
Mark the following questions True or False:
3 Chest wall lesions may sometimes be distinguished from pulmonary nodules by
identification of an incomplete border.
4 Lipoma is a common chest wall lesion.
5 Neurofibroma of an intercostal nerve will probably cause rib destruction.
6 Rib detail films or computed tomography (CT) scans are rarely needed to
identify the rib destruction of a primary bone tumor in the chest wall.
7 Multiple myeloma and metastases are among the most common causes of a chest
wall mass with associated rib destruction in an adult.
8 Ewing’s tumor and neuroblastoma should be considered when a chest wall mass
is observed in a child or young adult.
Chart 2-1 Pattern
Chest Wall Lesions
501 278I Nipples, supernumerary nipples?
II Artifact
117III Skin lesions (e.g., moles, neurofibromas, extrathoracic musculature)
181IV Mesenchymal tumors (muscle tumors, fibromas, lipomas, desmoid
143 251tumor, synovial sarcoma )
591V Neural tumors (schwannoma, neurofibroma, ganglioneuroma,
733neuroblastoma )
566VI Hodgkin’s and non-Hodgkin’s lymphoma
462,732,733VII Vascular tumors (angiosarcoma, glomus tumor, hemangioma)
VIII Benign bone tumors (fibrous dysplasia, osteochondroma, giant cell tumor,
732aneurysmal bone cyst, fibroma, chondromyxoid fibroma)
429IX Malignant bone tumors (metastases, multiple myeloma, Ewing’s sarcoma,
544 251chondrosarcoma, osteosarcoma, fibrosarcoma, malignant fibrous
733histiocytoma, plasmacytoma [solitary myeloma])
X Hematoma
XI Rib fractures
775 14XII Infection (actinomycosis, aspergillosis, nocardiosis, blastomycosis,
284tuberculosis, osteomyelitis [rare])
203XIII Thoracopulmonary small cell (“Askin”) tumor
216,409XIV Invasion by contiguous mass (lung cancer)
XV Lymphangioma (cystic hygroma)
Discussion
Chest wall opacities (Chart 2-1) may be observed as a result of shadows that arise
from both extrathoracic and intrathoracic normal and abnormal structures.
Common extrathoracic causes of radiographically visible opacities include nipples,
moles, and various cutaneous lesions (e.g., neuro bromas of von Recklinghausen’s
201,680disease). Extrathoracic chest wall opacities are seen as soft-tissue opacities
with an incomplete, sharp border (Fig 2-3). The border is produced by the interface
of the mass with air and is lost where the mass is continuous with the soft tissues of
the chest wall. Cutaneous lesions should not have the tapered borders that are seen?
?
?
in Figure 2-1. The tapered border indicates displacement of the pleura inward by
198the mass and has been described as an extrapleural sign. Physical examination
is also essential in the evaluation of cutaneous lesions. Nipple shadows may be
easily identi ed when they are symmetric and when their borders are incomplete,
501but caution is warranted. Repeat examination with small, lead nipple markers
should be performed if there is any possibility of confusing a nipple shadow with a
pulmonary nodule.
Figure 2-3 This large, left mass has a sharp lateral border because it is outlined
by air, but has no medial border illustrating the incomplete border sign. The mass is
obviously outside of the rib cage and easily identi ed as a chest wall mass. Physical
examination revealed this to be a soft, pliable mass in this neonate, making
lymphangioma the most likely diagnosis.
Intrathoracic chest wall lesions are radiologically visible because of their
interface with aerated lung. Like the cutaneous lesions, their borders are
173incomplete where they are contiguous with the chest wall (Fig 2-4, A). Thus the
incomplete border is helpful in distinguishing chest wall lesions from pulmonary
lesions (answer to question 3 is True), but not in distinguishing cutaneous from
intrathoracic chest wall lesions. The tapered superior and inferior borders,
however, are valuable signs for con rming an intrathoracic extrapulmonary
location. Unfortunately, the tapered border may not be observed if the lesion is
seen en face: In fact, the lesion may not be visible. Lateral and oblique coned-down
views are frequently helpful in eliciting this sign (Figs 2-4, B and C).?
Figure 2-4 A, This myeloma illustrates the incomplete border sign, which is useful
in distinguishing pulmonary from extrapulmonary masses. Note the sharp inferior
border and absence of a superior border. B, Entire border of a chest wall mass may
appear incomplete owing to tapering. Note bone destruction. This is another
example of myeloma. C, Coned-down lateral view of the mass illustrated in B
reveals tapered borders (arrows), which result from displacement of both layers of
the pleura, a valuable sign for distinguishing pulmonary from extrapulmonary
masses.
409Lipomas are common chest wall lesions and may be seen as either
subcutaneous or intrathoracic masses (Fig 2-5, A). (Answer to question 4 is True.)
They may even grow between the ribs, presenting as both intrathoracic and
subcutaneous masses. Physical examination reveals a soft, movable mass when
there is a signi cant subcutaneous component. CT should show the extent of the?
?
?
?
?
?
181mass and, more importantly, con rm that the lesion is of fat density (Fig 2-5,
B).
Figure 2-5 A, Chest wall lipoma appears to be of tissue opacity, in contrast to
aerated lung. Location of lipoma against the lateral chest wall and its incomplete
border (sharp medial but absent lateral border) suggest that it is nonpulmonary.
There is no rib destruction to con rm chest wall origin. Both chest wall and pleural
masses should be considered in diBerential. B, CT scan of another patient with a
chest wall lipoma shows a mass that is of greater opacity than the aerated lung but
less opaque than the musculature of the chest wall. This intermediate fat density
mass is shown to extend through chest wall muscles.
(Case courtesy of Thomas L. Pope, Jr., M.D.)
198Rib destruction is a key observation in Figure 2-6. This nding excludes
lipoma and other benign tumors, such as neuro broma, from the diagnosis. Benign
neural tumors, such as schwannoma and neuro broma, may erode ribs inferiorly
and even produce a sclerotic reaction (Fig 2-7). Multiple chest wall masses in
combination with rib deformities and inferior rib errosions should suggest
neuro bromatosis (Figs 2-8, A-C). Neural tumors should not destroy the rib, as
shown in Figure 2-6. (Answer to question 5 is False.) Rib destruction is not always
obvious on a frontal examination and may be better visualized with rib detail
examination or CT scan. (Answer to question 6 is False.)?
?
Figure 2-6 Same lm seen in Figure 2-1 shows rib destruction (arrows) and
con rms chest wall involvement. These observations narrow the diBerential to
metastasis vs. multiple myeloma. Myeloma is the diagnosis.?
Figure 2-7 Benign schwannoma has not destroyed the rib but has eroded its
inferior cortex. Note sclerotic border, which virtually ensures the benign nature of
the lesion.
Figure 2-8 A, Posteroanterior (PA) radiograph shows bilateral, elongated,
tapered, smooth, peripheral masses. Multiple ribs are eroded inferiorly. B, CT
con rms the peripheral masses with extension of the left lateral mass through the
chest wall. The posterior extension of the mass was not suspected from the?
?
radiograph. C, The right paraspinal mass extends through the neural foramen and
was also not detected on the radiograph. This is a common nding in patients with
neurofibromatosis.
Metastases and small, round cell tumors are the most common tumors to produce
the pattern of rib destruction seen in Figures 2-1 and 2-6. The most common
primary tumors to metastasize to the chest wall are lung, breast, and renal cell, but
knowledge of a primary tumor is essential, because any tumor that spreads by
hematogenous dissemination may produce a chest wall lesion (Figs 2-9, A-C).
Multiple myeloma, plasmacytoma (solitary myeloma), and Ewing’s tumors are
primary round cell tumors that may arise in the bones of the chest wall. The
diBerential diagnosis in the adult patient with a chest wall mass and bone
destruction is most often metastasis vs. multiple myeloma. (Answer to question 7 is
True.) In a child, however, the pattern is more suggestive of metastatic
neuroblastoma or Ewing’s tumor. (Answer to question 8 is True.) Figure 2-1 shows a
typical example of multiple myeloma (answer to question 1 is c), but there are a
number of common variations. Myeloma may occur with complete loss of a rib,
large expanded ribs, or only a small, ill-de ned area of bone destruction. The
patient may even present with a pathologic fracture of the involved rib.
Occasionally, the soft-tissue mass may be rather large and the bone lesion minimal.
Lymphoma is another tumor that may infrequently produce a peripheral soft-tissue
566mass with incomplete or tapered borders and extend through the chest wall.
This indicates an advanced stage of lymphoma and is not an expected abnormality
at the time of presentation. The chest wall extension may not be seen on the plain
film, but it can be confirmed with a CT scan (Figs 2-10, A and B).?
?
?

Figure 2-9 A, PA lm shows a large soft-tissue opacity projected over the left
upper chest. The inferior border is sharply de ned, appearing to follow the inferior
cortex of the fth left rib, and the fourth rib is missing. The mass has no superior,
medial, or lateral borders; therefore, this is another variation of the incomplete?
?
?
border sign. B, CT con rms a posterior soft-tissue mass with rib destruction. This is
a common appearance for a chest wall metastasis, but in this case the primary is a
rare cutaneous Merkel’s cell tumor. C, Lower CT image with lung windows shows
how the mass appears to change shape as it extends around the chest wall
following the rib. The only border of the mass that is visible on the plain lm is
produced by the interface of the mass with the lung.
Figure 2-10 A, Advanced Hodgkin’s lymphoma has caused this large soft-tissue
mass. The incomplete borders indicate an extrapulmonary location, but the plain
lm reveals no evidence of the chest wall extension. B, CT scan shows the large,
peripheral soft-tissue opacity to have tapered borders and to extend through the
chest wall. Multiple pulmonary nodules were also confirmed.?
?
?
?
?
?
Benign and malignant bone tumors may arise in the scapula, sternum, vertebra,
and ribs. Some of the common benign rib lesions, such as benign cortical defect
and brous dysplasia, do not produce soft-tissue masses, but hemangiomas and
osteochondromas do produce soft-tissue opacies that project inward and should be
considered in the diBerential diagnosis of intrathoracic chest wall masses.
Hemangiomas may produce a signi cant extraosseous mass and resemble other
chest wall masses, but they can best be identi ed by their typically reticular, or
“basket weave,” pattern of bone destruction. Osteochondromas may elevate the
pleura and present as an intrathoracic chest wall mass. The typical pattern of the
calci ed matrix should con rm the diagnosis of osteochondroma (Fig 2-11).
Hereditary multiple exostoses are the result of an autosomal dominant disorder that
frequently involves multiple Fat bones. These patients may have deformity of the
ribs and multiple osteochondromas. They are also at increased risk for the
development of chondrosarcoma. Malignant transformation of osteochondromas in
this group of patients has been reported to vary from 3% to 25%. Signs of
malignancy include pain, swelling, soft-tissue mass, and growth (Figs 2-12, A-C).
Both osteosarcoma and chondrosarcoma may arise from the bones of the chest wall
in patients without any known risk factors. Chondrosarcoma is the most common
primary bone tumor of the scapula, sternum, and ribs. Ten percent of all
544chondrosarcomas are reported to arise in the thorax. Chondrosarcoma might
have been considered in the case seen in Figure 2-2; however, the tumor matrix of
chondrosarcoma is typically more spotted with calci ed rings, arcs, dots, or bands
as compared with the more homogenous matrix seen in this case. In answer to
question 2, Ewing’s sarcoma, metastatic lung cancer, and plasmacytoma may all
involve the chest wall, but should be eliminated by the blastic appearance.
371Osteosarcoma typically produces a more homogeneous blastic matrix and is the
answer to question 2. Blastic metastases from breast and prostate cancer (Figs 2-13,
A and B) to the ribs and vertebrae are much more common.?
?
Figure 2-11 This mass has protruded into the thorax, elevating the pleura, as
evidenced by the tapered borders. The calci ed matrix has a speckled, reticulated
appearance that is typical of a cartilage matrix. In addition, there is a well-de ned,
calcified cortex. These features are diagnostic of an osteochondroma.
?
?
?
Figure 2-12 A, Multiple osteochondromas produce calci ed soft-tissue masses.
These masses may cause considerable chest wall deformity with spreading of ribs.
They may also cause intrathoracic and extrathoracic soft-tissue masses. This patient
with hereditary multiple exostoses has two large masses. The smaller superior mass
is an osteochondroma. The large inferior mass obliterates the costophrenic angle
and extends into the extrathoracic soft tissues. Because of recent growth, a biopsy
was performed con rming the diagnosis of chondrosarcoma. B, CT of the smaller
superior osteochondroma shows a typical pattern of calci cation. C, CT of the
larger inferior chondrosarcoma shows a large soft-tissue mass with irregular bands
of calcified matrix.?
Figure 2-13 A, Compare this case with the case seen in Figure 2-2, A. This
elongated opacity follows the left anterior third rib, indicating a chest wall origin.
The opacity is lobulated and blastic. Blastic rib lesions are a common appearance of
prostate metastases, but the lobulated, expansile chest wall mass is unusual. B, The
blastic lesion in the lower thoracic vertebra con rms the presence of multiple
blastic bone lesions. This is a common appearance of metastatic prostate cancer.
InFammatory lesions of the chest wall may arise from puncture wounds,
hematogenous seeding, or direct extension from intrathoracic infections.
Septicemia by bacterial infections and even miliary spread of tuberculosis may
cause osteomyelitis of the spine or ribs with chest wall involvement, but infectious?
chest wall masses most often arise from empyemas or pneumonias with empyemas.
Actinomycosis is one of the more aggressive granulomatous infections and may
produce a parenchymal opacity, pleural eBusion, chest wall mass, rib destruction,
213,775and even cutaneous stulas. Occasionally, air-Fuid levels are seen in the
soft tissues. Other granulomatous infections that produce a similar appearance
14include aspergillosis, nocardiosis, blastomycosis, and, rarely, tuberculosis.
Patients with these infections usually have a febrile course, although it may be
somewhat indolent.
Hematoma is usually suggested by a history of trauma and is frequently
associated with rib fractures (Figs 2-14, A-C). Care must be taken not to overlook
an underlying lytic lesion that would indicate that the fracture is pathologic.
Occasionally, old rib fractures may be mistaken for nodules because of their callus.
These are best evaluated with coned-down views of the ribs. Rarely, chest wall
397desmoid tumor occurs as a late complication of trauma. Desmoid tumors are
143locally invasive but histologically benign chest wall masses.?
Figure 2-14 A, There is a large, right-lower thoracic opacity with no detectable
borders. Based on this PA radiograph, this could be mistaken for a pleural Fuid
collection. B, The lateral review reveals a well-circumscribed, posterior, elongated,
masslike opacity. C, CT reveals mixed attenuation of the posterior opacity with an
associated rib fracture. This confirms a chest wall hematoma.
Primary lung abnormalities sometimes invade the pleura and chest wall with rib
destruction and resemble primary chest wall abnormalities. This is observed with
both infections and primary lung tumors. The apical lung cancer (Pancoast’s
tumor) is best known for this presentation. When a lung cancer invades the pleura,
it may spread along the pleura in a manner that produces a tapered border.
However, close observation often reveals irregular or even spiculated borders,
which should strongly suggest the pulmonary origin of the tumor (Figs 2-15, A-D).
CT is sometimes required to visualize the irregular interface with the lung and
con rm the pulmonary origin of the tumor. Patients with apical lung cancer often
present with shoulder and arm pain. This combination is described as Pancoast’s
syndrome. When the tumor invades the paravertebral sympathetic chain, the
19patient may also have Horner’s syndrome, which includes ipsilateral ptosis,
miosis, and anhidrosis. ?
?
Figure 2-15 A, This large, peripheral, right apical mass has an inferior sulcus,
suggesting that it is more likely a lung mass. B, CT reveals a lobulated mass and
con rms an acute interface with the pleura, suggesting that it is arising in the lung
rather than either the chest wall or pleura. C, Coronal reconstruction CT shows a
broad interface with the chest wall and pleura but con rms the superior and
inferior sulci that were suspected from the frontal radiograph. D, Bone windows
from the CT reveal destruction of a rib. This is a lung cancer invading the pleura
and chest wall. Because of its location in the apex of the lung, this is known as
Pancoast’s tumor.
Top 5 Diagnoses: Chest Wall Lesions
1 Metastases
2 Multiple myeloma
3 Neural tumors4 Invasive lung cancer
5 Hematoma
Summary
The incomplete border sign, which may be seen as the result of both extrathoracic
and intrathoracic chest wall masses, is suggestive of an extrapulmonary process.
Chest wall masses have smooth, tapered borders that are helpful in distinguishing
them from pulmonary lesions. These are best seen with tangential views.
Benign chest wall tumors such as lipoma, schwannoma, and neurofibroma should
not destroy ribs but may erode the inferior surface of a rib.
Chest wall tumors that destroy ribs are most commonly metastases or multiple
myelomas in adults and Ewing’s tumor or neuroblastoma in children.
Rib destruction may be subtle, requiring coned views, CTs, and even radionuclide
bone scans for visualization.
Actinomycosis, aspergillosis, nocardiosis, tuberculosis, and blastomycosis may all
produce chest wall lesions with rib destruction. The history and physical findings
should alert the radiologist to these possibilities.
A CT scan is often required to confirm chest wall involvement by metastases,
myeloma, lymphoma, and even benign masses.
Lung, breast, and renal cell tumors are the most common primary tumors to
metastasize to the chest wall.
Answer Guide
Legends for introductory figures
Figure 2-1 This mass is typical of a chest wall mass because of the smooth,
tapered medial border. The tapered border indicates an intrathoracic location.
(See Figure 2-6 on p. 11.)
Figure 2-2 This large, right-upper, lateral thoracic mass has tapered superior and
inferior borders with the additional finding of an opacity that follows the posterior
aspect of the right third and fourth ribs. The widening of the interspace between
the second and third ribs is the result of the mass. There is also lateral destruction
of the third rib. The opacity is greater than that of the surrounding ribs, indicating
a blastic bone reaction that is the result of calcified tumor matrix. This is a rare
case of osteosarcoma arising from the chest wall. Prostate and breast cancers arecommon primary tumors and are much more common causes of blastic bone
metastases that may involve the thoracic skeleton.
Answers
1. c 2. b 3. T 4. T 5. F 6. F 7. T 8. T3
Pleural and Subpleural Opacities
Questions
1 Referring to Figure 3-1, which of the following is the least likely diagnosis?
a Metastatic melanoma.
b Metastatic breast carcinoma.
c Invasive thymoma.
d Malignant mesothelioma.
e Metastatic ovarian carcinoma.
2 Referring to Figure 3-2, A and B, the most likely diagnosis for this case is:
a Rounded atelectasis.
b Localized fibrous tumor of the pleura.
c Multiple myeloma.
d Infarct.
e Mesothelial cyst.
3 Referring to Figure 3-3, A-C, the most likely diagnosis for this case is:
a Malignant mesothelioma.
b Neurofibromatosis.
c Metastases.
d Invasive thymoma.
e Loculated pleural effusion.Figure 3-1Figure 3-2
Figure 3-3Mark the following questions True or False:
4 Malignant mesothelioma may present with either solitary or multiple pleural
nodules.
5 A shaggy, irregular border favors a subpleural, parenchymal lung lesion over a
pleural lesion.
6 Mesothelioma frequently causes bone destruction.
7 Pleural lesions may be confused with mediastinal masses.
Chart 3-1 Solitary Pleural Opacity
I Loculated pleural effusion
172II Metastasis
65,768III Mesothelioma (benign or malignant)
200,207,237,256,598IV Lipoma
658,760,782V Organized empyema
VI Hematoma
VII Mesothelial cyst
591VIII Neural tumor (schwannoma, neurofibroma)
153,175,618IX Solitary fibrous tumor of the pleura
Chart 3-2 Multiple Pleural Opacities (Each >2 Cm)
414I Loculated pleural effusion
II Metastases (particularly from adenocarcinomas)
414,753III Invasive thymoma (rare)
346,637IV Mesothelioma (malignant)
613V Pleural plaques (asbestos-related)
361,630VI Splenosis
VII Neural tumors=
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>
Chart 3-3 Subpleural Parenchymal Lung Opacities
293I Infarct
II Granuloma (tuberculosis, fungus)
III Inflammatory pseudotumor
IV Metastasis
V Rheumatoid nodule
19,253VI Primary carcinoma of the lung including Pancoast’s tumor
71,714VII Lymphoma
45,485VIII Round atelectasis
Discussion
Solitary Pleural Opacity
The radiologic evaluation of a solitary pleural opacity (Chart 3-1) is complicated
658,741by the paucity of reliable signs for accurate localization. The opacity
should be in a peripheral extrapulmonary location, which may be con rmed by
identifying the incomplete border sign (see Figs 2-4, A-C). The peripheral position
is easily recognized when the mass is against the lateral chest wall, but the correct
location may be more di cult to identify when the mass is either anterior or
posterior (Fig 3-4, A). The lateral view (see Fig 3-2, A) or even a computed
163,401tomography (CT) scan (Fig 3-4, B) may be needed to con rm the
peripheral location. A peripheral mass requires consideration of three locations: (1)
the chest wall, (2) the pleura, and (3) the subpleural area of the lung. Smooth,
incomplete tapered borders with obtuse pleural angles localize a mass to either the
chest wall or pleura, while shaggy borders and acute pleural angles con rm the
diagnosis of a subpleural peripheral lung opacity (Figs 3-5, A and B, and Fig 3-6).
One pitfall is that a peripheral lung mass, such as a metastasis, may have smooth
borders. Some metastatic tumors and even lymphoma can also disseminate to both
lung and pleura. The foregoing signs for localizing peripheral masses are sometimes
indeterminate on the plain lm, but they are also applicable in CT interpretation.
In fact, CT is often required for the precise localization of abnormalities seen on the
plain film.=
=
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Figure 3-4 A, This solitary metastasis from a malignant brous histiocytoma
presents as a sharply circumscribed peripheral mass. Its pleural location may be
suspected because of the less de nite lateral borders, but this cannot be con rmed
on the PA lm. B, CT scan shows the mass to have a broad pleural attachment with
obtuse pleural angles, confirming its pleural origin.>
=
Figure 3-5 A, This right apical opacity extends to the medial and apical pleura. It
could arise from the mediastinum, pleura, or lung. The streaky linear opacities
along its lateral border could represent either atelectatic lung caused by
compression or extension of the mass into surrounding lung tissue. B, CT
demonstrates the relationship of the mass to mediastinal structures and shows an
irregular linear opacity extending through the lung to the lateral pleura. This is
most suggestive of a lung mass that has extended through the pleura into the
mediastinum. C, T –weighted axial MRI shows similar extension across the1
mediastinum with displacement of the esophagus. Biopsy con rmed primary lung
cancer. This case illustrates the di culty of precise localization of some masses
even with CT and MRI.=
=
Figure 3-6 A, PA chest shows a poorly de ned opacity in the periphery of the left
upper lobe. B, CT section of the upper portion of the opacity shows a tapered
border suggesting either a pleural mass or pleural extension of a lung mass. C, A
lower CT section shows irregular margins con rming a subpleural origin of a
pulmonary mass. Biopsy confirmed primary lung cancer.
Some pleural tumors lack the broad-based pleural signs described previously
because they have a small area of attachment to either pleural surface and appear
more round. The case shown in Figure 3-2, A and B, was described at surgery as a
58pedunculated pleural mass. Berne and Heitzman reported that pedunculated
pleural tumors may be Auoroscopically observed to change shape or move with=
=
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respiration. This motion may also be recorded on inspiration and expiration lms.
Documentation of free movement in the pleural space distinguishes chest wall from
pleural masses.
Probably the most confusing pleural opacity is the one that presents in a medial
location. A mass in this position is often more suggestive of a mediastinal mass.
(Answer to question 7 is True.) Because both pleural masses and mediastinal
masses are seen as a result of their interface with the lung, both have a sharp,
incomplete border that is frequently tapered; therefore, diagnosis of a medially
located mesothelioma can be made only by biopsy. Similarly, mesothelioma arising
from an interlobar ssure is di cult to correctly identify as a pleural mass. This is
best accomplished by identi cation of the ssures on the lateral lm, or even with
a CT scan.
The distinction of loculated pleural Auid from a solid pleural tumor may also be
760di cult (Figs 3-7, A-C). The most practical approach to this problem is to
review serial lms. Because localized collections of pleural Auid may change
rapidly, they are frequently referrred to as vanishing tumors. These collections may
occur in either the lateral pleural space or the interlobar ssures. Both
posteroanterior (PA) and lateral lms are required for their localization because a
localized eDusion in the ssure may mimic an intrapulmonary lesion.
331Ultrasound may be useful for determining that a lesion is Auid lled rather than
solid, but successful ultrasound examination requires that the mass be contiguous
with the chest wall. CT scans are very sensitive for separating pulmonary from
pleural opacities and correctly identifying pleural Auid collections (Figs 3-8, A and
B). Laterally located collections are easily accessible to direct needle puncture,
which not only rules out a mass lesion but also provides Auid for culture when an
empyema is suspected. Correlation with the clinical history is also important. A
296,658history of recent pneumonia is evidence in favor of a loculated empyema.=
=
=
=
Figure 3-7 A, This large, mass-like opacity lls the left-lower chest, obscuring the
costophrenic angle. The smooth, tapered, superior-lateral border (arrows) suggests a
pleural opacity. B, The lateral lm further con rms a well-circumscribed opacity
suggestive of a pleural mass, but the history of a recent left lower-lobe pneumonia
favors the diagnosis of a loculated eDusion. C, Ultrasound demonstrates a large
sonolucency between the posterior chest wall (thick arrows) and the lung (thin
arrows). This con rms the presence of a loculated eDusion consistent with an
empyema.=
=
=
Figure 3-8 A, This well-circumscribed oval opacity appears to be in the center of
the lung, but note the oblique orientation. B, CT scan reveals large bilateral pleural
eDusions. The oval opacity on the chest radiograph is a loculated Auid collection in
the oblique fissure.
Pleural tumors, cysts, and loculated eDusions all appear homogeneous on plain
lms, but should be distinguished with ultrasound, CT, or magnetic resonance
imaging (MRI) scans. Pleural tumors may be regarded as solid, but they are not
always entirely homogeneous. The large mass shown in Figure 3-2, A and B is
shown by CT to be heterogeneous with soft-tissue opacity, a calci cation, and areas
of low attenuation caused by necrosis. It does not have uniform low attenuation,
which is expected with a mesothelial cyst.
Localized brous tumor of the pleura (previously called solitary mesothelioma)=
=
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probably arises from submesothelial mesenchymal cells rather than mesothelial
cells and is usually benign, although 37% of such tumors have been reported to be
163,618malignant. Localized brous tumor of the pleura should present as a
wellcircumscribed peripheral mass and should never invade the chest wall or lung. The
case shown in Figure 3-2 is a benign, localized brous tumor of the pleura. (Answer
to question 2 is b.) The plain lms in this case are not adequate for exclusion of a
chest wall mass, but the CT shows the mass to be separate from the chest wall and
thus makes multiple myeloma an unlikely choice. The CT appearance of this
heterogeneous mass further excludes mesothelial cyst. Both pulmonary infarcts and
rounded atelectasis are pulmonary processes that typically have a subpleural
location. They usually have poorly marginated borders, and the CT scan should
485confirm their pulmonary origin.
Malignant solitary mesothelioma may be radiographically similar but is probably
not related to the localized brous tumor of the pleura. When it occurs in
combination with a history of asbestos exposure, it probably should be considered
an early stage of the malignant mesothelioma. (Answer to question 4 is True.) At
this early localized stage, a malignant solitary mesothelioma is not expected to
extend into either the chest wall or lung.
A solitary pleural metastasis is impossible to diDerentiate on the basis of its
radiologic features from the mass seen in this case. The similarity of a solitary
metastasis is illustrated in Figure 3-4, A and B. Metastatic disease is the most
common cause of a pleural mass with lung and breast cancer accounting for 60%
of cases.
Multiple Pleural Opacities
Multiple pleural opacities (Chart 3-2) are usually the result of loculated eDusion,
pleural masses, or a combination of the two. The radiologic appearance is that of
multiple, separate, sharply circumscribed, smooth, tapered opacities (see Fig 3-1)
or of diDuse pleural thickening with lobulated inner borders. Loculated pleural
eDusion is probably the most common cause of this appearance. The causes of
loculated eDusion include empyema, hemorrhage, and neoplasms. Lateral
decubitus lms are of little value in recognizing the condition because some free
Auid may coexist with either loculated collections of Auid or solid masses.
Sequential lms showing a change over a short time period should con rm the
presence of loculated Auid collections (Fig 3-9). Ultrasound and CT scans may be
useful for con rming the presence of loculated Auid collections and for
thoracentesis or drainage procedures. As with a solitary pleural opacity, a history of
previous pneumonia or a distant primary tumor may suggest the correct cause of
the pleural thickening.=
Figure 3-9 A, This diDuse, mass-like pleural thickening was the result of
hemothorax in a hemophiliac. B, Follow-up PA chest lm after 2 weeks from the
case illustrated in A reveals complete resolution of the pleural thickening,
confirming a suspected diagnosis of pleural effusion.
Metastases are the most common cause of multiple pleural nodules.
Adenocarcinomas are particularly known for their tendency to produce pleural
metastases. Knowledge of either a primary lung tumor or an extrathoracic primary
tumor, such as breast cancer or melanoma, should strongly suggest the diagnosis.
The radiologic combination of bilateral lobulated pleural thickening and a previous
mastectomy virtually ensure the diagnosis of metastatic breast carcinoma; however,
metastatic breast cancer is often unilateral (Fig 3-10).=
=
Figure 3-10 A, Patient with prior right mastectomy for breast cancer has
developed extensive opaci cation of the right hemithorax with nodular thickening
of the lateral pleura. B, Lateral view shows the largest portion of the opacity to
represent posterior pleural thickening. There is also thickening of the minor ssure.
This metastatic breast cancer has spread around the pleura, resembling the
appearance expected with diDuse malignant mesothelioma. (Compare with Fig
311.)
Invasive thymoma typically spreads contiguously, invades the pleura, and
spreads around the lung with the radiologic appearance of multiple pleural masses
(see Fig 3-1).=
=
=
71,741In the terminal stages of lymphoma, spreading to the pleura is rare. This is
714most often in the form of pleural eDusion, but nodular masses may also be
observed.
Multiple myeloma often presents with extrapulmonary masses (see Chapter 2)
and may mimic multiple pleural masses. It is not likely to result in the appearance
of diDuse nodular pleural thickening as seen in either pleural metastases or
mesothelioma (Fig 3-11; see Fig 3-1). Bone destruction is a reliable feature of
multiple myeloma (see Fig 2-1, B).
Figure 3-11 DiDuse nodular pleural thickening with thickening of interlobar
ssures was unilateral in this case of diDuse malignant mesothelioma. Solitary
mesothelioma may be either benign or malignant, but diDuse mesothelioma is
always malignant.
Neuro bromatosis may present with multiple tapered masses that require
217consideration of chest wall vs. pleural masses. These masses arise from the
intercostal nerves and are expected to erode or scallop their associated ribs, but
they may not always show this feature. Without the rib erosion, their appearance is
more suggestive of pleural masses (see Figs 3-3, A and B). (Answer to question 3 is
b.) The plain lm in this case shows bilateral smooth, tapered peripheral masses
without evidence of rib erosion and requires consideration of metastases.
Mesothelioma is not likely because the masses are bilateral. Multiple myeloma is=
>
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unlikely in the absence of rib destruction. A CT scan of the spine (see Fig 3-3, C)
shows an additional mass in the posterior mediastinum that is enlarging the spinal
canal with vertebral erosion and sclerosis. The CT is diagnostic of a neural mass
and therefore con rms the diagnosis of neuro bromatosis. Physical ndings of
multiple cutaneous neuro bromas may also be con rmatory. The other diagnoses
oDered in question 3 are ruled out by the CT ndings. Invasive thymoma usually
presents with an anterior mediastinal mass that may invade the pleura, but does
not cause a posterior mass with spinal erosion. Loculated pleural eDusions are of
low attenuation on CT and do not account for the spinal abnormalities seen in this
case.
DiDuse malignant mesothelioma is another important cause of lobulated or
163,172,319,540nodular pleural thickening (see Fig 3-11). In contrast to the
condition illustrated in Figure 3-1, diDuse malignant mesothelioma is virtually
always unilateral. (Answer to question 1 is d.) However, radiologic distinction of
mesothelioma from diDuse pleural metastases and, rarely, local spread of a
163,327bronchioloalveolar carcinoma is often impossible. Either may have an
associated bloody pleural eDusion. Even the histologic distinction of these two
lesions may be di cult, requiring special stains. CT studies have shown these
tumors to be more extensive than suspected from plain lms, with extension into
13the lung, chest wall, and mediastinum (Figs 3-12, A and B). Invasion of lung or
bone is considered evidence of advanced disease and is not common. (Answer to
question 6 is False.)=
Figure 3-12 A, This diDuse mesothelioma appears less nodular than that seen in
Figure 3-10, possibly because of the associated pleural eDusion. The linear opacities
in the right lung could be the result of compressive atelectasis or extension of the
tumor. B, CT scan con rms the presence of peripheral linear pulmonary opacities
that are continuous with the pleural tumor. These occur when mesothelioma follows
the interlobar fissures and invades the interlobular septae.
The association of asbestos exposure with both primary carcinoma of the lung
65,319,486,657and malignant mesothelioma is well known. Because the incidence
of both primary lung and pleural tumors is increased by asbestos exposure, a
history of exposure is of no value in making the distinction of metastasis vs.=
=
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mesothelioma. Another curious feature of the relationship between asbestos
exposure and these tumors is that patients who develop the neoplasms usually do
not have the typical pulmonary findings of asbestosis (see Chapters 18 and 19).
Asbestos-related pleural plaques may be Aat or nodular. They are easily
246,613overlooked or mistaken for artifacts in the early stages of the disease. These
plaques most commonly cause areas of Aat pleural thickening, but occasionally
they produce a nodular appearance. They do not spread around the lung and are
not seen in the apex. Although they may be confused with the early stages of
mesothelioma, they should not be confused with advanced cases such as that
illustrated in Figure 3-11.
361,630Splenosis occurs after the autotransplantation of splenic tissue into the
pleural space following combined splenic and diaphragmatic injuries. The presence
of multiple masses in the left pleural space requires questioning of the patient for a
history of prior severe upper abdominal or lower thoracic trauma. This is
particularly important when the patient has undergone splenectomy and repair of a
ruptured diaphragm.
Subpleural Parenchymal Lung Opacities
Another problem to be considered in the evaluation of a peripheral opacity is the
distinction of a true pleural abnormality from a subpleural lung lesion (Chart 3-3).
Sometimes peripheral lung opacities are so sharply de ned that they completely
mimic a true pleural opacity. Additional signs that suggest the true nature of the
opacity are (1) ill-de ned or shaggy borders, (2) associated linear opacities, (3) a
heterogeneous texture, such as small areas of lucency or air-bronchograms, and (4)
acute pleural angles. These clues to a pulmonary origin of the opacity may be
enhanced by CT scan, which enhances the texture of a suspected mass and its
253interface with the surrounding lung. This provides a sensitive means for
detecting local invasion of lung parenchyma and even con rming a pulmonary
origin (see Figs 3-6, A-C). CT has the added advantage of being more sensitive for
the detection of very small lesions. The latter fact is most important in evaluating
patients with a known primary neoplasm. (Answer to question 5 is True.)
Neoplasms, including metastases and primary lung cancer, often develop in a
peripheral subpleural location. The frequency with which metastases occur in this
setting was not appreciated prior to the use of CT scanning for staging metastatic
disease. Metastatic nodules are typically well-circumscribed opacities. Some have
acute pleural angles and can be labeled intrapulmonary, whereas others have more
obtuse angles indicating pleural involvement (see Fig 3-4, B). Because they are
incompletely surrounded by air and are often small, the plain lm is not sensitive
for the detection of small subpleural metastases.=
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538Apical primary carcinoma of the lung (Pancoast’s or superior sulcus tumor)
represents a common presentation of a peripheral subpleural primary lung cancer.
These masses grow by contiguous invasion and are distinguished radiologically
from pleural masses by their irregular, poorly marginated, or even spiculated
borders (see Figs 3-5, A-C). Because they are locally very invasive, they often
spread through the pleura into the chest wall. The plain lm nding of bone
destruction indicates advanced disease (Fig 3-13). In the absence of bone
involvement on the plain lm, CT and MRI scans are used for detecting extension
into the soft tissues of the chest wall, particularly in seeking brachial plexus
invasion. The superiority of CT over plain lm for staging these tumors is well
documented, but the axial display of CT does not optimally show the pleural fat
planes. Coronal MRI scans may provide the optimal means for detecting
penetration of the mass through the apical pleura. The cell types of apical lung
cancer include adenocarcinoma, bronchioloalveolar cell carcinoma, and squamous
cell carcinoma. These tumors are accessible to needle-aspiration biopsy, which
yields a diagnosis in a high percentage of cases. Scar carcinoma is another variant
of lung cancer that often occurs in the apices. This variant includes all lung cancers
that arise around a preexistent scar. Scar carcinoma may be suggested by serial
lms that reveal an old calci ed scar from previous granulomatous infection and
an associated growing soft-tissue opacity. Lymphoma may also cause an irregular
apical mass that resembles a superior sulcus or Pancoast’s tumor. It is usually
associated either with evidence of lymphadenopathy or with a history of previously
treated nodal disease.
Figure 3-13 Superior sulcus (or Pancoast’s) tumors are primary lung cancers that
often invade the pleura and chest wall. Notice the poorly marginated inferior=
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border of the mass that distinguishes it from a chest wall or pleural mass. The tumor
has destroyed multiple ribs and vertebrae.
Organizing pulmonary processes, including organizing pneumonia, inAammatory
pseudotumor, granulomas, infarcts, and rounded atelectasis, must also be
considered in the diDerential diagnosis of subpleural pulmonary opacities.
Granulomas are often peripheral and may resemble either metastases or primary
lung tumors. Likewise, infarcts may organize into well-circumscribed, subpleural
opacities that are radiologically indistinguishable from granulomas, metastases, or
lung cancers, but they more typically form pleural-based triangular opacities. This
characteristic triangular or wedge-shaped opacity may be more con dently
identi ed by CT. A history of prior pleuritic chest plain or thrombophlebitis should
provide further confirmatory evidence of an infarct.
Rounded atelectasis or folded lung is another benign cause of peripheral lung
85,91opacities that resemble lung cancer. These opacities are associated with
pleural thickening and may be caused by retracting pleural brosis. They are
usually spherical with irregular borders, typically extend to the pleura with an
acute angle, and are most often posterior. Air bronchograms may be observed at
the periphery. This phenomenon is usually seen in patients with a history of
asbestos exposure and must be distinguished from mesothelioma and lung cancer.
CT may be diagnostic in revealing the associated pleural thickening and
characteristic retraction of pulmonary vessels and bronchi into a curved shape
91,161,485following the contour of the mass of scarred, collapsed lung (Fig 3-14).
Con rmation of stability with old lm is essential because lung cancer may appear
to be nearly identical, sometimes requiring biopsy.
Figure 3-14 Rounded atelectasis causes a peripheral, masslike opacity with
associated pleural thickening. The volume loss leads to retraction of surroundingpulmonary vessels with a characteristic CT appearance. Also note the plaques of
pleural thickening, which are the result of asbestos exposure.
Top 5 Diagnoses: Pleural and Subpleural Opacities
1 Metastases
2 Loculated pleural effusion
3 Mesothelioma
4 Neural tumor
5 Hematoma
Summary
Pleural opacities may be confused with either chest wall lesions or subpleural
parenchymal lung lesions.
Identification of bone destruction or extension of the mass through the ribs is the
most reliable plain film method of localizing a chest wall lesion.
A solitary pleural opacity may be caused by a loculated fluid collection or a solid
mass such as a metastasis, mesothelioma, or lipoma.
Localized fibrous tumor of the pleura (solitary benign mesothelioma) has no
association with asbestos exposure. Malignant solitary mesothelioma represents the
early phase of diffuse mesothelioma, is related to asbestos exposure, and requires
175histologic diagnosis.
Multiple pleural opacities result from loculated effusion, malignant mesothelioma,
and metastases from adenocarcinomas (particularly lung or breast primaries) or
melanoma, or spread from an invasive thymoma.
Splenosis is a rare cause of multiple pleural masses that should be suspected on the
basis of a history of prior splenic injury and thoracoabdominal surgery.
Ill-defined or shaggy borders, associated linear opacities, and a heterogeneous
appearance with air bronchograms should be reliable findings for the
identification of a subpleural parenchymal lung process that may have secondarily
involved the pleura. These findings should suggest tuberculosis, a fungal infection,
an organizing infarct, or even a primary lung tumor.
Rounded atelectasis is associated with pleural scarring, occurs in patients with a
history of asbestos exposure, and must be distinguished from primary lung cancer