5 6287273689696174255

What Radiology
Residents Need to Know:

Chest Radiology
Ronald L. Eisenberg
123
What Radiology Residents Need
to Know: Chest Radiology
Ronald L. Eisenberg
What Radiology Residents

Need to Know: Chest
Radiology
Ronald L. Eisenberg, MD, JD
Department of Radiology
Beth Israel Deaconess Medical Center
Boston, MA
USA
ISBN 978-3-030-16825-4 ISBN 978-3-030-16826-1 (eBook)

https://doi.org/10.1007/978-3-030-16826-1
© Springer Nature Switzerland AG 2020

This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of
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To Zina, Avlana, and Cherina
Preface
Each first-year rotation is a scary experience for new radiology resi-

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

Radiology Media Specialist at Beth Israel Deaconess Medical Center,
for adding arrows and cropping the large number of illustrations in the
print and electronic formats, as well as ensuring that all images have
been transformed into a resolution level suitable for printing. I also
want to thank the faculty of our chest section and the residents rotat-
ing through it for their tireless efforts in identifying many of the excel-
lent examples used in this book.
ix
Contents
1 Introduction �� 1

Search Pattern�� 1
Comparison with Old Studies/Reports: Better or Worse�� 2
The Value of Symmetry�� 2
All Abnormalities Can Look the Same �� 2
Special Areas for Focus�� 4
Dictations as Conversations�� 5
2 Fissures, Lines, and Stripes�� 7
Fissures�� 7
Anterior Junction Line�� 8
Posterior Junction Line�� 9
Hilum Overlay Sign�� 9
Right Paratracheal Stripe�� 9
Aorticopulmonary (AP) Window�� 11
Paraspinal Lines �� 11
Right Paraspinal Line�� 13
Left Paraspinal Line �� 14
Retrosternal Stripe �� 14
Posterior Tracheal Stripe �� 14
Azygoesophageal Line and Recess �� 15
References �� 16
3 Patterns of Lung Disease�� 17
Other Classic Patterns and Signs�� 19
Ground-Glass Opacity �� 19
Tree-in-Bud Pattern �� 20
xi
xii Contents
Mosaic Attenuation Pattern �� 21

Silhouette Sign �� 22
Spine (Vertebral Fade-Off) Sign �� 22
4 Tubes, Lines, and Catheters and Their Complications�� 25
Endotracheal (ET) Tube�� 25
Tracheostomy Tube �� 27
Peripherally Inserted Central Catheters (PICC lines) �� 28
Port-a-Cath and Other Tunneled Catheters �� 32
Swan-Ganz Catheters�� 32
Intra-Aortic Balloon Pump (IABP) �� 34
Nasogastric/Orogastric Tube �� 35
Dobhoff (Feeding) Tube�� 36
Cardiac Devices�� 38
Chest Tube�� 40
Reference�� 42
5 Volume Loss �� 43
Subsegmental/Discoid/Platelike Atelectasis�� 43
Relaxation (Compressive) Atelectasis�� 44
Obstructive Atelectasis�� 45
Round Atelectasis �� 45
Lobar Collapse�� 46
Right Upper Lobe �� 46
Golden S Sign �� 47
Right Middle Lobe �� 48
Lingula �� 48
Lower Lobe �� 49
Left Upper Lobe �� 50
Total Lung �� 51
6 Pneumonia�� 55
Caveats�� 55
Types of Pneumonia�� 56
Community-Acquired Pneumonia (CAP)�� 56
Hospital-Acquired Pneumonia (HAP) �� 57
Ventilator-Acquired Pneumonia (VAP) �� 57
Imaging Patterns�� 57
Lobar Pneumonia �� 57
Lobular Pneumonia (Bronchopneumonia) �� 58
Contents xiii
Interstitial Pneumonia�� 59

Round Pneumonia �� 59
Aspiration Pneumonia�� 60
Follow-up of Pneumonia�� 62
Complications of Pneumonia�� 62
Pneumatocele �� 62
Lung Abscess �� 63
Empyema �� 64
Empyema Necessitans �� 66
Special Types of Bacterial Pneumonia�� 66
Klebsiella �� 66
Septic Emboli �� 67
Loeffler’s Syndrome�� 68
Chronic Eosinophilic Pneumonia �� 69
Fungal Pneumonia�� 70
Aspergillosis�� 70
Other Fungal Diseases �� 72
Pneumocystis Jirovecii (formerly Carinii) Pneumonia �� 72
Viral Pneumonia�� 74
Infectious Mononucleosis (Epstein-Barr virus) �� 74
Varicella (Chickenpox) Pneumonia �� 74
Tree-in-Bud Pattern in Other Viral Pneumonias�� 75
Tuberculosis�� 75
7 Pleural Effusion �� 83
Caveats�� 83
Imaging �� 85
Subpulmonic Effusion �� 88
Loculated Effusion �� 89
Fissural Pseudotumor �� 90
Hemothorax �� 90
Chylothorax �� 91
8 Pulmonary Edema�� 93
Imaging�� 94
Neurogenic Pulmonary Edema�� 97
Pulmonary Hemorrhage�� 101
Adult Respiratory Distress Syndrome (ARDS)�� 101
xiv Contents
9 Pulmonary Vascular Diseases�� 105

Pulmonary Embolism�� 105
Non-thrombotic Pulmonary Emboli�� 110
Chronic Pulmonary Thromboembolism�� 111
Pulmonary Arterial Hypertension�� 112
Pulmonary Veno-occlusive Disease�� 115
10 Solitary Pulmonary Nodule (SPN)/Pulmonary
Neoplasms�� 117
Imaging Criteria for Benignancy�� 118
Mimics of Nodules �� 123
Follow-Up of Nodules (Fleischner Criteria) �� 124
Benign Nodule(s)�� 124
Granuloma�� 124
Hamartoma�� 125
Pulmonary Arteriovenous Fistula (AVM)�� 125
Rheumatoid Necrobiotic Nodule �� 125
ANCA-Associated Granulomatous Vasculitis �� 126
Lung Cancer�� 126
Adenocarcinoma�� 127
Adenocarcinoma in Situ�� 127
Squamous Cell Carcinoma�� 130
Small Cell Lung Carcinoma (SCLC)�� 132
Large Cell Carcinoma�� 133
Carcinoid Tumor�� 133
Pancoast (Superior Sulcus) Tumor�� 135
Metastases to the Lungs�� 136
Hematogenous Spread �� 136
Lymphangitic Spread �� 139
Direct Spread �� 141
Lymphoma �� 142
Kaposi’s Sarcoma�� 144
Sequestration �� 145
11 Pleural Neoplasms �� 147
Mesothelioma�� 147
Metastases �� 149
Fibrous Tumor of the Pleura�� 150
Contents xv
Pleural Lipoma�� 151

12 Emphysema�� 153
Centrilobular Emphysema �� 153
Panlobular (Panacinar) Emphysema �� 154
Paraseptal Emphysema �� 155
Bullous Disease �� 157
Alpha-1 Antitrypsin Deficiency�� 158
Congenital Lobar Emphysema�� 159
13 Pulmonary Fibrosis �� 161
Chronic�� 161
Usual Interstitial Pneumonia (UIP)�� 161
Nonspecific Interstitial Pneumonia (NSIP)�� 163
Acute and Subacute�� 164
Cryptogenic Organizing Pneumonia (COP)�� 164
Acute Interstitial Pneumonia (AIP) �� 166
Smoking-Related�� 167
Respiratory Bronchiolitis-Interstitial Lung
Disease (RB-ILD)�� 167
Desquamative Interstitial Pneumonia (DIP)�� 168
Pulmonary Langerhans Cell Histiocytosis (PLCH)�� 169
14 Inhalational Diseases�� 173
Pneumoconioses�� 173
Silicosis �� 174
Asbestosis�� 176
Hypersensitivity Pneumonitis�� 177
Allergic Bronchopulmonary Aspergillosis (ABPA)�� 180
Crack Lung�� 182
15 Miscellaneous Diffuse Pulmonary Diseases�� 183
Sarcoidosis�� 183
Lymphangioleiomyomatosis (LAM)�� 188
Pulmonary Alveolar Proteinosis�� 190
ANCA-Associated Granulomatous Vasculitis�� 191
Scleroderma�� 193
xvi Contents
Cystic Fibrosis�� 194

Drug Toxicity�� 195
Radiation-Induced Lung Disease�� 197
Lymphoid Interstitial Pneumonia (LIP)�� 199
Amyloidosis�� 200
16 Mediastinal Masses �� 203
Anterior Mediastinum �� 203
Middle Mediastinum �� 203
Posterior Mediastinum�� 204
ITMIG Classification of Mediastinal Compartments�� 205
Prevascular (Anterior)�� 206
Visceral (Middle) �� 206
Paravertebral (Posterior)�� 206
Anterior Mediastinal Masses (Superior Mediastinum) �� 207
Thymoma �� 207
Thymoma Versus Thymic Carcinoma�� 209
Thymic Hyperplasia�� 210
Thymic Cyst�� 210
Teratoma �� 211
Thyroid Mass �� 213
Lymphoma Lipoma �� 214
Hemorrhage �� 215
Aneurysm of the Ascending Aorta
or Sinus of Valsalva �� 216
Anterior Mediastinal Masses (Lower Mediastinum)�� 216
Pericardial Cyst�� 216
Epicardial Fat Pad �� 217
Morgagni Hernia �� 217
Middle Mediastinal Masses�� 218
Lymphadenopathy �� 218
Enlarged Pulmonary Artery �� 219
Bronchogenic Cyst �� 219
Posterior Mediastinal Masses�� 220
Hiatal Hernia �� 220
Bochdalek Hernia �� 220
Foregut Duplication Cyst (Esophageal Duplication,
Neurenteric, or Bronchogenic Cyst)�� 221
Esophageal Dilatation �� 221
Contents xvii
Esophageal Neoplasm (Benign or Malignant)�� 222

Esophageal Varices�� 223
Neurogenic Tumor �� 223
Spinal Neoplasm or Infection�� 223
Meningocele �� 224
Extramedullary Hematopoiesis �� 224
Descending Thoracic Aortic Aneurysm �� 225
Diffuse Mediastinal Processes�� 226
Mediastinal Lipomatosis �� 226
Acute Mediastinitis �� 226
Fibrosing Mediastinitis �� 226
17 Trachea and Bronchi�� 229
Tracheobronchomegaly �� 229
Relapsing Polychondritis�� 230
Tracheomalacia �� 231
Saber-Sheath Trachea�� 232
Post-intubation Stenosis�� 232
Other Causes of Tracheal Stenosis and Wall
Thickening�� 235
Bronchiectasis �� 235
Mucoid Impaction �� 241
Broncholithiasis�� 242
Bronchopleural Fistula (BPF) �� 243
Foreign Body �� 244
Trauma�� 245
18 Aorta�� 247
Acute Aortic Injury�� 247
Aortic Dissection�� 250
Aortic Aneurysm �� 252
Pseudoaneurysm of the Aorta�� 254
Coarctation of the Aorta�� 254
Reference�� 255
19 Cardiac-Pericardial Disease �� 257
Mitral Annulus Calcification �� 262
Myocardial Infarction: Complications�� 262
High-Output Failure�� 264
xviii Contents
Pericardial Disease�� 265

Pericardial Effusion�� 265
Constrictive Pericarditis�� 268
Pericardial Calcification�� 268
20 Diaphragm �� 271
Eventration �� 273
Phrenic Nerve Paralysis �� 274
Traumatic Rupture of Hemidiaphragm �� 275
Diaphragmatic Herniation �� 276
Juxtaphrenic Peak �� 277
21 Esophagus�� 279
Achalasia �� 279
Boerhaave Syndrome�� 281
Foreign Body�� 282
22 Abnormal Air�� 285
Pneumothorax�� 285
Mimics of Pneumothorax�� 288
Tension Pneumothorax�� 290
Pulmonary Interstitial Emphysema �� 291
Pneumomediastinum �� 291
Pneumopericardium�� 293
Subcutaneous Emphysema�� 294
23 Abnormalities Outside the Thorax�� 297
Mass Impressing/Displacing the Lower
Cervical Trachea�� 297
Cervical Rib�� 298
Gastrointestinal Abnormalities�� 299
Pneumoperitoneum�� 300
Injuries to the Bones of the Thorax �� 304
Miscellaneous �� 309
Index�� 313
Introduction
1
For many first-year residents, the chest is their most challenging rota-
tion. The major reason is that interpretations of chest radiographs are
often subjective. One attending may read a radiograph as entirely nor-
mal, while another may detect a subtle consolidation or mild elevation
of pulmonary venous pressure. Also, technical factors may play an
important role. Many inpatient studies are portable AP images, which
are more difficult to interpret than the standard upright PA and lateral
views. Differences in the degree of inspiration and obliquity of the
patient can make it difficult to compare the current study with previ-
ous examinations.
Search Pattern
It is essential to develop a rigorous search pattern to ensure that you

do not miss anything on chest radiographs (and CT). At some point,
you need to evaluate the size and shape of the heart and mediastinum,
the pulmonary markings, and the lungs; check for pleural effusion and
pneumothorax; and make certain that the monitoring and support
devices (various tubes and catheters) are in the proper position.
Electronic Supplementary Material The online version of this chapter (https://

doi.org/10.1007/978-3-030-16826-1_1) contains supplementary material, which
is available to authorized users.
© Springer Nature Switzerland AG 2020 1

R. L. Eisenberg, What Radiology Residents Need to Know: Chest Radiology,
https://doi.org/10.1007/978-3-030-16826-1_1
2 1 Introduction
Some experienced readers prefer to first examine everything out-

side the chest (bones, soft tissues, trachea, upper abdomen) because of
the danger of satisfaction of search. Once you have found an abnor-
mality in the heart or lungs, there is less chance that you will remem-
ber to also look at the other structures visible on chest radiographs. A
popular system utilized by our residents is to begin with “ABCD” –
airways, bones, cardiomediastinal silhouette, and diaphragm.
Comparison with Old Studies/Reports: Better or Worse
Failure to examine one (or more) prior studies and the dictated report
is a cardinal sin. Much of chest radiology, especially in ICU patients
undergoing frequent portable studies, revolves around the determina-
tion of whether there has been any interval change. Indeed, when
viewing a new image, it is important to answer the following ques-
tion: better, worse, or no change. This decision will influence how you
shape your eventual report.
The Value of Symmetry
The markings in the right and left lung should be symmetric. Therefore,
part of your search pattern should be to artificially divide the chest
from top to bottom into a series of horizontal rectangular areas and
compare the appearance of the right and left lungs. Any asymmetric
increase in opacification on one side should raise the suspicion of an
abnormality (Figs. 1.1 and 1.2; see Fig. e1.1).
(All electronic images (Figs. e1.1–e1.4) can be found on
this chapter’s website on SpringerLink: [https://doi.org/10.1007/
978-3-030-16826-1_1])
All Abnormalities Can Look the Same
An important limitation of chest radiography is that most disorders

produce an abnormal area of opacification that is similar for a wide
variety of underlying causes. The specific appearance, combined with
the clinical history and location within the lung, may be sufficient to
make a precise diagnosis. However, at times it may be impossible
All Abnormalities Can Look the Same 3
Fig. 1.1 Value of asymmetry. The large mass in the right apex (arrow) is
somewhat obscured by overlying bony structures in this region. However, it is
clearly asymmetric with the opposite side. (Courtesy of Gillian Lieberman,
MD, Boston)
a b
Fig. 1.2 Value of asymmetry and old studies. Subtle pneumonia. (a) Increased
opacification with air bronchograms in the left perihilar region when compared
with the opposite side (arrow), consistent with developing pneumonia. (b) On
the normal study obtained 3 weeks previously, this area was completely clear,
and there has been a definite change
to distinguish among various diagnostic possibilities. The classic

example is the ICU patient with increased opacification at the left
base and obscuration of the hemidiaphragm. This could represent vol-
ume loss in the lower lobe, pleural effusion, aspiration, or pneumo-
nia – and in most cases there is a combination of two or more of these
4 1 Introduction
possibilities. In the appropriate clinical setting, there also could be an

underlying primary or metastatic malignancy that adds to the area of
opacification. If necessary clinically, CT can distinguish among these
various possibilities (see Figs. e1.2 and e1.3).
Special Areas for Focus
Apices – overlapping ribs and clavicle and cartilage calcification in

the first rib can hide areas of consolidation and especially neoplasms,
only showing mild asymmetry. Also, it may be difficult to determine
whether a round opacification in the apex represents a lung nodule or
merely a bone island in a rib. In both of these cases, consider an api-
cal lordotic view. This effectively lifts up the bony structures, so that
the lung parenchyma can be seen much better. An opacification that
persists is in the lung and can be characterized better on this view
(Fig. 1.3).
Hila – the overlapping tangle of normal arteries and veins makes it

difficult to detect small abnormalities in this region, especially in
patients with vascular congestion.
a b
Fig. 1.3 Value of apical lordotic projection. (a) Initial radiograph demonstrates
asymmetric increased opacification in the right apical region. (b) Apical lordotic
view clearly shows that parenchymal nodule in the right upper lung (arrow)
Dictations as Conversations 5
Dictations as Conversations
Consider your report as a conversation between you and the referring

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

fications (batwing pattern). However, in the appropriate clinical setting, other
possibilities could be suggested as alternative diagnoses
6 1 Introduction
As long as you are not using structured reporting for chest radio-
graphs, remember English 101 and write a coherent narrative, relating
your findings in a logical fashion in flowing sentences. You may have
to include a host of impertinent negatives during your first rotation on
chest. However, as you progress, think back to internship. Did you
want the radiology report to be a long dissertation or just provide the
answer to your clinical question? Remember that an endless rambling
report is not a sign of erudition, and this practice will pose a major
problem when you finally take call.
Fissures, Lines, and Stripes
2
Fissures (Fig. 2.1)
• Lines composed of layers of visceral and parietal pleura that sepa-

rate the lobes of the lungs
• Major fissures – run obliquely from superior to inferior and extend
from the fifth thoracic vertebra to the diaphragm, separating the
lower lobe (posteriorly) from the anterior and middle lobe/lingula
• Minor (horizontal) fissure – runs anteriorly and laterally from the
right hilum to the lateral chest wall, separating the anterior segment
of the right upper lobe (above) from the right middle lobe
• Accessory fissures
○○ Azygos fissure – normal anatomic variant, in which a deep pleu-
ral fissure into the apical segment of the right upper lobe during
embryologic development is caused by a laterally displaced azy-
gos vein, which takes a curvilinear path from the upper aspect of
the right lung to end in a teardrop shadow just above the right
hilum
○○ Superior accessory fissure – separates the superior segment from
the lower basal segments of the lower lobe, more commonly on
the right, and runs in a horizontal plane posterior to the minor
fissure


https://doi.org/10.1007/978-3-030-16826-1_2
8 2 Fissures, Lines, and Stripes
a b
c d
Fig. 2.1 Normal fissures. (a) Minor fissure (arrow). Note the markedly
enlarged heart without vascular congestion, a discordance consistent with the
diagnosis of cardiomyopathy. (b) Minor fissure (black arrow) and portions of
the major fissures (white arrows). (c, d) Azygos fissure (arrow)
○○ Inferior accessory fissure – separates the medial basal segment

from the rest of the lower lobe, extending superiorly and slightly
medially from the inner third of the hemidiaphragm
○○ Left minor fissure – separates the lingula from the superior seg-
ment of the left upper lobe
Anterior Junction Line (See Figs. e2.1 and e2.2)
(All electronic images (Figs. e2.1–e2.14) can be found on this chapter’s

website on SpringerLink: [https://doi.org/10.1007/978-3-030-16826-1_2])
• Formed by apposition of the visceral and parietal pleura of the

anteromedial aspects of the lungs with a small amount of interven-
ing mediastinal fat
Right Paratracheal Stripe 9
• Appears on up to 50% of radiographs as an oblique line crossing the

superior two-thirds of the sternum from upper right to lower left
• Obliteration of the line
○○ Because of its location in the anterior mediastinum, obliteration
or abnormal convexity of the line suggests underlying anterior
mediastinal disease (thyroid mass, lymphadenopathy, neoplasm,
thymic mass, lipomatosis, volume loss, or hyperinflation of the
adjacent lung)
Posterior Junction Line (See Figs. e2.3 and e2.4)
• Formed by the apposition of the visceral and parietal pleura of the

posteromedial portion of the lungs, posterior to the esophagus and
anterior to the third through fifth thoracic vertebrae
• Appears as a straight or mildly leftward convex line, typically pro-
jecting through the trachea
• The posterior junction line demonstrates more cranial extension
than the anterior junction line and, unlike its counterpart, is seen
above the clavicles
Hilum Overlay Sign (Fig. 2.2; See Figs. e2.5 and e2.6)
• To distinguish true cardiomegaly from a large anterior mediastinal

mass mimicking cardiac enlargement
• Normally, the main pulmonary artery is always lateral to the car-
diac shadow or just within its outer edge
• An anterior mediastinal mass often overlaps a main pulmonary
artery, which is then clearly visible within the margins of the mass
(which extends >1 cm beyond the pulmonary artery margin)
Right Paratracheal Stripe (Figs. 2.3 and 2.4; See Fig. e2.7)
• Formed when the visceral and parietal pleura of the right upper
lobe come in contact with the right lateral border of the trachea and
the intervening mediastinal fat
• Air within the right lung and trachea outlines these entities to form
the right paratracheal stripe, which has a maximum normal thick-
ness of 4 mm
Fig. 2.2 Hilum overlay sign. The right hilar mass overlaps the main pulmonary
artery, unlike the normal appearance on the left. (Heilman/Wikimedia)
a b
Fig. 2.3 (a, b) Normal right paratracheal stripe (arrow) [1]
• It begins superiorly at the level of the clavicles and extends inferiorly

to the right tracheobronchial angle at the level of the azygos arch
• The right paratracheal stripe is the most commonly seen mediastinal
line or stripe, visualized in up to 97% of posteroanterior chest radio-
graphs as it courses through the right brachiocephalic vein and SVC
Paraspinal Lines 11
Fig. 2.4 Abnormal right paratracheal stripe. Paramediastinal opacification

(arrow) obliterating the right paratracheal stripe represents mediastinal hemor-
rhage related to the insertion of the right subclavian catheter
• Widening or obliteration of the right paravertebral stripe is an indi-

cation of mediastinal bleeding in trauma and of lymphadenopathy
in sarcoidosis and lymphoma
• The similar left paratracheal stripe is less frequently evident,
extending from the reflection of the left subclavian artery to the
aortic arch
orticopulmonary (AP) Window (Figs. 2.5 and 2.6;

A
See Fig. e2.8)
• Shallow concave interface between the aorta and pulmonary artery.

• Convexity of the AP window interface indicates a mediastinal
abnormality, most frequently lymphadenopathy or a saccular tho-
racic aortic aneurysm
Paraspinal Lines (Figs. 2.7 and 2.8; See Fig. e2.9)
• Formed by the lungs and pleura coming into tangential contact with
the posterior mediastinal fat, paraspinal muscles, and adjacent soft
tissues on each side
a b
Fig. 2.5 Normal AP window. (a) Shallow concave interface (∗) between the
aorta and the pulmonary artery. (b) CT image shows the normal AP window (∗).
The concave interface seen in (a) actually represents the lateral border (arrow)
of the AP window formed by the left lung and pleura contacting the aortic arch
and extending to the pulmonary artery [1]
a b
Fig. 2.6 Abnormal AP window (bronchogenic carcinoma). (a) In addi-

tion to the abnormal bulge in the AP window (arrow), there is thickening of
the right paratracheal stripe (∗), left lower lobe consolidation, and left pleu-
ral effusion. (b) CT image shows a significant soft-tissue mass within the AP
window and subcarinal space, compatible with metastatic lymphadenopathy.
Lymphadenopathy in the paratracheal region accounted for the thickened right
paratracheal stripe [1]
Paraspinal Lines 13
Fig. 2.7 Normal right and left paraspinal lines (arrows) [1]
a b
Fig. 2.8 Abnormal paraspinal lines (abscess). (a) Mass (arrow) effacing the
left paraspinal line. The lateral wall of the descending aorta is seen as a separate
entity (arrowhead). (b) CT image confirms the presence of an abscess (arrow)
that effaces the paraspinal lines. The air-soft tissue interface between the lung
and aorta remains intact on the left (arrowhead), thereby preserving the normal
radiographic appearance of the lateral aortic wall [2]
RIGHT PARASPINAL LINE
• Seen on about 25% of PA radiographs, it appears straight and typi-

cally extends from the 8th to 12th thoracic vertebral levels
• Lateral displacement may reflect osteophytes, prominent mediasti-
nal fat, or such posterior mediastinal disorders as hematoma, mass,
and extramedullary hematopoiesis
LEFT PARASPINAL LINE
• Seen on about 40% of PA radiographs, it extends vertically from

the aortic arch to the diaphragm, typically lying medial to the lat-
eral wall of the descending thoracic aorta
• Lateral displacement may reflect osteophytes, prominent mediasti-
nal fat, tortuosity of the descending thoracic aorta, or such posterior
mediastinal abnormalities as hematoma, mass, extramedullary
hematopoiesis, and esophageal varices
Retrosternal Stripe (See Figs. e2.10 and e2.11)
• Formed by the interface between the anterior lungs and the retroster-
nal soft tissues (fat, internal mammary vessels)
• Normally measures <7 mm
Posterior Tracheal Stripe (Figs. 2.9 and 2.10; See Fig. e2.12)
• Thin vertical stripe, posterior to the trachea, which is formed by air

within the trachea and right lung outlining the posterior tracheal
wall and intervening soft tissues
a b
Fig. 2.9 (a, b) Normal posterior tracheal stripe (arrows)

Azygoesophageal Line and Recess 15
Fig. 2.10 Abnormal posterior tracheal stripe. Marked widening of the stripe
(arrows) following tracheobronchoplasty
• Typically measures up to 2.5 mm in thickness

• When the posterior trachea comes in contact with the anterior
wall of the esophagus, the combination of esophageal wall,
posterior tracheal wall, and intervening soft tissues forms a
thicker tracheoesophageal stripe, which may measure up to
5.5 mm
• A thickened posterior tracheal stripe may be seen with congenital
anomalies of the aortic arch, acquired vascular lesions, esophageal
lesions (achalasia, neoplasm), lymphatic malformations, mediasti-
nitis, and post-traumatic hematomas
Azygoesophageal Line and Recess (See Figs. e2.13 and e2.14)
• Interface formed by the right lower lobe outlining the mediastinum

adjacent to the esophagus and azygos vein
• On a PA radiograph, there is a mild leftward convexity superiorly
and straight edge inferiorly (lower third)
• On an axial CT scan, the azygoesophageal recess is located poste-

rior and to the right of the esophagus and anterior to the vertebral
bodies
• Filling of the azygoesophageal recess may reflect lymphadenopa-
thy, esophageal neoplasm, pleural abnormality, or enlargement of
the left atrium
References
1. Gibbs JM, Chandrasekhar CA, Ferguson EC, Oldham SAA. Lines and stripes:
where did they go? —from conventional radiography to CT. Radiographics.
2007;27:33–48.
2. Whitten CR, Khan S, Munneke GJ, Grubnic S. A diagnostic approach to
mediastinal abnormalities. Radiographics. 2007;27:657–71.
Patterns of Lung Disease
3
Pulmonary diseases are generally classified into two major categories

according to their predominant radiographic appearance:
• Air-space (alveolar) disease – fluffy confluent opacities with indis-
tinct margins and often containing air bronchograms (Fig. 3.1; see
Fig. e3.1)
Fig. 3.1 Air-space disease (Pneumocystis jiroveci pneumonia). Severe, bilat-

eral air-space consolidation with air bronchograms [1]


https://doi.org/10.1007/978-3-030-16826-1_3
18 3 Patterns of Lung Disease
Fig. 3.2 Interstitial disease (chronic fibrotic pulmonary disease).

Extensive prominence of reticular markings bilaterally

website on SpringerLink: [https://doi.org/10.1007/978-3-030-16826-1_3])
• Interstitial (reticular) disease – reticular, nodular, or reticulonodu-
lar pattern with relatively sharp margins, normal intervening lung,
and infrequent air bronchograms (Fig. 3.2; see Fig. e3.2)
Air-space diseases – filling of the air spaces with:
• Fluid (pulmonary edema, ARDS with excessive capillary permea-
bility) (see Fig. e3.3)
• Blood (pulmonary hemorrhage) (see Fig. e3.4)
• Pus (inflammatory exudate, as in pneumonia) (see Fig. e3.5)
• Gastric contents (aspiration) (see Fig. e3.6)
Interstitial diseases – involvement of the supporting structures of the
lung (bronchi, blood vessels, lymphatics, and connective tissue) with
three basic patterns:
• Reticular
○○ Interstitial pulmonary edema (increased capillary pressure in con-
gestive heart failure) (see Fig. e3.7)
○○ Interstitial lung disease – UIP (usual interstitial pneumonia), NSIP
(nonspecific interstitial pneumonia) (see Fig. e3.8)
○○ Lymphangitic metastases (see Fig. e3.9)
• Nodular
○○ Miliary tuberculosis (Fig. 3.3)
○○ Hematogenous pulmonary metastases (see Fig. e3.10)
Other Classic Patterns and Signs 19
Fig. 3.3 Miliary tuberculosis. Innumerable small pulmonary nodules
• Reticulonodular
○○ Sarcoidosis (see Figs. e3.11 and e3.12)
○○ Silicosis
Of course, this division into two major parenchymal patterns of
disease is somewhat artificial and serves only as a general guide.
Some disorders can present as both air space and interstitial
patterns. Classic examples include elevated pulmonary venous
pressure (interstitial and alveolar edema), tuberculosis (can appear
as a pneumonia, extensive scarring, or military nodules), and
sarcoidosis.
Other Classic Patterns and Signs

Ground-Glass Opacity (Fig. 3.4)
• On CT scans, area of hazy increased attenuation, with preservation

of bronchial and vascular margins
• Caused by partial filling of air spaces, interstitial thickening (due to
fluid, cells, and/or fibrosis), partial collapse of alveoli, increased
capillary blood volume, or a combination of these; the common
factor is the partial displacement of air
• Less opaque than consolidation, in which bronchovascular margins
are obscured
Fig. 3.4 Ground-glass opacifications. Multiple areas of hazy increased opac-

ity, less dense than in consolidation, with preservation of bronchial and vascular
margins
Fig. 3.5 Tree-in-bud pattern. Centrilobular bronchial dilatation and filling by

mucus associated with a linear branching pattern (arrows) [1]
Tree-in-Bud Pattern (Fig. 3.5)
• Centrilobular bronchial dilatation and filling by mucus, pus, or fluid,

associated with a linear branching pattern that resembles a budding
tree and is generally more pronounced in the lung periphery
Other Classic Patterns and Signs 21
• Although first described in cases of endobronchial spread of tuber-

culosis and considered pathognomonic of this condition, this pat-
tern is now recognized as a CT manifestation of various other
infectious and noninfectious entities
Mosaic Attenuation Pattern (Fig. 3.6)
• Heterogeneous CT lung attenuation with well-defined borders, cor-

responding to the secondary pulmonary lobules
• The name derives from mosaic artwork, which consists of variously
colored glass or stone inlaid in a contrasting pattern
• Major pathologic causes:
○○ Pulmonary vascular disease – hypoperfused lung appears lower in
attenuation than adjacent normal or hyperperfused lung
○○ Small airways disease – regional variations in the presence of air-
trapping lead to a patchwork of low-attenuation lung that is inter-
posed with normally ventilated, higher-attenuation lung
○○ Primary parenchymal disease – higher-attenuation lung is abnormal
and, when heterogeneously distributed, contrasts with adjacent nor-
mal, lower-attenuation lung to produce a patchwork mosaic pattern
Fig. 3.6 Mosaic attenuation. Ground-glass opacification that spares single and
multilobular regions in a patient with chemical bronchiolitis following a witnessed
episode of aspiration [4]
a b c
Fig. 3.7 Silhouette sign. (a) In this normal patient, the right heart border is
sharply seen (arrows) since it is in contact with normally aerated lung. (b) In
another patient, increased opacification at the right base medially silhouettes the
right heart border. (c) Lateral view shows that the opacification projects over the
cardiac shadow, consistent with right middle lobe pneumonia
Silhouette Sign (Fig. 3.7; See Fig. e3.13)
• When two opacities of the same density are in contact with each
other, their contours disappear; when they are separated by a tissue of
different density (usually air), their individual contours are visible
• In the chest, loss of normal borders between structures is usually
due to a soft-tissue lesion (e.g., pneumonia or mass) adjacent to the
border of the heart, aorta, or diaphragm
• Recognition of the silhouette sign indicates the presence of a lesion,
and the normal margin that is obscured indicates the lobe in which
the abnormality is situated
• On the frontal view:
○○ Right heart border – right middle lobe (or medial right lower lobe).
○○ Left heart border – lingula
○○ Right hemidiaphragm – right lower lobe
○○ Left hemidiaphragm – left lower lobe
○○ Aortic knob – left upper lobe.
○○ Descending aorta – left lower lobe
Spine (Vertebral Fade-Off) Sign (Fig. 3.8)
• On a lateral chest radiograph, the thoracic vertebral bodies nor-

mally appear blacker from top to bottom (due to increased penetra-
tion of the X-ray beam through the more aerated lower lungs)
References 23
a b c
Fig. 3.8 Spine sign. (a) In a normal patient, the vertebral bodies of the thoracic
spine appear to become blacker from top to bottom. (b) In another patient, the
vertebral bodies appear dramatically whiter below the level of the arrow. (c) On
the frontal view, the right lower lobe pneumonia is much less well seen (arrow).
(Courtesy of Jennifer Ni Mhuircheartaigh, MD, Boston)
• Reversal of this normal appearance indicates that the air in the

lower lung has been displaced by something of higher opacity, such
as pneumonia, pleural effusion, or a mass
• The spine sign is especially valuable for detecting a lower lobe
pneumonia that is situated below the apex of the ipsilateral hemi-
diaphragm and thus cannot be visualized on the frontal view
References
1. Eisenberg RL. Clinical Imaging: An Atlas of Differential Diagnosis.
Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins; 2010.
2. Eisenberg RL, Johnson NM, editors. Comprehensive Radiographic
Pathology. 6th ed. St. Louis: Elsevier/Mosby; 2016.
3. Franquet E. Pneumonia. Semin Roentgenol. 2017;52:27–34.
4. Ridge CA, Bankier AA, Eisenberg RL. Mosaic attenuation. AJR.
2011;197:W970–7.
5. Nemec SF, Bankier AA, Eisenberg RL. Lower lobe-predominant diseases of
the lung. AJR. 2013;200:712–28.
6. Nemec SF, Bankier AA, Eisenberg RL. Upper lobe-predominant diseases of
the lung. AJR. 2013;200:W222–37.
Tubes, Lines, and Catheters
and Their Complications 4
Endotracheal (ET) Tube
Proper position depends on the patient’s head

• Neutral position (bottom of the mandible at the C5-C6 level) –
3–5 cm above the carina (usually about halfway between the carina
and the medial ends of the clavicles) (Fig. 4.1)
• Flexion – tip of the ET tube is about 2 cm lower
• Extension – causes tip of the ET tube to be about 2 cm higher
Complications
• Malposition into the right main bronchus (more vertical course),
leading to volume loss in the left lung and sometimes the right
upper lobe (Fig. 4.2; see Fig. e4.1)
(All electronic images (Figs. e4.1–e4.22) can be found on this
chapter’s website on SpringerLink: [https://doi.org/
10.1007/978-3-030-16826-1_4])
• Malposition in the neck:
○○ Risk of extubation and ineffective ventilation
○○ Damage to the vocal cords by the cuff balloon
• Overdistension of the cuff balloon may cause ischemic damage to
the inner wall of the trachea and result in tracheal stenosis (Fig. 4.3)
Electronic Supplementary Material The online version of this chapter

(https://doi.org/10.1007/978-3-030-16826-1_4) contains supplementary mate-
rial, which is available to authorized users.

https://doi.org/10.1007/978-3-030-16826-1_4
26 4 Tubes, Lines, and Catheters and Their Complications
Fig. 4.1 Proper position of endotracheal tube. The tip of the tube (white
arrow) is approximately 3 cm above the carina (black arrow)
Fig. 4.2 Malpositioned endotracheal tube. The tip extends into the right
main bronchus (arrow), causing collapse of the left lung. (Courtesy of Jennifer
Ni Mhuircheartaigh, MD, Boston)
Tracheostomy Tube 27
Fig. 4.3 Overdistension of balloon cuff of an endotracheal tube (arrow).

(Courtesy of Paul Spirn, MD, Boston)
Tracheostomy Tube
Correct position (Fig. 4.4)
• Tip should be about midway between the stoma in which the tra-
cheostomy was inserted and the carina
• Unlike an endotracheal tube, a tracheostomy tube does not move
with flexion and extension of the neck
• The width of a tracheostomy tube should be about two-thirds of the
width of the trachea
Complications (see Fig. e4.2)
• Excessively long tube too close to the carina

• Small amount of pneumomediastinum may occur after placement
• Large amount of pneumomediastinum may reflect a tracheal leak
or injury to the trachea or esophagus
• After removal, granulation tissue may lead to tracheal stenosis at
the tracheostomy site (see Fig. 17.3, page 234)
Fig. 4.4 Proper position of tracheostomy tube. The tip (white arrow) is
about half way between the point of insertion and the carina (black arrow)
Peripherally Inserted Central Catheters (PICC lines)
Correct position
• Within the distal superior vena cava (SVC), at or above the cavoatrial
junction (Fig. 4.5)
• These small catheters may be difficult to visualize radiographi-
cally, and oblique views may be required to precisely demonstrate
the tip
Abnormal positions (in up to 30% of cases)
• Right atrium – can cause arrhythmia due to irritation of the sino-

atrial node (Fig. 4.6)
○○ Determining the position of the cavoatrial junction:
• 1 cm below the site where the right atrial appendage bulges
outward from the SVC
• 2.3 vertebral bodies and disc spaces below the carina (derived
from CT study)
Peripherally Inserted Central Catheters (PICC lines) 29
Fig. 4.5 Proper PICC line position. The tip (arrow) is at the cavoatrial
junction (arrow)
Fig. 4.6 Malpositioned PICC line. The tip (arrow) extends well into the
right atrium
Note: The frequently stated concept that the cavoatrial junction is

4 cm below the carina is NOT valid experimentally or logically.
Consider two patients, one a jockey and the other an NBA center.
Would they have the same distance from the carina to the cavoatrial
junction?
• Internal jugular vein (Fig. 4.7; see Fig. e4.3)

• Crossing the midline to the contralateral brachiocephalic or subcla-
vian vein (Fig. 4.8)
• Azygos vein (Fig. 4.9)
• Small thoracic vein (internal mammary, superior intercostal vein) –
risk of perforation, thrombosis, inadequate infusion of fluid.
• Persistent left superior vena cava (see Fig. e4.4)
• Situs inversus – left subclavian PICC line appears to extend to a
persistent left SVC (see Fig. e4.5)
• Coiled along the course from its insertion in the arm to the SVC
(Fig. 4.10; see Fig. e4.6)
• Subclavian artery (see Fig. e4.7)
○○ Pulsatile flow with abnormal course paralleling the aortic arch or
failing to descend to the right of the thoracic spine
Fig. 4.7 Malpositioned large-bore right subclavian central catheter

(arrows). The tip extends into the ipsilateral jugular venous system
Peripherally Inserted Central Catheters (PICC lines) 31
Fig. 4.8 Malpositioned right internal jugular catheter. The catheter crosses
the midline into the left brachiocephalic venous system (arrows)
a b
Fig. 4.9 Azygos placement of central catheter. (a) Frontal projection shows
that the catheter takes a sharp turn upward and medially at the level of the azy-
gos vein (arrow). (b) On the lateral view, the catheter takes a characteristic
posterior course (arrows). (Courtesy of Paul Spirn, MD, Boston)
Fig. 4.10 PICC line coiled in the axillary and subclavian veins (arrows)
Port-a-Cath and Other Tunneled Catheters
• Right atrium (because they are larger catheters most commonly

used for the introduction of chemotherapy medications or antibiot-
ics, which may be toxic in the low-flow SVC but not in the right
atrium, where there is much higher blood volume)
• Post-procedure radiography – to detect the infrequent complication
of pneumothorax (this does not occur with smaller PICC lines,
which are not direct sticks) and perforation (see Fig. e4.8)
• Rarely, during removal a portion of the catheter may shear off and
remain in the chest (see Fig. e4.9)
Swan-Ganz Catheters

• Within the pulmonary artery (usually the right), no more than 2 cm
beyond the hilum
Abnormal position
• Placement beyond the proximal interlobar pulmonary artery (or
proximal left descending pulmonary artery), because of the danger
of pulmonary infarction due to occlusion of a more peripheral pul-
monary artery by the catheter (see Fig. e4.10)
Swan-Ganz Catheters 33
Fig. 4.11 Hemodialysis catheter tip extending to the right atrium (arrow)
a b
Fig. 4.12 Swan-Ganz catheter. (a) Standard position with tip (black arrow)
in the right pulmonary artery, overlying the spine. Note the substantial collapse
of the right upper lobe (white arrows). (b) In another patient, the tip (arrow)
extends into the left pulmonary artery
Intra-Aortic Balloon Pump (IABP)
• Circulatory assist device that inflates during diastole and deflates

during systole to provide support to patients with cardiogenic shock
and to enhance perfusion through the coronary arteries
• Opaque tip should be about 2 cm below the top of the transverse
aortic arch (generally about midway between it and the superior
border of the left main bronchus)
Abnormal positions
• Too low – inflated balloon may occlude the renal artery (and be
ineffective) (see Fig. e4.11)
• Too high – inflated balloon may occlude a great vessel, leading to
stroke (see Fig. e4.12)
Note: The inflated balloon appears as a cylindrical lucency (arrows)
along the course of the aorta (see Fig. e4.13)
Fig. 4.13 Proper position of IABP. The opaque tip (arrow) is about 2 cm
below the transverse arch of the aorta and about halfway between it and the
main bronchus
Nasogastric/Orogastric Tube 35
Nasogastric/Orogastric Tube
Correct position
• Tip should be well into the stomach so that the side hole (about 10 cm
from the tip) is beyond the level of the esophagogastric junction
• Positioning of the side hole above the esophagogastric junction
(arrow) can lead to aspiration of tube feedings (Fig. 4.14)
Abnormal positions
• Main bronchus (most commonly the right)

• Rarely, can be pushed into more distal bronchi and even perforate
into the pleural space
• Coiled in the neck (always check this area if the tube is not seen in
the esophagus)
• Extending to the distal esophagus before turning back on itself with
the tip pointing upward
Fig. 4.14 Malpositioned nasogastric tube. The tip (white arrow) extends
only to the esophagogastric junction, and the side hole (black arrow) is in the
lower esophagus
Dobhoff (Feeding) Tube
Correct position
• Opaque tip ideally at or just beyond the ligament of Treitz

(Fig. 4.15), usually acceptable if the opaque tip is in the duodenum
so as to minimize the risk of a large amount of residual gastric fluid
that may lead to aspiration
• Nevertheless, in practice the opaque tip often is only in the distal
antrum (Fig. 4.16), due to the difficulty in passing the tube beyond
the pylorus
Abnormal position (Fig. 4.17; see Figs. e4.14–e4.17)
• As with nasogastric/orogastric tube (see above), in the distal esoph-

agus, coiled in the neck, or extending into a main bronchus
Fig. 4.15 Ideal position of Dobhoff tube. The tip (arrow) is at the ligament of
Treitz
Dobhoff (Feeding) Tube 37
Fig. 4.16 Dobhoff tube tip in the distal stomach (arrow)
Fig. 4.17 Malpositioned Dobhoff tube. The tip (white arrow) is in the left
bronchial tree. Note the extensive coiling of the tube in the neck (black arrows).
(Courtesy of Paul Spirn, MD, Boston)
Cardiac Devices
• Pacemaker and automatic implantable cardiac defibrillator (AICD),

which has a thicker electrode on at least one lead (Fig. 4.18)
Correct position
• Single channel – lead in the apex of the right ventricle, to the left of
the spine (often only temporary) (Fig. 4.19; see Fig. e4.18)
Fig. 4.18 Difference between cardiac pacer (black arrow) and AICD
(white arrows). Both extend to the right ventricle in this patient
a b
Fig. 4.19 Proper position of single-channel cardiac device (arrows). (a, b)

The leads extend to the right ventricle (anteriorly in b)
Cardiac Devices 39
a b
Fig. 4.20 Proper position of dual-channel cardiac device. (a, b) The leads
extend to the right atrium (white arrows) and right ventricle (black arrows).
Note the anterior position of both of these cardiac chambers
• Dual channel – leads in the right atrium (usually in the right atrial
appendage, with an upward curve) and the apex of the right ven-
tricle (with both leads seen anteriorly on a lateral view) (Fig. 4.20;
see Figs. e4.19 and e4.20)
• Biventricular (three channel) – used to synchronize contractions
in the right and left ventricles, it also directly paces the left ven-
tricular epicardium via an additional lead within the coronary
sinus or great cardiac vein (seen posteriorly on a lateral view)
(Fig. 4.21)
Complications (see Fig. e4.21)

• Pneumothorax on insertion
• Fractured lead
• Cardiac perforation or tamponade
• Twiddler’s syndrome (patient inadvertently twists the subcutane-
ous generator so that the lead tip is retracted from the inner wall of
the heart)
a b
Fig. 4.21 Proper position of three-channel (biventricular) device. (a, b)

The additional third channel lead extends above the right ventricular lead and
posteriorly (arrows)
Chest Tube
• To treat a pneumothorax – most effective if directed anteriorly or to

the apex of the lung
• To drain a pleural effusion – generally paced posteriorly and at the
lung base
Complications/poor drainage
• Proximal side hole located outside of the chest wall – leads to air
leak with improper drainage and subcutaneous emphysema
(Fig. 4.23)
• Tip not within a loculated effusion causes failure to drain it prop-
erly (may require placement under image guidance) (see Fig. e4.22)
Chest Tube 41
Fig. 4.22 Proper position of chest tubes. The white arrows point to a chest
tube directed toward the apex to treat a pneumothorax. The black arrows point
to a chest tube directed toward the base to drain a pleural effusion
• Removal of a large pleural effusion and rapid re-expansion of a col-

lapsed lung may lead to re-expansion edema in the underlying lung
(see Figs. 8.8 and e8.12)
• Kinking of the tube (especially with the smaller pigtail catheters
and not with the larger surgical chest tubes)
Fig. 4.23 Side hole of chest tube outside of thoracic cage (arrow). There is
extensive subcutaneous gas along the chest wall and between pectoral muscle
bundles. (Courtesy of Paul Spirn, MD, Boston)
Reference
1. Eisenberg RL, Johnson NM, editors. Comprehensive Radiographic Pathology.
6th ed. St. Louis: Elsevier/Mosby; 2016.
Volume Loss
5
Volume loss in the lung spans a spectrum of appearances, ranging

from streaks of atelectasis to collapse of a lobe or an entire lung.
Subsegmental/Discoid/Platelike Atelectasis
• Linear opacities of varying thickness that usually occur at the lung

bases and are parallel to the hemidiaphragm (though they may run
obliquely) (Fig. 5.1)
Fig. 5.1 Platelike atelectasis. Bilateral lines of opacification at the bases (arrows)
in a patient with low lung volumes. There also is a small left pleural effusion

https://doi.org/10.1007/978-3-030-16826-1_5
44 5 Volume Loss
• Caused by conditions that limit diaphragmatic excursion (e.g.,

splinting following thoracic or abdominal surgery or trauma) and in
supine bedridden patients
• Differentiation from chronic fibrous scarring
○○ Atelectasis usually clears within a few days, once the patient
resumes normal deep breathing
• Differentiation from pneumonia
○○ Atelectasis develops and resolves more rapidly than pneumonia
○○ Atelectasis is associated with volume loss (elevation of the ipsi-
lateral hemidiaphragm and displacement of fissures)
○○ On contrast CT, atelectasis shows intense enhancement due to
crowding of blood vessels (Fig. 5.2)
○○ Therefore, if differentiating between atelectasis and pneumonia
is a key clinical issue in an ICU patient, a non-contrast CT scan
is of no value and should not be ordered
Fig. 5.2 Atelectasis versus pneumonia. Contrast CT scan demonstrates that

the degree of enhancement is key to differentiating between these two condi-
tions. On the right, there is little enhancement compared to the dorsal muscles
(white arrow), consistent with pneumonia. On the left, there is substantial con-
trast enhancement (black arrow), indicative of atelectasis
Relaxation (Compressive) Atelectasis
• Decrease in lung volume due to compression from a space-occupy-

ing structure (pneumothorax, large pleural effusion, or mass)
• In lung collapse, proximal segmental bronchi usually remain patent
and filled with air (air bronchograms within the airless parenchyma).
Round Atelectasis 45
• The absence of proximal air bronchograms within a collapsed lung

suggests endobronchial obstruction (see below)
Obstructive Atelectasis
• With a bronchial obstruction, inspired air cannot replace the alveolar

air that normally diffuses into the adjacent pulmonary capillary bed
• Obstruction of a main bronchus leads to a gasless lung within
18–24 hours, without air bronchograms
• When the obstruction is more peripheral, such as from a mucous
plug, air bronchograms often are visible
Round Atelectasis (Fig. 5.3; See Figs. e5.1 and e5.2)

this chapter’s website on SpringerLink: [https://doi.org/
10.1007/978-3-030-16826-1_5])
Fig. 5.3 Round atelectasis in asbestos-related disease. Left lung mass (black
arrow) abuts the pleura and has a “comet tail” of bronchovascular structures
(white arrow) extending into the mass [1]
46 5 Volume Loss
• Atypical form of lung collapse that usually occurs adjacent to

scarred pleura and may mimic lung cancer
• Most commonly related to exposure to mineral dust (asbestosis,
pneumoconiosis) or an exudative pleural effusion (tuberculosis,
hemothorax)
Imaging
• Focal peripheral, round, or oval opacity that typically occurs in a

lower lobe posteriorly and is associated with pleural thickening
• The mass usually has an acute angle with the adjacent aerated
lung
• More than half demonstrate air bronchograms
• “Comet tail” sign – characteristic CT appearance of whorled/swirl-
ing or curving pattern of crowded bronchovascular structures as
they extend from the lower border of the mass and converge toward
the adjacent hilum (rare in other pleural-based masses)
• If the CT findings are equivocal, it may require fine-needle aspiration
biopsy to exclude malignancy (especially if the patient is a smoker)
Lobar Collapse
• Almost always due to bronchial obstruction secondary to mucous
plug or malignancy (with resorption of alveolar air via the pulmo-
nary capillary bed)
• Occasionally, may be caused by inflammatory scarring (such as
tuberculosis) or by foreign body aspiration in children
• The airless collapsed lung produces a characteristic pattern depend-
ing on the lobe involved, with associated displacement of fissures
• The affected lobe has a triangular appearance, with the apex point-
ing centrally toward the hilum
Right Upper Lobe (Fig. 5.4; See Fig. e5.3)
• Frontal view
○○ Elevation of the minor fissure and obscuration of the right con-
tour of the superior mediastinum
• Lateral view
○○ Upward shift of the minor fissure and anterior shift of the major
fissure
Lobar Collapse 47
a b
Fig. 5.4 Right upper lobe collapse. (a, b) Elevation of the minor fissure
(white arrows) and anterior shift of the major fissure (black arrow). (Courtesy of
Gillian Lieberman, MD, Boston)
Fig. 5.5 Golden S Sign. Typical reversed S-shaped curve representing col-
lapse of the right upper lobe, with the lower bulge produced by the obstructing
hilar carcinoma (arrow) [2]
Golden S Sign (Fig. 5.5)
• Reversed S-shaped curve seen on frontal chest radiographs, which

represents a combination of collapse of the right upper lobe and a
hilar mass (usually bronchogenic carcinoma)
48 5 Volume Loss
○○ Upper, laterally concave segment of the S is formed by the ele-

vated minor fissure
○○ Lower, medial convexity is produced by the tumor mass, which has
caused bronchial narrowing that is responsible for the collapse
Right Middle Lobe (Fig. 5.6; See Figs. e5.4 and e5.5)
• Frontal view
○○ Downward displacement of the minor fissure with varying degree
of obscuration of the right heart border
○○ May be a triangular opacity with the base silhouetting the right
heart border and the apex pointing toward the lateral chest wall
• Lateral view
○○ Linear band or triangular opacity overlying the heart (base ante-
riorly and apex pointing toward the hilum)
○○ Inferior displacement of the minor fissure and superior displace-
ment of the major fissure
a b
Fig. 5.6 Right middle lobe collapse. (a) Minimal silhouetting of the right
hear border (arrows). (b) Lateral view shows collapse of the right middle lobe
(arrows) [2]
Lingula (See Fig. e5.5)
• Same as right middle lobe collapse, except there is varying degree

of obscuration of the left heart border on the frontal view
Lobar Collapse 49
Lower Lobe (Figs. 5.7 and 5.8; See Figs. e5.6–e.5.8)
• Frontal view
○○ Right – triangular opacity that obscures the medial part of the
right hemidiaphragm but does not silhouette the heart border
Fig. 5.7 Right lower lobe collapse. Triangular opacity (arrows) obscures the
medial aspect of the right hemidiaphragm. (Hellerhoff / Wikimedia)
Fig. 5.8 Left lower lobe collapse. Retrocardiac opacification with character-
istic oblique margin (arrow) and silhouetting of the hemidiaphragm
50 5 Volume Loss
○○ Left – triangular opacity behind the heart that obscures the

medial part of the left hemidiaphragm and the aorta
○○ There may be inferomedial displacement of the ipsilateral hilum
and shift of the mediastinum to that side
• Lateral view
○○ Posterior displacement of the ipsilateral major fissure, which
appears as an interface between the collapsed lower lobe and the
hyperexpanded upper lobe
○○ Loss of the outline of the posterior half of the hemidiaphragm
○○ Spine sign (lower vertebral bodies appear more opaque than the
upper ones, the reverse of normal) (see Fig. 3.8)
○○ Lower lobe collapses posteriorly and inferiorly
Left Upper Lobe (Fig. 5.9; See Fig. e5.9)
• Frontal view
○○ Hazy opacification extending outward from the left hilum that
often reaches the apex of the left lung and tends to fade laterally
and inferiorly
a b
Fig. 5.9 Left upper lobe collapse. (a) Generalized increased opacity of the left
hemithorax without silhouetting of the aortic knob or proximal descending aorta
(luftsichel sign). The visualized vascular markings reflect lower lobe vessels. (b)
Lateral view confirms the anterior position of the collapsed left upper lobe [2]
Lobar Collapse 51
○○ With complete collapse, the upper margin of the aortic arch and
the proximal descending aorta (posterior structures) remain visible
because the superior segment of the lower lobe expands to such a
degree that it replaces the posterior segment of the upper lobe
○○ Classic appearance of a crescentic paramediastinal lucency
(luftsichel sign), which reflects interposition of the apex of the
hyperexpanded lower lobe between the aortic arch and the col-
lapsed upper lobe
○○ Parenchymal opacity of left upper lobe collapse may mimic pneu-
monia, though this error can be avoided by recognizing indirect
signs of volume loss (elevated left hilum and hemidiaphragm, shift
of mediastinal structures to the left, partial loss of the left heart
border, and an almost horizontal course of the left main bronchus)
• Lateral view
○○ Band of increased retrosternal opacification (representing the
collapsed left upper lobe)
○○ Anterior displacement of the left major fissure (paralleling the
sternum)
Total Lung (Fig. 5.10)
• Central bronchial obstruction due to mucous plug or malignancy
a b
Fig. 5.10 Total lung collapse. (a) Baseline radiograph is within normal limits.
Note the calcified granuloma in the left perihilar region (arrow). (b) Complete
collapse of the left lung after the lodging of a mucous plug in the left main bron-
chus. Note the change in position of the calcified granuloma when the left lung
collapses [2]
52 5 Volume Loss
Fig. 5.11 Pneumonectomy. Opacification of the left hemithorax with multi-

ple surgical clips. The trachea and other mediastinal contents are shifted to the
affected side, and there is compensatory hyperexpansion of the right lung [2]
• Complete opacification of the entire affected lung

• Elevation of the ipsilateral hemidiaphragm
• Mediastinal shift to the affected side
• On the lateral view, generalized hazy opacification caused by the
collapsed lung
• Especially after pneumonectomy, there may be substantial com-
pensatory hyperexpansion of the contralateral lung (may cross the
midline anteriorly, producing a large retrosternal air space on the
lateral view) (Fig. 5.11)
To differentiate between total lung collapse and pleural effusion

• Lung collapse – mediastinal shift TOWARD the affected side (see
Fig. e5.10)
• Pleural effusion (or tension pneumothorax) – mediastinal shift
AWAY FROM the affected side (see Figs. e5.11 and e5.12)
• If no mediastinal shift – balance between pleural effusion and
degree of underlying collapse (see Figs. e5.13 and e5.14)
Fallen lung sign

• Collapsed lung due to complete rupture of a main bronchus
• The affected lung “falls” away from the mediastinum into a depen-
dent position (hanging onto the hilum only by its vascular
attachments)
References 53
• Should be suspected if there is persistence of a large post-traumatic

pneumothorax after chest tube insertion
Imaging (see Fig. e5.15)

• In an upright patient, the collapsed lung falls inferiorly and laterally
away from the hilum (unlike the typical appearance in a large pneu-
mothorax, where the lung collapses inward toward the hilum)
• In a supine patient, as on CT, the collapsed lung falls posteriorly
References
the lung. AJR. 2013;200:712–28.
Pneumonia
6
Caveats
1. You cannot interpret what you cannot see. On a supine AP image,

enlargement of the cardiac silhouette, pulmonary edema, and layer-
ing pleural effusions make detection of a small pneumonia almost
impossible. Indicate this limitation to the referring physician by
stating something like: “In the appropriate clinical setting, it would
be extremely difficult to exclude superimposed pneumonia.”
2. Especially in the retrocardiac area on the lateral view, it may be difficult
to detect a subtle pneumonia. Normally, you should see discrete tubular
structure representing pulmonary vessels. Opacification obscuring
these vessels is the earliest sign of pneumonia (Fig. 6.1; see Fig. e6.1).
chapter’s website on SpringerLink: [https://doi.org/10.1007/
978-3-030-16826-1_6])
3. Any asymmetry in the lungs on a frontal view may be the earliest
sign of an area of consolidation (Fig. 6.2).
4. In hospitalized, bedridden patients, it often is impossible to deter-
mine whether a consolidation represents aspiration or infectious
pneumonia. Consider using the term “aspiration/pneumonia” to
indicate this to the referring physician.


https://doi.org/10.1007/978-3-030-16826-1_6
56 6 Pneumonia
a b
Fig. 6.1 Subtle retrocardiac pneumonia. (a) Lateral view shows normal dis-
crete tubular vessels behind the heart. (b) Obscuration of the vessels behind the
heart (arrows) indicates pneumonia
a b
Fig. 6.2 Subtle pneumonia. (a) Initial radiograph obtained several months
previously is normal. (b) Subsequent study shows a small, ill-defined area of
opacification in the left mid-lung (arrow). This can be identified because of
asymmetry with the opposite side and a change from the initial study
Types of Pneumonia
Community-Acquired Pneumonia (CAP)
• A pneumonia contracted by a person who has little contact with the

healthcare system
• Affects individuals of all ages and most commonly arises as a viral
infection (though there may be bacterial superinfection)
Imaging Patterns 57
Hospital-Acquired Pneumonia (HAP)
• Any pneumonia developing in a patient at least 48 hours after being

hospitalized
• Second most common nosocomial infection (after urinary tract
infections)
• Unlike community-acquired pneumonia, HAP is usually caused by
a bacterial infection, rather than a virus
• High morbidity and mortality rates and the primary cause of death
in intensive care units
Ventilator-Acquired Pneumonia (VAP)
• Any pneumonia developing in a patient at least 48–72 hours after

endotracheal tube intubation
• Typically affecting critically ill patients in an intensive care unit,
VAP develops in up to 30% of ventilated individuals and is associ-
ated with a mortality rate of up to 80%
Imaging Patterns
Lobar Pneumonia
• Homogeneous consolidation of all or a substantial percentage of a

single lobe
• Sharply marginated by one or more fissures (Fig. 6.3)
• Air bronchograms (larger bronchi remain patent) (see Fig. e6.2)
Fig. 6.3 Lobar pneumonia (right upper lobe). Homogeneous consolidation

bounded inferiorly by the minor fissure [1]
58 6 Pneumonia
a b
Fig. 6.4 Lobar pneumonia (left lower lobe). (a, b) Homogeneous consolidation
of the left lower lobe (arrows). On the frontal view, the left heart border (anterior)
is sharply seen because it is not silhouetted by the posterior pneumonia
• Silhouette sign when the consolidation is adjacent to the heart,

aorta, or hemidiaphragm (Fig. 6.4)
• Most commonly bacterial, especially due to Streptococcus pneumoniae
obular Pneumonia (Bronchopneumonia) (Fig. 6.5; See Figs.

L
e6.3–e6.7)
• Patchy, poorly defined, heterogeneous air-space consolidation that

tends to involve the peripheral portions of the lungs
• Frequently multifocal, involving several areas at the same time
• Tends to have indistinct margins (unless touching a pleural fissure)
• Associated with exudate filling the bronchi, leading to associated
atelectasis and absence of air bronchograms
• Patchy areas may coalesce to mimic lobar pneumonia
Fig. 6.5 Lobular pneumonia (right base). Ill-defined, heterogeneous con-

solidation [1]
Imaging Patterns 59
Fig. 6.6 Interstitial pneumonia (Pneumocystis jirovecii). Diffuse reticular

pattern in a patient with acute myelogenous leukemia. Note the early develop-
ment of alveolar consolidations at the bases. A later image showed the typical
pulmonary edema pattern [1]
Interstitial Pneumonia
• Involvement of the walls of the alveoli and airways producing a

fine, reticular pattern (Fig. 6.6)
• Diffuse or patchy ground-glass opacification on CT (see Fig.
e6.8)
• Caused by viral pneumonias, mycoplasma, and chlamydia
• In immunosuppressed patients (CD4 counts under 200/mm2), likely
to be Pneumocystis, with the classic pattern of bilateral prominence
of reticular markings radiating outward from the hila (may mimic
pulmonary edema)
Round Pneumonia (Fig. 6.7; See Figs. e6.9 and e6.10)
• Infectious mass-like opacity, usually seen in children who have a

history of infectious symptoms and recent normal chest radiograph
(making a neoplasm unlikely)
• Imaging appearance is due to underdeveloped pores of Kohn and
the absence of canals of Lambert, which limit the centrifugal spread
of early bacterial infection
• Most commonly due to Streptococcus pneumoniae or Haemophilus
influenzae
60 6 Pneumonia
Fig. 6.7 Round pneumonia. 6-cm consolidation with ill-defined margins in

the right lung of a woman with streptococcal pneumonia [2]
Aspiration Pneumonia
• Foreign material entering into the tracheobronchial tree second-

ary to gastroesophageal reflux, altered mental status (drug over-
dose, anesthesia), or neurologic disorder (stroke, traumatic brain
injury)
• Often develops in intubated patients, despite the presence of an
inflatable cuff
• Usually occurs in the most dependent portions of the lung
○○ Supine – superior and posterior basal segments of the lower
lobes or posterior segment of the upper lobes (Fig. 6.8)
○○ Upright – lower lobes (typically on the right, because the right
main bronchus runs more vertically and is wider)
• Rapid appearance of air-space consolidation, especially in bedrid-
den patients.
• Noninfectious aspiration – usually clearance in less than 1 week
○○ Mendelson syndrome – large-volume aspiration of gastric acid,
which produces a chemical pneumonitis and acute lung injury
(even ARDS) and a diffuse radiographic pattern simulating pul-
monary edema (Fig. 6.9; see Fig. e6.11)
○○ Lipoid pneumonia – chronic aspiration of ingested exogenous
lipid material (such as mineral oil for chronic constipation);
appears radiographically as chronic consolidation or mass, which
has low attenuation on CT (Fig. 6.10; see Fig. e6.12)
Imaging Patterns 61
Fig. 6.8 Aspiration pneumonia. Bilateral patchy, ill-defined areas of consoli-

dation in the lower lobes [2]
Fig. 6.9 Aspiration pneumonia. Ill-defined areas of opacification in the left

lung of a patient with chemical bronchiolitis [4]
Fig. 6.10 Lipoid pneumonia. Multiple opacities with fat attenuation in the
right lung (arrows), diagnostic of lipoid pneumonia in a patient with chronic use
of oily laxatives
62 6 Pneumonia
Follow-up of Pneumonia
• Radiographic clearance of pneumonia usually lags well behind

clinical improvement
• Follow-up chest radiographs are recommended in approximately
4–6 weeks to ensure complete resolution of the consolidation and
to assess persistent abnormality of the lung parenchyma (scarring,
bronchiectasis)
• Failure of a pneumonia to resolve by 8 weeks suggests an inaccu-
rate diagnosis or an endobronchial obstruction as a cause of post-
obstructive pneumonia (Fig. 6.11)
• Especially in patients with smoking history or over age 40, CT
should be considered to exclude an underlying bronchial lesion
(see Fig. e6.13)
Fig. 6.11 Post-obstructive pneumonia. Homogeneous increased opacification in

the right upper lobe secondary to carcinoma of the lung. The patchy opacification at
the right base is due to a combination of atelectasis and infiltrate secondary to exten-
sion of the tumor into neighboring bronchi [1]
Complications of Pneumonia
Pneumatocele
• Thin-walled, gas-filled cyst in the lung parenchyma that is most
frequently caused by pneumonia (especially in children following
staphylococcal pneumonia), trauma, or the inhalation of hydrocar-
bon fluid (Fig. 6.12; see Fig. e6.14)
Complications of Pneumonia 63
Fig. 6.12 Pneumatocele. Residual bilateral, thin-walled cystic spaces (arrows)

in the pulmonary parenchyma after a staphylococcal pneumonia during child-
hood [1]
• Single or multiple thin-walled cystic spaces (may be thick-walled

in the acute phase and mimic a lung abscess)
• CT may show scattered thin-walled cysts interspersed with nor-
mal lung in areas previously affected by pneumonia or trauma
(see Fig. e6.15)
Lung Abscess (Fig. 6.13; See Figs. e6.16–e6.19)

• Irregular infectious cavity containing necrotic debris or fluid.
• Often an air-fluid level, which usually has the same extent on both
frontal and lateral views
Fig. 6.13 Lung abscess. Large right middle lobe cavity containing an
air-fluid level (arrows) in an intravenous drug abuser [1]
64 6 Pneumonia
• The wall of the abscess may be smooth or ragged, with an unusual

nodular appearance suggesting a cavitating malignancy
• If it extends to the pleural surface, a lung abscess forms an acute
angle (unlike the obtuse angle formed by an empyema)
Empyema (Figs. 6.14 and 6.15; See Figs. e6.20 and e6.21)
• Loculated infection within the pleural space

• Stages of parapneumonic effusions:
○○ Initially sterile (exudative stage) with normal glucose levels
⚬⚬ As white blood cells and bacteria accumulate in the fluid collec-
tion (fibropurulent stage), the glucose level and pH decrease
○○ Finally, in the chronic organizing stage, the fluid is thick and
purulent, and there is the development of a fibrin peel
• Initially, may appear as a typical pleural effusion (usually
unilateral)
Fig. 6.14 Empyema. Classic lenticular appearance of an empyema posteriorly

(arrows). Courtesy of Gillian Lieberman, MD, Boston)
Complications of Pneumonia 65
Fig. 6.15 Empyema with split pleura sign. This woman with tuberculosis
presented with weight loss, malaise, and chills. Loculated right pleural effusion
with thickened, enhancing pleura (arrows) infiltrates into the extrapleural fat
(arrowhead) [6]
• As it reaches the fibropurulent stage, an empyema may become

loculated with a characteristic lenticular shape and smooth border
that is convex to the lung and forms an obtuse angle with the chest
wall
• Disparity in the lengths of air-fluid levels on PA and lateral
projections
• Presence of an air-fluid level or pockets of air within a pleural col-
lection suggests a bronchopleural fistula
• CT – Classic split pleura sign (smooth thickening and contrast
enhancement of the visceral and parietal pleura surrounding the
loculated collection of fluid in the pleural space)
Table 6.1 Differentiation between empyema and lung abscess

Empyema Lung Abscess
Sharply defined margin with the lung Lack of discrete boundary with the
lung
Elliptical (lenticular) Round
Obtuse angle with chest wall Acute angle with chest wall
Smooth inner surface Thicker, often irregular wall
Disparity in length of air-fluid levels Air-fluid levels of relatively equal
lengths
Split pleura sign on CT
66 6 Pneumonia
Empyema Necessitans (Fig. 6.16)
• Chronic empyema draining via a sinus tract into the subcutaneous

tissues of the chest wall, most commonly related to tuberculosis or
fungal infection (actinomycosis, aspergillosis, blastomycosis,
mucormycosis)
• Loculated pleural fluid collection or mass with associated rib
destruction and often bubbles of loculated gas in soft tissues
Fig. 6.16 Empyema necessitans. Pleural calcifications (arrowheads), a locu-

lated pleural effusion, and extension into the chest wall (arrows) [6]
Special Types of Bacterial Pneumonia

Klebsiella
• Gram-negative bacterial pneumonia that is most common in debili-

tated middle-aged and older men with alcoholism (about two-thirds
of cases); high mortality rate
• Tends to form a voluminous exudate that produces a homogeneous
parenchymal consolidation containing an air bronchogram
• Lobar enlargement (especially the right upper) with the character-
istic bulging fissure sign (Fig. 6.17)
○○ Bulging fissure sign also in Haemophilus influenzae pneumonia
(predominantly in compromised hosts, such as chronic pulmonary
disease, immune deficiency, alcoholism, diabetes) (see Fig. e6.22)
Special Types of Bacterial Pneumonia 67
Fig. 6.17 Bulging fissure sign (Klebsiella). Downward bulging of the minor
fissure (arrow) due to massive enlargement of the right upper lobe with inflam-
matory exudate [1]
• High frequency of abscess and cavity formation (ischemic necrosis

and death of a portion of the lung may result in sloughed lung
within a thick-walled cavity, known as “pulmonary gangrene”)
Septic Emboli (Figs. 6.18 and 6.19; See Figs. e6.23–e6.25)
• Most frequently result from infectious particles reaching the lung

from an infected heart valve (especially the tricuspid), intravenous
catheter, or injected debris
• Persons at risk include drug abusers, immunocompromised patients,
individuals with septal defects, and those with indwelling venous
catheters, pacemakers, or prosthetic heart valves
• Initially, multiple ill-defined round or wedge-shaped opacities with
a swirling pattern that are usually peripheral and tend to involve the
lower lobes (starry night sign – mimicking the brush strokes in van
Gogh’s painting of that name)
• Cavitary pulmonary nodules tend to develop rapidly (1–2 days)
68 6 Pneumonia
a b
Fig. 6.18 Septic emboli. (a, b) Large cavitary lesions (arrow) in the lungs of
two intravenous drug abusers with septic thrombophlebitis [1]
Fig. 6.19 Septic emboli. Multiple cavitating nodules in a young immunocom-

promised male. Arrows point to vessels leading directly to several nodules
(feeding vessel sign) [1]
Loeffler’s Syndrome
• Transient, rapidly changing, migrating, nonsegmental areas of

parenchymal consolidation, which are associated with blood eosin-
ophilia and minimal (or no) pulmonary symptoms
• Bilateral patchy consolidations with ill-defined margins that are
predominantly located in the periphery of the lung
Special Types of Bacterial Pneumonia 69
Fig. 6.20 Loeffler’s syndrome. Peripheral air-space nodule with surrounding

ground-glass opacity in the right lower lobe (arrow). Follow-up study showed
that the nodule had disappeared [7]
• May produce single or multiple air-space nodules with surrounding

ground-glass opacities (Fig. 6.20)
• Unlike chronic eosinophilic pneumonia (see below), the transient
air-space abnormalities resolve in some areas and reappear in oth-
ers over days
• Loeffler’s syndrome (also known as simple pulmonary eosino-
philia) is applied to idiopathic cases; a similar imaging pattern can
occur in response to parasitic infection or be drug-induced
Chronic Eosinophilic Pneumonia (Fig. 6.21; See Fig. e6.26)
• Classic appearance of multifocal areas of consolidation in both

lungs, especially the upper lobes, reflecting inflammatory eosino-
phils filling alveoli and infiltrating the interstitium
• Characteristic peripheral predominance (“reverse pulmonary
edema pattern”)
• Rapid response to steroid therapy (clinical improvement within
hours, radiographic clearing within a few days)
70 6 Pneumonia
Fig. 6.21 Chronic eosinophilic pneumonia. Bilateral patchy infiltrates with a

peripheral distribution [1]
Fungal Pneumonia
Aspergillosis
• Common fungus found in soil, on plants, and in decaying matter, as

well as in household dust and building materials, which does not
harm persons with normal immune systems and no allergic
hypersensitivity
• Invasive aspergillosis (most aggressive form) is essentially limited to
debilitated patients, diabetics, and neutropenic individuals with
severely compromised immune systems (organ or bone marrow trans-
plants, high-dose steroids or chemotherapy, lymphoma, leukemia)
• Central mass within a cavity in invasive aspergillosis is almost
always necrotic lung (Fig. 6.22; see Figs. e6.27–e6.29)
• CT halo sign – early finding of a zone of ground-glass opacity (usu-
ally related to hemorrhage) surrounding a nodule or mass is strongly
suggestive of invasive aspergillosis in an immunocompromised
patient (Fig. 6.23; see Fig. e6.30)
• Aspergilloma – solid homogeneous, rounded, mobile mycetoma
that develops in a pre-existing cyst or cavity (primarily upper lobe)
in a patient with underlying lung disease and is separated from its
wall by a crescentic air space (air crescent sign) (see Fig. e6.31)
Fungal Pneumonia 71
Fig. 6.22 Aspergillosis. A mycetoma (solid arrow) appears as a homogeneous

rounded mass that is separated from the thick wall of the cavity by a crescent-
shaped collection of air [1]
Fig. 6.23 Invasive pulmonary aspergillosis. Multiple pulmonary nodules

with the characteristic halo sign [1]
72 6 Pneumonia
Other Fungal Diseases
• Histoplasmosis – central United States; nodules often calcify

(Fig. 6.24)
• Coccidioidomycosis – southwestern United States (also northern
Mexico and Central and South America)
• Actinomycosis, Nocardia – pleural effusion and extension to the
chest wall are common (may develop empyema) (see Fig. e6.32)
• Candidiasis, aspergillosis, sporotrichosis, and mucormycosis –
essentially limited to debilitated patients and those with underlying
diseases (diabetes mellitus, lymphoma, leukemia) (see Fig. e6.33)
Fig. 6.24 Histoplasmosis. Miliary calcifications with a dominant calcified

granuloma in the right mid-lung (arrow)
Pneumocystis Jirovecii (formerly Carinii) Pneumonia

(Figs. 6.25 and 6.26; See Figs. e6.34–e6.36)
• Caused by a yeast-like fungus and almost exclusively seen in

immunosuppressed patients (especially AIDS, lymphoproliferative
diseases, or renal transplants)
• Initially, bilateral diffuse interstitial opacities spreading outward
from the hila
Fungal Pneumonia 73
Fig. 6.25 Pneumocystis jirovecii pneumonia. Diffuse bilateral opacifications

radiating outward from the hila in a patient with AIDS [1]
Fig. 6.26 Pneumocystis jirovecii pneumonia. Diffuse ground-glass attenu-

ation with intralobular lines (crazy-paving pattern) in a young man with
AIDS [1]
• If untreated, this soon progresses to a homogeneous diffuse alveo-

lar consolidation that may simulate pulmonary edema
• Thin-walled, air-filled lung cysts (especially apical and subpleural)
occur in about 40% of patients and may cause a pneumothorax
• Thick-walled cavities usually indicate superinfection
• Hilar adenopathy and significant pleural effusions are rare (their
presence should raise the possibility of an alternate diagnosis)
74 6 Pneumonia
Viral Pneumonia
Infectious Mononucleosis (Epstein-Barr Virus)
• Although a clinical diagnosis, may appear on chest radiographs as

bilateral hilar enlargement due to lymphadenopathy (see Fig. e6.37)
• Important to look for medial displacement of gas within the stom-
ach and splenic flexure caused by splenomegaly
Varicella (Chickenpox) Pneumonia (Fig. 6.27; See Fig. e6.38)
• Diffuse distribution of small (1–10 mm), poorly defined nodules,

which may coalesce to produce extensive bilateral fluffy infiltrates
that tend to develop near the hilum and lung bases
• Healed varicella pneumonia classically appears as tiny military cal-
cifications scattered widely throughout both lungs (develops sev-
eral years after the pulmonary infection)
• No calcification of hilar lymph nodes (unlike histoplasmosis or tubercu-
losis, the two other major causes of diffuse pulmonary calcifications)
Fig. 6.27 Varicella pneumonia. Bilateral, coarse military nodules distributed

diffusely throughout both lungs [1]
Tuberculosis 75
Tree-in-Bud Pattern in Other Viral Pneumonias
• Cytomegalovirus, which typically occurs in immunosuppressed

individuals (especially after transplantation) (Fig. 6.28)
• Respiratory syncytial virus in infants and young children (see Fig.
e6.39)
Fig. 6.28 Tree-in-bud pattern (cytomegalovirus). Centrilobular ground-

glass opacities in addition to nodules and “tree-in-bud” opacities in a patient
with chronic myelogenous leukemia who underwent bone marrow transplanta-
tion [1]
Tuberculosis
Primary
• Although traditionally considered a disease of children and young
adults, with the dramatic decrease in the prevalence of tuberculosis
(especially in children and young adults), primary pulmonary dis-
ease can develop at any age
• Primary tuberculosis may affect any lobe, so that the diagnosis can-
not be excluded because the infection is not in the upper lobe
76 6 Pneumonia
• “Latent” TB refers to someone who has a positive TST with no his-

tory of tuberculous infection or imaging evidence of active or old
disease (most often detected when undergoing routine screening
for employment or school)
• “Inactive” TB refers to someone with imaging evidence of prior
tuberculosis but no sign of active disease
Imaging
• One or more foci of lobar or segmental air-space consolidation that

is usually homogeneous, dense, and well defined (Fig. 6.29)
• If multiple, randomly distributed throughout the lungs
• Cavitation is infrequent.
• Associated enlargement of hilar or mediastinal lymph nodes (usu-
ally unilateral) is seen in about one-third of patients (may be the
only imaging finding, especially in children and immunocompro-
mised adults with AIDS) (Fig. 6.30; see Fig. e6.40)
• Unilateral pleural effusion often occurs, especially in adults, and is
usually associated with pulmonary parenchymal abnormalities (see
Fig. e6.41)
• In patients with an adequate host immune response, the consolida-
tion slowly decreases in size and may form a well-circumscribed
nodule that may eventually calcify (Ghon lesion) and be associated
with an ipsilateral calcified lymph node (Ranke complex) (see Figs.
e6.42 and e6.43)
Fig. 6.29 Primary tuberculosis. Consolidation of the right upper lobe

(arrow) [1]
Tuberculosis 77
Fig. 6.30 Primary tuberculosis. Unilateral enlargement of right hilar nodes

(arrow) without a discrete parenchymal infiltrate [1]
Fig. 6.31 Inactive tuberculosis. Bilateral fibrocalcific changes at the apices,

with upward retraction of the hila [1]
• Characteristic apical pleural thickening and fibronodular appear-

ance in one or both upper lungs (Fig. 6.31; see Fig. e6.44)
• CT – enlarged lymph nodes typically have a low-density center
(due to caseous necrosis) with rim enhancement (reflecting granu-
lomatous tissue); may demonstrate subtle cavitation that is not vis-
ible on chest radiographs (see Fig. e6.45)
78 6 Pneumonia
Postprimary (Reactivation/Active)
• Results from either activation of a latent primary infection or,
less commonly, from a repeat infection in a previously sensitized
host
• About 10% of all infected patients with tuberculosis develop reac-
tivation (highest risk within the first 2 years or during periods of
immunosuppression)
Imaging
• Initially, a nonspecific hazy, poorly marginated alveolar infiltrate

that most commonly affects the upper lobes, especially the apical
and posterior segments (Figs. 6.32; see Fig. e6.46)
• Bilateral (though often asymmetric) upper lobe disease is common
and is almost diagnostic of postprimary tuberculosis
• Because an apical lesion may be obscured by overlying clavicle or
ribs, an apical lordotic view is often of value
• Cavitation is common (about 50%) and characteristic of postpri-
mary disease (Figs. 6.33 and 6.34; see Fig. e6.47)
• The presence of cavitation indicates that the disease is highly con-
tagious, and this finding alone warrants putting the patient in respi-
ratory isolation
• Air-fluid levels in cavities are uncommon and usually a manifesta-
tion of superinfection (see Fig. e6.48)
• Tuberculous cavities may result in endobronchial spread and the
classic “tree-in-bud” pattern of centrilobular bronchial dilatation
and filling by mucus, pus, or fluid, associated with a linear
a b
Fig. 6.32 Active tuberculosis. (a, b) Heterogeneous consolidation in the api-

cal posterior segment of the left upper lobe (arrows) [8]
Tuberculosis 79
Fig. 6.33 Active tuberculosis. Bilateral cavitary lesions (arrows) with relatively
thick walls [1]
Fig. 6.34 Active tuberculosis. Large thick-walled cavity associated with mul-
tiple peripheral small nodules and branching linear structures (black arrows).
Note the thickening of bronchial walls (white arrow) [1]
80 6 Pneumonia
branching pattern that resembles a budding tree and is generally

more pronounced in the lung periphery (see Figs. e6.49–e6.51)
• Other complications of cavitation include rupture into the pleural
space (leading to empyema or bronchopleural fistula) and the devel-
opment of a pseudoaneurysm of the pulmonary artery (Rasmussen
aneurysm)
• Pleural effusion and lymph node enlargement are rare in postpri-
mary tuberculous disease (though common and sometimes the only
finding in primary disease)
• As the disease heals, fibrotic changes develop in the surrounding
lung, which cause volume loss in the affected segment with dis-
placement of the fissures and hilar structures (see Fig. e6.52)
• CT – because the diagnosis of typical postprimary tuberculosis is
generally evident on chest radiographs, CT is primarily used to assess
the extent and nature of the disease (more sensitive for demonstrating
cavitation and such complications as vascular erosion, rupture into
the pleural space, and miliary and endobronchial spread)
Miliary
• Hematogenous dissemination that usually occurs in patients with
altered host resistance to the primary infection
• Almost invariably leads to a dramatic febrile response with night
sweats and chills
• There may be minimal symptoms in severely debilitated patients,
especially elderly persons and those receiving steroids
Imaging
• Diffuse pattern of innumerable tiny (1–2 mm), discrete, relatively

well-defined pulmonary nodules distributed uniformly throughout
both lungs (Fig. 6.35; see Figs. e6.53 and e6.54)
• CT – may detect the presence of diffuse lung involvement when
corresponding chest radiographs are normal or show only minimal
or limited disease
References 81
Fig. 6.35 Miliary tuberculosis. Multiple tiny nodules throughout both lungs [1]
References
2. Franquet E. Pneumonia. Semin Roentg. 2017;52:27–34.
the lung. AJR. 2013;200:712–28.
2011;197:W970–7.
5. Cantin L. Multiple cystlike lung lesions in the adult. AJR. 2010;194:W1–W11.
6. Nachiappan AC, Rahbar K, Xiao S, et al. Pulmonary tuberculosis: role of
radiology in diagnosis and management. Radiographics. 2017;37:52–72.
7. Jeong JJ, Kim K-I, Seo IJ, et al. Eosinophilic lung diseases: a clinical, radio-
logic, and pathologic overview. Radiographics. 2007;27:617–37.
the lung. AJR. 2013;200:W222–37.
9. Gosset N, Bankier AA, Eisenberg RL. Tree-in-bud pattern. AJR. 2009;193:
W472–7.
Pleural Effusion
7
Caveats
1. Substantial amounts of pleural fluid may be present without being

apparent on a supine frontal view.
2. Beware of the effect of patient position in assessing changes in
pleural effusion from a prior study. A more upright position could
falsely suggest clearing of a layering pleural effusion. Conversely,
a more supine position could suggest a new pleural effusion that
previously was clearly evident on the lateral view, but not on the
frontal PA projection (Fig. 7.1; see Fig. e7.1).
978-3-030-16826-1_7])
Pleural fluid is produced by the pulmonary capillary bed at the pari-
etal pleura and resorbed at the visceral pleura and by lymphatic drain-
age. Pleural effusion develops if the rate of formation of pleural fluid
exceeds the rate of resorption.


https://doi.org/10.1007/978-3-030-16826-1_7
84 7 Pleural Effusion
a b
Fig. 7.1 Effect of patient position on pleural effusions. (a) Initial image taken
with the patient supine shows large bilateral layering pleural effusions that obscure
the hemidiaphragms and the lower lungs (arrows). (b) On a repeat study a few min-
utes later with the patient in a more upright position, the pleural effusions “decrease”
and no longer layer along the posterior thoracic wall. With the lower lungs now vis-
ible, it is possible to detect the presence of pneumonia at both bases (arrows)
Two major types (identical radiologic appearance):
• Transudate – rate of formation of pleural fluid exceeds its resorption

(congestive heart failure, cirrhosis, hypoalbuminemia, nephrotic
syndrome)
• Exudate – increased permeability of the pleural surface leading to
the accumulation of proteinaceous pleural fluid (malignancy, infec-
tion, connective tissue disease, pulmonary embolism, drug-induced)
or a decrease in lymphatic flow
Common causes
• Congestive heart failure (usually bilateral but larger on the right)

• Neoplasm (primary or metastatic lung cancer, lymphoma)
• Pneumonia/abscess
• Ascites
• Pancreatitis (usually left-sided)
• Tuberculosis (often unilateral in a child and may be only imaging
manifestation)
• Pulmonary embolism (small)
• Mixed connective tissue disease (lupus, rheumatoid arthritis)
• Trauma (hemothorax – higher attenuation than plain fluid on CT)
Imaging 85
Imaging
• Radiographs
○○ Upright view (Fig. 7.2; see Fig. e7.2)
• Classic blunting or meniscus appearance at the lateral and
posterior costophrenic angles
• Lateral view can detect as little as 50–75 mL of pleural fluid in
the posterior costophrenic angles, compared with about 200 mL
of pleural fluid that must accumulate before it can be identified
in the lateral costophrenic angles on the frontal projection
○○ Supine view (see Fig. 7.1a; see Fig. e7.1a)
• Hazy opacification of the hemithorax (most prominent at the
base), without obscuration of vascular markings (Fig. 7.3)
• Tracking of fluid into the fissures and around the apex of the
lung (apical cap) (Fig. 7.4)
• Large effusions may opacify an entire hemithorax and shift
the mediastinum to the opposite side (see Fig. e7.3), unless
there is compensatory collapse of the ipsilateral lung (Fig. 7.5)
Fig. 7.2 Pleural effusion. Blunting of the normally sharp angle between the
diaphragm and the rib cage (arrows), along with a characteristic upward con-
cave border (meniscus) of the fluid level [1]
Fig. 7.3 Layering pleural effusion. There is hazy opacification of the left
hemithorax with silhouetting of the hemidiaphragm, but no obscuration of
underlying vessels
Fig. 7.4 Apical pleural cap. Right pleural fluid extends from the costophrenic
angle along the lateral chest wall and around the apex of the lung (arrows)
○○ Lateral decubitus view (Fig. 7.6)

• With the patient lying on the side of a suspected effusion, free
fluid will layer out along the inner margin of the chest cage of
the dependent side
• Failure of an opacification to layer out along the dependent
chest wall indicates either that it is prevented from doing so by
adhesions (loculated effusion, see below) or does not represent
pleural fluid
Imaging 87
Fig. 7.5 Pleural effusion producing complete homogeneous opacification of

the left hemithorax. This massive pleural effusion in a patient with coccidioido-
mycosis must be associated with virtually complete collapse of the left lung, as
there is no contralateral shift of the mediastinal structures [1]
a b
Fig. 7.6 Value of the lateral decubitus view. (a) Initial frontal radiograph
shows apparent elevation of the left hemidiaphragm (arrow) with absent lung
markings below it and mild blunting of the costophrenic angle, suggesting a
subpulmonic effusion. (b) Lateral decubitus view with the left side down shows
layering of opacification along the dependent lateral chest wall (arrows), con-
firming the presence of a large amount of free pleural fluid
• CT
○○ Far more sensitive in detecting a free-flowing pleural effusion,
which appears as an area of water attenuation layering along the
posterior chest wall (see Fig. e7.4)
○○ Can document a loculated effusion and permit image-guided
drainage
• Ultrasound (see Figs. e7.5 and e7.6)

○○ The normal pleural interface appears as an echogenic line, while
on a high-resolution scan, the visceral and parietal portions of
the pleura can be resolved
○○ A transudative pleural effusion appears as an echo-free space
between the visceral and parietal pleura
○○ An exudative pleural collection (infectious, inflammatory, hem-
orrhagic, chylothorax) produces a complex pattern with septa-
tions and echogenic contents
○○ An empyema can result in an echogenic collection that mimics a
solid lesion
Subpulmonic Effusion (Fig. 7.7; See Fig. e7.7)
• Accumulation of fluid between the inferior border of the lung and

the hemidiaphragmatic pleura
a b
Fig. 7.7 Subpulmonic effusion. (a) Initial image shows the normal midline
position of the apex of the right hemidiaphragm (arrow). (b) Subsequent image
shows lateral displacement of the apex of the hemidiaphragm, consistent with
subpulmonic effusion [1]
Loculated Effusion 89
• Classic appearance is an unusually lateral position of the apex of

the hemidiaphragmatic contour, with the lateral costophrenic angle
remaining sharp
• On upright films, subpulmonic effusion can produce an abnormal
distance between the gastric fundus and the apparent left hemidia-
phragmatic contour
Loculated Effusion (Fig. 7.8; See Fig. e7.8)
• Usually exudative, a loculated effusion represents a fluid collection

that is no longer free-flowing and is unable to shift with gravity, fre-
quently because of adhesions between the visceral and parietal pleura
• Radiographically, there is no change in the position of the effusion
with the patient in various positions (upright, supine, decubitus)
• On the frontal view, the fluid collection typically has an elliptical
(lenticular) appearance and is often lobulated, is longer in the verti-
cal direction, and makes obtuse angles with the chest wall
• An infected loculated fluid collection is termed an empyema (see
page 64)
a b
Fig. 7.8 Loculated effusion. (a) On an upright frontal radiograph, the fluid
opacification at the right base (arrow) does not produce the typical meniscus
appearance at the costophrenic angle with extension along the lateral chest wall,
suggesting that it is loculated. (b) Upright lateral radiograph demonstrates a
lenticular opacification that is longer in the vertical direction and makes obtuse
angles with the chest wall (arrows), an appearance classic for a loculated effu-
sion. (Courtesy of Gillian Lieberman, MD, Boston)
a b
Fig. 7.9 Fissural pseudotumor and loculated effusion. (a, b) Elliptical fluid-
filled mass in the right hemithorax (white arrow), representing a pseudotumor in
the minor fissure. Note the loculated effusion along the left lateral chest wall
(black arrow)
Fissural Pseudotumor (Fig. 7.9; See Figs. e7.9–e7.11)
• Sharply marginated, lenticular collection of pleural fluid confined

to a minor (75%) or major fissure
• Frequently an incidental finding in a patient with radiographic fea-
tures of congestive heart failure
• May mimic a solitary pulmonary mass, though a pseudotumor typi-
cally is elongated along the course of a fissure and often has tapered
ends
• Pseudotumors in a major fissure may only be apparent on a lateral
view
Hemothorax
• Blood within the pleural space, most commonly related to chest

trauma
• May develop in patients with pulmonary infarction, neoplasm, or
infection (especially tuberculosis) or in patients with coagulopathies
• Radiographically indistinguishable from pleural effusion, though
there often is a suggestive clinical history (acute trauma) and other
imaging findings (rib fracture, pneumothorax) (see Fig. e7.12)
References 91
• CT
○○ Recent pleural hemorrhage has a high attenuation value when
compared to the homogeneous water attenuation of serous pleu-
ral fluid (see Fig. e7.13)
○○ May be a fluid-fluid level (hematocrit level) produced by layer-
ing of the more serous components above and the denser cellular
elements of blood below (see Fig. e7.14)
Chylothorax (See Fig. e7.15)
• Leakage of chyle (lymphatic fluid of intestinal origin with large

amounts of triglycerides and cholesterol) into the pleural space
• Most commonly related to disruption or obstruction of a major
lymphatic channel (thoracic duct or a tributary) secondary to a neo-
plasm (especially lymphoma), trauma (surgical or nonsurgical), or
infection
• Virtually identical radiographic appearance as transudative pleural
effusion on both radiographs and CT (attenuation value usually is
close to that of water)
References
2. Kim EA, Lee KS, Shim YM, et al. Radiographic and CT findings in compli-
cations following pulmonary resection. Radiographics. 2002;22:67–86.
3. Palas J, Matos AP, Mascarenhas V, et al. Multidetector computed tomog-
raphy: Evaluation of blunt chest trauma in adults. Radiol Res Pract.
2014;2014:864369.
Pulmonary Edema
8
Pulmonary edema is defined as excess extravascular fluid in the lungs.

The most common cause is cardiogenic pulmonary edema, due to
increased pulmonary venous pressure related to disease of the left
side of the heart. This most frequently is the result of left ventricular
failure (with associated cardiomegaly) but also can be a manifestation
of mitral valve disease, left atrial myxoma, or the hypoplastic left
heart syndromes.
Cardiogenic pulmonary edema generally begins with involvement
of the interstitial compartment and then extends to fill the alveoli with
fluid as the severity of the disease increases. Indeed, it is the most
common cause of the “pulmonary edema pattern” of symmetric bilat-
eral alveolar opacities. There often is a right-sided pleural effusion at
wedge pressures >20 mm Hg, and radiographic clearing of pulmonary
edema typically lags behind the clinical status of the patient.
Other causes of a similar pulmonary edema pattern include:
• Fluid overload (hypervolemia, hypoproteinemia) – common cause,

particularly during the postoperative period and in elderly patients,
in whom there is rapid clearing with appropriate treatment
• Overtransfusion or incompatible blood transfusion


https://doi.org/10.1007/978-3-030-16826-1_8
94 8 Pulmonary Edema
• Renal failure/uremia – complex mechanism (left ventricular fail-

ure, decreased oncotic pressure, hypervolemia, increased capillary
permeability)
Another cause of this pattern is neurogenic and other types of non-

cardiogenic pulmonary edema, in which there is no enlargement of the
cardiac silhouette unless there is unrelated heart disease (see below).
Imaging
• Interstitial edema – earliest stage

○○ Loss of the normal sharp definition of pulmonary vascular mark-
ings (especially in the lower lungs) (Fig. 8.1)
○○ Redistribution of blood flow to the upper lungs (cephalization)
(Fig. 8.2)
○○ Perihilar haze
○○ Peribronchial cuffing (see Fig. e8.1b)
978-3-030-16826-1_8])
○○ Thickening of the interlobular septa, which appear as fine, short, lin-
ear horizontal opacities extending to the pleura (Kerley B lines) and
may develop when the wedge pressure is >13 mm Hg (see Fig. e8.1)
Fig. 8.1 Interstitial pulmonary edema. Loss of the normal sharp definition of
pulmonary vascular markings and a perihilar haze. At the bases, note the thin
horizontal lines of increased opacity (Kerley B lines) that represent fluid in the
interlobular septa [1]
Imaging 95
Fig. 8.2 Redistribution of pulmonary blood flow. Apical vascular redistribu-

tion, as indicated by the diameters of upper lobe vessels (arrows) equal to those
of lower lobe vessels (open arrows). Note the moderate enlargement of the
heart [2]
a b
Fig. 8.3 Batwing appearance of alveolar edema. (a) Frontal radiograph and
(b) CT image demonstrate diffuse alveolar filling through both lungs. Note the
characteristic sparing of the outermost portions of the lungs
○○ Enlargement of the azygos vein may be seen in overhydration

edema (see Fig. e8.2)
• Alveolar edema (Fig. 8.3; see Figs. e8.3 and e8.4)
○○ Typical appearance of bilateral air-space opacifications (butterfly
or batwing pattern), which are most prominent in the central peri-
hilar regions and develop when the wedge pressure is >25 mm Hg
○○ Generally spares the outermost portions of the lungs
Fig. 8.4 Unilateral pulmonary edema. Diffuse alveolar pattern is limited to

the dependent left lung in a homeless patient who developed pulmonary edema
while sleeping on a park bench lying on his left side [1]
• Asymmetric pulmonary edema usually most prominently affects

the right lung
• Unilateral appearance is most frequently related to dependency of
the affected side (Fig. 8.4; see Figs. e8.5 and e8.6)
• In acute mitral insufficiency secondary to papillary muscle rupture
or other cause, pulmonary edema primarily involves the right upper
lung (see Fig. e8.7)
• Patchy asymmetric pattern may develop in patients with pre-exist-
ing lung disease, especially emphysema, because only areas with
intact pulmonary vessels are affected (see Fig. e8.8)
• Recurrent episodes of interstitial and alveolar edema and hemor-
rhage in patients with chronic left heart failure may result in the
development of a coarse, often poorly defined reticular pattern
that predominantly involves the middle and lower lung zones
(may be impossible to distinguish from COPD in older patients
and often represents both conditions coexisting in the same
patient) (see Fig. e8.9)
• Radiographic resolution of pulmonary edema usually occurs hours
or days after symptoms improve and wedge pressure measurements
have returned to normal (especially in patients with left-sided heart
failure), because of the time lag before the large amount of extra-
cellular fluid is reabsorbed
Neurogenic Pulmonary Edema 97
Fig. 8.5 CT of interstitial edema. In a patient with postoperative fluid over-

load and a pulmonary capillary wedge pressure of 20 mm Hg, there are interlo-
bar septal lines predominating in the anterior portion of the left lung, along with
some peribronchial cuffing (arrow). Both lungs display diffuse ground-glass
areas of increased attenuation with a gravitational anteroposterior gradient [3]
• Serial widening of the vascular pedicle (width of the superior medi-

astinum measured from the right lateral border of the SVC at the
point where it crosses the right main bronchus to the left lateral
margin of the left subclavian artery as it arises from the aortic arch)
• CT
○○ Smooth thickening of interlobular septa, which appear as lines in
the lung periphery running perpendicular to the pleura (Kerley B
lines) (Fig. 8.5)
○○ Ground-glass, low-grade lung opacification or frank air-space
consolidation with a central distribution (see Fig. e8.10)
Neurogenic Pulmonary Edema
• Important cause of non-cardiogenic pulmonary edema that is

reported to develop in up to 30% of patients after head trauma, sei-
zures, or stroke (Fig. 8.6)
• Related to increased intracranial pressure, neurogenic pulmonary
edema typically disappears within several days of surgical relief
Fig. 8.6 Non-cardiogenic pulmonary edema. Pulmonary vascular conges-

tion with a normal cardiac silhouette following a stroke
Differences between the two major types of edema
• Cardiac
○○ Low-protein transudate due to increased hydrostatic pressure
generated across the capillary membrane
○○ Initially accumulates in the connective tissues surrounding the
blood vessels and secondary pulmonary lobules
• Noncardiac
○○ Protein-rich exudate that accumulates in the extravascular space
as a consequence of increased microvascular permeability
○○ Because of inherent disruption of the alveolocapillary membrane
in this condition, water may not flow into the loose connective
tissue, instead directly flooding the alveolar space
○○ Clearance of the protein-rich exudate is slower than with a non-
proteinaceous transudate
Other causes of non-cardiogenic pulmonary edema
• Inhalation of toxic gases (e.g., hydrocarbons, chlorine, sulfur diox-
ide, nitrogen dioxide in silo-filler’s disease) (see Fig. e8.11)
• Near-drowning (Fig. 8.7)
Neurogenic Pulmonary Edema 99
Fig. 8.7 Near-drowning. Diffuse pulmonary edema pattern [1]
a b
Fig. 8.8 Re-expansion edema after thoracentesis. (a) Initial radiograph

shows a massive left malignant effusion. (b) Repeat examination 2 hours after
the rapid removal of 2500 mL of fluid shows re-expansion pulmonary edema on
the left (arrows). The segment of left lung not compressed by effusion remains
free of edema. Over the next 6 days, the edema resolved spontaneously [1]
• Rapid re-expansion of lungs – unilateral pulmonary edema pattern

that follows the rapid removal of large amounts of air or fluid from
the pleural space (Fig. 8.8; see Fig. e8.12)
• Chronic renal failure (see Fig. e8.13)
• Non-traumatic pulmonary hemorrhage (bleeding diatheses, idio-

pathic pulmonary hemosiderosis, Goodpasture’s syndrome, polyar-
teritis nodosa, ANCA-associated granulomatous vasculitis)
• Narcotic abuse (heroin, methadone, cocaine) (Fig. 8.9; see Figs.
e8.14 and e8.15)
• ARDS (sepsis, oxygen toxicity, disseminated intravascular coagu-
lation, cardiopulmonary bypass)
Fig. 8.9 Cocaine abuse. Extensive bilateral heterogeneous central and parahi-
lar opacities, representing cardiogenic pulmonary edema in a woman who pre-
sented with shortness of breath and chest pain after smoking crack cocaine [1]
Imaging – chest radiographs can distinguish between cardiac and non-

cardiogenic (permeability) edema in about 80% of patients (Table 8.1)
Table 8.1 Cardiac and Cardiac Noncardiac

noncardiac edema Major signs
Kerley lines Present Less common
Pleural effusions Present Less common
Cardiomegaly Present Less common
Opacities in lung Diffuse Patchy and
peripheral
Minor signs
Air bronchograms Rare Often present
Perihilar haze Present Infrequent
Peribronchial cuffing Present Unusual
Adult Respiratory Distress Syndrome (ARDS) 101
Pulmonary Hemorrhage
• Alveolar process that is extremely difficult to differentiate radio-

graphically from pulmonary edema and pneumonia (see Fig. e8.16)
Adult Respiratory Distress Syndrome (ARDS)
• Severe, unexpected acute respiratory distress (usually requiring

mechanical ventilation) that develops in a patient with no major
underlying lung disease
• Diffuse alveolar damage from increased pulmonary capillary per-
meability, which develops in response to numerous types of lung
injury and results in leakage of proteinaceous fluid into the
alveoli
• This process eventually results in alveolar disruption and hemor-
rhage, a reduction in surfactant, and alveolar collapse
• Causes include:
○○ Diffuse severe pulmonary infection (bacterial or viral)
○○ Prolonged or profound shock
○○ Inhalation of toxins and irritants
○○ Oxygen toxicity
○○ Systemic reaction to a broad spectrum of non-pulmonary
processes
• Diagnosis is based on clinical grounds – acute onset of bilateral
lung opacities, no clinical signs of congestive failure (pulmonary
artery wedge pressure ≤ 18 mm Hg), PaO2/FIO2 ≤ 300 mm Hg.
• High mortality rate of up to 60%
Imaging (Figs. 8.10 and 8.11; see Fig. e8.17)
• Bilateral pulmonary edema pattern that is typically delayed 12 hours

or more after the clinical onset of respiratory failure (unlike cardio-
genic pulmonary edema, in which the chest radiograph is often
abnormal before or concurrent with the onset of symptoms)
• Cardiac silhouette is not enlarged (unless there is underlying heart
disease), and there is infrequently any associated pleural effusion
• Lung opacities evolve rapidly (maximum during the first 3 days)
and may progress to areas of consolidation
Fig. 8.10 ARDS. Diffuse bilateral pulmonary edema pattern with normal car-
diac silhouette. No evidence of appreciable pleural effusion
Fig. 8.11 ARDS. Diffuse bilateral alveolar process involving all lobes with no
cardiomegaly or pleural effusion. (Courtesy of Jeffrey Klein, MD, Burlington,
CT)
References 103
• Radiographic findings may be less severe than expected by the clin-

ical degree of hypoxemia
• CT – diffuse ground-glass opacities (but a more patchy distribution
with some portions of normal-appearing lung)
• In those who survive ARDS, there is clearing of the ground-glass
opacifications and consolidations but frequently a residual promi-
nence of interstitial markings with traction bronchiectasis, archi-
tectural distortion, and functional disability
• Need for prolonged mechanical ventilation and decreased lung
compliance frequently leads to the development of barotrauma
(pneumothorax, pneumomediastinum, pulmonary interstitial
emphysema, pneumatoceles)
References
the lung. AJR. 2013;200:712–28.
3. Gluecker T, Capasso P, Schnyder P, et al. Clinical and radiological features
of pulmonary edema. Radiographics. 1999;19:1507–31.
4. Gotway MB, Marder SR, Hanks DK, et al. Thoracic complications of illicit
drug use: an organ system approach. Radiographics. 2002;22:S119–35.
5. Rossi SE, Erasmus JJ, McAdams HP, et al. Pulmonary drug toxicity: radio-
logic and pathologic manifestations. Radiographics. 2000;20:1245–59.
Pulmonary Vascular Diseases
9
Pulmonary Embolism
• Third most common form of acute cardiovascular disease (after

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


https://doi.org/10.1007/978-3-030-16826-1_9
106 9 Pulmonary Vascular Diseases
Imaging
• Radiographs
○○ Usually normal (may be nonspecific opacity, pleural effusion,
atelectasis, or elevation of the hemidiaphragm indistinguishable
from other pulmonary or pleural processes)
○○ Primarily performed to exclude other disorders that could mimic a
pulmonary embolism (pneumonia, rib fracture, pneumothorax)
○○ Classic peripheral, pleural-based, wedge-shaped opacity
(Hampton hump) is seen in a minority of cases with pulmonary
infarction (Fig. 9.1)
○○ Uncommon findings of:
• Focal oligemia (Westermark sign) (Fig. 9.2; see Fig. e9.1)
this chapter’s website on SpringerLink: [https://doi.
org/10.1007/978-3-030-16826-1_9])
• Enlargement of the ipsilateral pulmonary artery (Fleischner
sign) (Fig. 9.3) associated with rapid tapering of the occluded
pulmonary artery distally (knuckle sign)
○○ Essential for accurate interpretation of radionuclide ventilation-
perfusion (V/Q) lung scan
a b
Fig. 9.1 Hampton hump sign of pulmonary embolism/infarction. (a, b)

Wedge-shaped, pleural-based areas of increased opacification/attenuation
(arrows) in two different patients. (a) From [1]; (b) from [2]
Pulmonary Embolism 107
a b
Fig. 9.2 Westermark sign of pulmonary embolism. (a) Hyperlucency of the

left lung. (b) CTPA demonstrates a large pulmonary embolism filling the left
pulmonary artery (arrow)
a b
Fig. 9.3 Fleischner sign of pulmonary embolism. (a) Enlargement of the

ipsilateral pulmonary artery (arrow), associated with rapid tapering of the
occluded pulmonary artery distally. (b) CT image confirms the clot-filled pul-
monary artery (arrow). (Courtesy of Jeffrey Klein, MD, Burlington, CT)
• CT pulmonary angiogram (CTPA) (Fig. 9.4; see Figs. e9.2–e9.7)

○○ Has replaced V/Q lung scanning in most institutions as the pre-
ferred imaging modality for detecting and excluding pulmonary
emboli
○○ Shows a pulmonary embolus as a central filling defect sur-
rounded by contrast within the pulmonary artery or as an abrupt
cutoff (complete obstruction) of a pulmonary artery branch
Fig. 9.4 Acute pulmonary embolus. Large filling defects in the right main
(white arrow) and left interlobar (black arrow) pulmonary arteries [3]
Fig. 9.5 Acute pulmonary embolism. Eccentric partial filling defect, which is
surrounded by contrast material and forms acute angles with the arterial wall
(arrows) [3]
○○ If eccentric, the filling defect forms an acute angle with the pul-
monary artery wall (Fig. 9.5)
○○ Saddle embolism is the infrequent development a large pulmo-
nary embolism that straddles the main pulmonary arterial trunk
at its bifurcation (Fig. 9.6)
○○ Pulmonary infarcts appear as peripheral ground-glass opacifica-
tions or consolidations that often have a wedge-shaped configu-
ration (see Fig. e9.6)
○○ May demonstrate other diseases that could mimic pulmonary
embolism
Pulmonary Embolism 109
Fig. 9.6 Saddle embolus. The pulmonary embolism straddles the main pul-
monary arterial trunk at its bifurcation. (Glitzy queen00 / English Wikipedia)
○○ Part of the three-pronged study in which patients presenting with

chest pain are also assessed for coronary artery disease and aor-
tic dissection
• Radionuclide ventilation-perfusion (V/Q) lung scan (see Fig. e9.7)
○○ Normal perfusion study excludes significant embolization, and
no further examinations are needed
○○ Two or more segmental or larger perfusion defects with normal
ventilation in these areas (V/Q mismatch) are highly likely for
pulmonary embolism
○○ Relatively large number of indeterminate examinations, espe-
cially in patients with chronic obstructive pulmonary disease or
parenchymal abnormalities seen on chest radiographs
Management
• Clinical significance of small emboli is unclear (if there is no
impairment of cardiopulmonary reserve, these small clots may be
left untreated without adverse effect)
• Immediate anticoagulation therapy (heparin) for patients with sus-
pected DVT or pulmonary embolism reduces mortality rates from
30% to <10%
• Thrombolytic therapy can be used within the first 4 hours in patients
with hemodynamic compromise (if low risk for bleeding)
Non-thrombotic Pulmonary Emboli
• Septic emboli – see Figs. 6.18 and 6.19; e6.24 and e6.25
• Fat embolism syndrome
○○ Fat emboli occur in a large majority of patients with severe traumatic
long bone fractures, but fewer than 10% become symptomatic
○○ Fat embolism syndrome refers to the combination of acute respi-
ratory failure and hypoxia, neurologic manifestations, and a
petechial rash, all of which develop following long bone fracture
after an asymptomatic interval of 12–72 hours
○○ Initial symptoms are probably caused by mechanical occlusion
of blood vessels by fat globules or the bone marrow (too large to
pass through the capillaries), which were released into the venous
system following trauma
○○ Late symptoms are believed to result from endothelial damage
and permeability edema caused by irritating free fatty acids pro-
duced by hydrolysis due to the actions of intrapulmonary lipase
○○ Although usually resolving completely, fat embolism syndrome
is associated with a mortality rate of 10–20%
Imaging (Fig. 9.7)
○○ Diffuse parenchymal opacities (mimicking non-cardiogenic pul-

monary edema, diffuse pneumonia, or ARDS) that develop after
an asymptomatic interval following long bone fracture
• Amniotic fluid emboli (see Fig. e9.8)
○○ Rare, but often fatal (80%) complication of pregnancy
○○ Related to amniotic fluid entering the bloodstream through small
tears in the uterine veins
○○ Can occur due to uterine contractions during normal labor or be
a complication of abortion, amniocentesis, or cesarean delivery
• Foreign body emboli (see Figs. e9.9 and e9.10)
○○ Most commonly related to talc and cellulose used to cut heroin
and other drugs in addicts
○○ These substances are trapped in the pulmonary vasculature,
where they incite thrombosis and inflammation
○○ Chest radiographs demonstrate a broad spectrum of findings,
from multiple small nodules to large areas of increased opacity
simulating the progressive massive fibrosis of silicosis
• Tumor emboli (intravascular pulmonary metastases) (see Fig. e9.11)
Chronic Pulmonary Thromboembolism 111
a b
Fig. 9.7 Fat embolism syndrome. (a) Diffuse bilateral air-space consolidation
due to alveolar hemorrhage and edema that developed 3 days after a leg fracture.
Unlike cardiogenic pulmonary edema, the distribution in this patient is predomi-
nantly peripheral rather than central, and the heart is not enlarged. (b) Recumbent
radiograph of the knee obtained with a horizontal beam shows the characteristic
fat-blood interface (FBI sign, arrow) in a large suprapatellar effusion [1]
Chronic Pulmonary Thromboembolism
• Reported to occur in about 4% of patients with acute pulmonary

embolism, in whom repetitive thromboembolism leads to elevated
pulmonary artery pressure
• Risk factors include malignancy, splenectomy, chronic inflamma-
tory conditions, and ventriculo-atrial shunts
Imaging
• Eccentric, crescentic intraluminal defect forming obtuse angles

with the vessel wall (Fig. 9.8)
• May be complete occlusion of a vessel, which appears smaller than
others situated at a similar distance from the hilum
• Contrast within a thickened (often small) recanalized vein
• Web or flap within a contrast-filled pulmonary artery, serpiginous
pulmonary arteries, and extensive tortuous and enlarged bronchial
artery collaterals (see Fig. e9.12)
• May have mosaic attenuation with well-defined borders and scar-
ring at the site of previous infarcts
• Enlargement of central pulmonary arteries and right ventricular
hypertrophy (signs of secondary pulmonary artery hypertension)
Fig. 9.8 Chronic pulmonary thromboembolism. Eccentric thrombus forms

obtuse angles with the vessel wall (white arrows). Note the dilated collateral
bronchial artery (black arrow) [3]
Pulmonary Arterial Hypertension
• Elevation of mean pulmonary artery pressure (>25 mm Hg at rest,

>30 mm Hg during exercise)
• General causes
○○ Increased pulmonary blood flow (left-to-right shunt)
○○ Narrowing of pulmonary vessels (chronic pulmonary embolism)
○○ Increased resistance to pulmonary venous drainage (mitral valve
disease)
• Major types
○○ Primary
• Uncommon subtype of sustained elevation of pulmonary
artery pressure in which no underlying cause is identified
• Typically affects young females (20–45 years)
○○ Secondary
• Diffuse lung disease (obstructive emphysema, interstitial
fibrosis)
• Diffuse pulmonary arterial disease (thromboembolism, arteritis)
• Chronic heart disease (mitral valve disease, left ventricular
failure)
Pulmonary Arterial Hypertension 113
• Chronic hypoxia (chest deformity, neuromuscular disease,

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

great increase in the size of the pulmonary trunk. The right and left pulmonary
arteries are huge (arrows), but the peripheral pulmonary vasculature is relatively
sparse. Note the hilum convergence sign on the right. Long-standing pulmonary
hypertension has produced degenerative intimal changes in the pulmonary
arteries, which have become densely calcified. The patient had an atrial septal
defect and Eisenmenger’s physiology (reversed left-to-right shunt) [1]
a b
Fig. 9.10 Prominence of pulmonary outflow tract (arrow). (a) Normal

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

(with normal pulmonary vessels and no associated cardiac
abnormality) is a common appearance in adolescents and
adults younger than 30 years of age (especially in women)
(Fig. 9.10a); however, if there is an appropriate murmur, fur-
ther studies must be performed to exclude pulmonic stenosis
(Fig. 9.10b)
• CT (see Figs. e9.13 and e9.14)
○○ Much more accurate for detecting pulmonary artery enlargement
when the diameter of the main pulmonary artery is greater than
that of the ascending aorta or ≥3 cm
○○ Pulmonary artery calcifications are virtually pathognomonic
○○ Demonstrates right ventricular enlargement and bulging of the
interventricular septum
○○ Mosaic attenuation that is heterogeneous or patchy, with a peri-
vascular distribution (regions of hypoattenuation reflecting
areas of hypoperfusion interposed with areas of hyperattenua-
tion where there is normal or excessive perfusion); this differs
from the typical segmental and well-defined distribution of
mosaic attenuation associated with chronic pulmonary
embolism
References 115
Pulmonary Veno-occlusive Disease
• Rare subtype of pulmonary arterial hypertension, in which pulmo-

nary venous thrombosis and fibrosis cause narrowing or occlusion
of the pulmonary veins
• Although the etiology is unknown, this condition has been associ-
ated with viral infection, chemotherapy, autoimmune disease, bone
marrow transplantation, intracardiac shunts, radiation injury, and a
genetic predisposition
• Typically affects children and young adults
• Classic triad of severe pulmonary artery hypertension, radiographic
evidence of pulmonary edema, and normal wedge pressure (though
not seen in many patients)
• The combination of smooth interlobular septal thickening and ill-

defined diffuse centrilobular ground-glass opacities in a patient
with enlarged pulmonary arteries is highly suspicious for pulmo-
nary veno-occlusive disease
References
1. Eisenberg RL. Clinical Imaging: An Atlas of Differential Diagnosis. 5th ed.
2. Frazier AA, Galvin JR, Franks TJ, Rosado-de-Chrsitenson ML. Pulmonary
vasculature: hypertension and infarction. Radiographics. 2000;20:491–524.
3. Wittram C, Maher MM, Yoo AJ. CT angiography of pulmonary embo-
lism: diagnostic criteria and causes of misdiagnosis. Radiographics.
2004;24:1219–38.
4. Arnold HR, Gardner JE, Goodman PH. Amniotic pulmonary embolism.
Radiology. 1961;77:629–43.
5. Restreppo CS, Carrillo JA, Martinez S, et al. Pulmonary complications
from cocaine and cocaine-based substances: imaging manifestations.
Radiographics. 2007;27:941–56.
6. Gotway MR, Marder SR, Hanks DK, et al. Thoracic complications of illicit
drug use: an organ system approach. Radiographics. 2002;22:S119–35.
7. Gladdish GW, Sabloff BM, Munden RF, et al. Pulmonary thoracic sarcomas.

2011;197:W970–7.
9. Peña E, Dennie C, Veinot J, Muñiz SH. Pulmonary hypertension: how the
radiologist can help. Radiographics. 2012;32:7–32.
10. Gluecker T, Capasso P, Schnyder P, et al. Clinical and radiological features
of pulmonary edema. Radiographics. 1999;19:1507–31.
Solitary Pulmonary Nodule (SPN)/
Pulmonary Neoplasms 10
Solitary round or oval pulmonary opacifications are common inciden-

tal findings on a chest radiograph or chest CT performed for another
indication. They are especially common in smokers, up to half of
whom have tiny nodules, almost all of which are benign. By defini-
tion, the opacification is termed a nodule if ≤3 cm in diameter and a
mass if >3 cm.
When encountering a solitary pulmonary nodule, the critical deci-
sion is whether this represents a benign or malignant process.
Numerous criteria can be used to assess the risk of cancer.
Age effect
• <Age 30 – cancer risk <1%
• Ages 30–45 – cancer risk about 15%
• >Age 50 – cancer risk about 50%
Size effect
• The smaller the nodule, the more likely it is to be benign
○○ <6 cm – rarely malignant
○○ <2 cm – 80% of nodules are benign
○○ >5 cm – 95% are malignant


https://doi.org/10.1007/978-3-030-16826-1_10
118 10 Solitary Pulmonary Nodule (SPN)/Pulmonary Neoplasms
• However, relatively small size does not exclude lung cancer

○○ About 15% of malignant nodules are <1 cm in diameter
○○ About 40% of malignant tumors are <2 cm
• Nodules <9 mm are infrequently visible radiographically unless
they are diffusely calcified
Major clinical risk factors of malignancy
• Smoking history (almost all squamous and small cell carcinomas)

• Exposure to asbestos or radon
• Pulmonary fibrosis
• Positive family history
Imaging Criteria for Benignancy
Margins
• Smooth, well-defined – likely benign (but 20% of malignant nod-
ules also have this appearance) (Fig. 10.1; see Figs. e10.1 and e10.2)
Fig. 10.1 Benign tuberculoma. Smooth, well-defined pulmonary SPN [1]

Imaging Criteria for Benignancy 119
Fig. 10.2 Malignant bronchogenic carcinoma. Ill-defined, irregular, and

spiculated SPN [1]

this chapter’s website on SpringerLink: [https://doi.org/
10.1007/978-3-030-16826-1_10])
• Irregular, spiculated – malignant (Fig. 10.2) (Lobular contour
implies uneven growth, which is associated with malignancy, but
this appearance is seen in up to 25% of benign nodules.)
Calcification
• Central, diffuse solid, laminated, or popcorn calcification – benign
(but a substantial number of benign nodules are not calcified)
(Figs. 10.3–10.5)
• Eccentric or multiple dense or part solid calcifications – worrisome
for neoplastic engulfment of a preexistent calcified granuloma or
metastases from osteosarcoma or chondrosarcoma (Fig. 10.6; see
Figs. e10.3 and e10.4)
Fig. 10.3 Benign central calcification in a SPN [1]
Fig. 10.4 Benign diffuse solid calcification in a SPN (arrows) [1]

Imaging Criteria for Benignancy 121
Fig. 10.5 Benign irregular scattered “popcorn” calcifications in a SPN.

This pattern is characteristic for a hamartoma [1]
Fig. 10.6 Malignant eccentric, punctate calcification in a SPN. This pattern

represents an “engulfed” granuloma [1]
Cavitation
• Smooth and thin (<4 mm) wall – benign (Fig. 10.7)
• Thick, irregular wall – malignant (Fig. 10.8) or an abscess with air-
fluid level (see Fig. e10.5)
Doubling time
• <20 days or > 400 days – usually benign (exception may be adeno-
carcinoma in situ, which may have a doubling time >1 year)
Fig. 10.7 Pneumatocele (benign). Large, thin-walled cystic space (arrows) that
developed following hydrocarbon poisoning [1]
Fig. 10.8 Squamous cell cancer. The cavitary mass has a thick, irregular wall
(arrow)
Mimics of Nodules 123
• Between 20 and 400 days – malignant (with exception noted above)

(see Fig. e.10.6)
Fat within a mass
• Highly specific for benign hamartoma (occasionally lipoid granu-
loma) (see Fig. e10.11b)
Feeding artery and draining vein (see Fig. e10.12)
• Virtually pathognomonic for benign arteriovenous malformation
Air bronchogram within a nodule
• About five times more common with malignancy (30% versus 6%)
(see Fig. e10.7)
Clustering of nodules – benign (usually an infectious process)
Stability of a pulmonary nodule (>1 cm) for 2 years or more
• Benign – therefore it is critical to compare with prior images (may
require contacting another institution where previous radiographs
were obtained)
CT
• Contrast enhancement <15 HU – very high negative predictive
value for malignancy
• Ground-glass nodules (or mixed-attenuation lesions with ground-
glass and solid components) – more likely to be malignant than a
solid nodule (see Fig. e10.7)
PET-CT (see Fig. e10.8)
• High isotope avidity – strong likelihood for malignancy (false posi-
tives include inflammatory nodules and hamartomas).
• For nodules >1 cm – a negative study has high negative predic-
tive value for excluding malignancy (exceptions are adenocarci-
noma in situ, well-differentiated adenocarcinomas, and peripheral
carcinoid tumors)
Mimics of Nodules (Fig. 10.9; See Fig. e10.9)
• Nipples – symmetric and not seen on lateral view; if unsure, repeat

study with nipple markers
• Calcification in costal cartilage of the first rib; if unsure, apical lor-
dotic view
• Blood vessel seen on end (if same size as nearby blood vessel)
• Bone island (constant relationship with an osseous structure on
serial images; high attenuation on CT)
• Pleural plaque
Fig. 10.9 Mimic of pulmonary nodules. Nipple shadows (arrows) in a

45-year-old man. The lateral view was normal
• Round atelectasis (abuts the pleura and characteristic comet tail

sign on CT)
• Soft-tissue nodules (skin lesions, neurofibromatosis)
Follow-Up of Nodules (Fleischner Criteria) [6]
• Does not apply to lung screening, patients with immunosuppres-

sion, or those with known primary cancer
• Based on the type of nodule
○○ Solid nodule – follow-up based on nodule size and smoking
history
○○ Subsolid nodule (ground-glass/part solid) – based on CT appear-
ance and multiplicity
Benign Nodule(s)
Granuloma
• Tuberculosis – primarily East Coast and west of the Rocky

Mountains (see Fig. e10.10)
• Histoplasmosis – central United States
• Coccidioidomycosis – southwestern United States
Benign Nodule(s) 125
Imaging
• Clearly benign when calcified (central, diffuse solid, or laminated)

• Worrisome for malignancy if eccentric calcification (see above)
Hamartoma
• Acquired benign abnormality consisting of disorganized growth of

mesenchymal tissue normally found in the lung
• Histologically, the tumor contains variable amounts of fat, carti-
lage, and connective and epithelial tissue (may also be bone, blood
vessel, and smooth muscle elements)
• Constitutes up to 10% of all solitary lung nodules
Imaging
• Lobulated contours and well-defined margins.

• 90% in lung periphery
• Extensive popcorn pattern of calcification is virtually diagnostic of
a benign hamartoma (though detected on chest radiographs in only
about 10% of cases) (see Fig. e10.11a)
• CT – characteristic fat attenuation (−50 to −150 HU) within the
lesion (see Figs. e10.10 and e10.11b)
Pulmonary Arteriovenous Fistula (AVM)
• Direct communication between a pulmonary artery and vein with-

out an intervening capillary network
• Sharply defined, round or oval, often slightly lobulated nodule (approx-
imately one-third are multiple), predominantly in a lower lobe
• Diagnosis requires identification of the feeding artery and draining
vein (see Fig. e10.12)
• Common finding in hereditary hemorrhagic telangiectasia (Rendu-
Osler-Weber disease)
Rheumatoid Necrobiotic Nodule (See Fig. e10.13)
• Smooth, well-circumscribed nodule(s), predominantly occurring in

a peripheral subpleural location
• Cavitation is common (thick-walled with smooth inner margins)

• A rare manifestation of rheumatoid lung disease, it tends to wax
and wane in relation to the activity of the rheumatoid arthritis and
the presence of subcutaneous nodules
ANCA-Associated Granulomatous Vasculitis
(formerly known as Wegener’s granulomatosis)
• Round, fairly well-circumscribed nodule that may simulate metastases

• Cavitation (thick-walled with irregular, shaggy inner margins)
develops in approximately half of the patients
• CT – ground-glass halo sign surrounding the nodules indicates
hemorrhage (see Fig. e10.14)
Lung Cancer
• Leading cause of death in the United States (overall 5-year survival
rate of about 15%)
• More people die of lung cancer than colon, breast, and prostate
cancers combined
• Vast majority (85%) of cases of lung cancer are due to long-term
tobacco smoking (almost all cases of squamous and small cell
carcinomas)
• About 10–15% of cases occur in people who have never smoked,
often caused by a combination of genetic factors and exposure to
radon gas, asbestos, second-hand smoke, or other forms of air
pollution
• Up to one-third of lung cancers initially present as solitary pulmo-
nary nodules
• Nearly 40% of those newly diagnosed with lung cancer already
have metastases to other parts of the body (most commonly lymph
nodes, liver, bones, brain, and adrenal glands)
• Lung cancer is traditionally divided into two categories – non-
small cell lung cancer (NSCLC), which is primarily adenocarci-
noma and squamous cell carcinoma, and small cell lung cancer
(SCLC)
Lung Cancer 127
○○ NSCLC often is detected at an early stage and is treated with

surgery alone
○○ SCLC typically presents at a late stage and requires a combina-
tion of radiation therapy and chemotherapy
Adenocarcinoma
• Most frequent non-small cell lung cancer (about 40–50% of all

bronchogenic carcinomas)
• Usually occurs as a solitary pulmonary nodule in the periphery of
the lung (especially the upper lobes) and is the slowest growing
type of lung cancer
• May arise from a pre-existing lung scar (“scar carcinoma”)
• Most common type of lung cancer in women and non-smokers
• Weak association with cigarette smoking
Imaging
• Solitary pulmonary nodule with margins that may be well-defined,

lobulated, irregular, or spiculated (due to reactive fibrosis) (see Fig.
e10.15)
Adenocarcinoma in Situ
• Previously known as bronchoalveolar carcinoma (BAC), this sub-

type of adenocarcinoma of the lung is distinguished by its periph-
eral location, well-differentiated cytology, growth in a single layer
along intact alveolar septa (“lepidic” growth pattern), and tendency
for both bronchial and lymphatic spread
• The new lung cancer classification (2011) uses the terms adenocar-
cinoma in situ and minimally invasive adenocarcinoma (mainly
based on the pathology of the lesion, and it is very difficult to dis-
tinguish among these lesions radiographically)
○○ Adenocarcinoma in situ – lepidic growth pattern, spreading along
the walls of the lung (≤3 cm) without destroying the underlying
architecture and without stromal, vascular, or pleural invasion
○○ Minimally invasive adenocarcinoma – small solitary adenocarci-

nomas (≤3 cm) with either pure or predominantly lepidic growth
with ≤5 mm of stromal invasion
• About 3–4 times more common to develop in smokers, especially
heavy smokers with long-term exposure; nevertheless, about one-
third of cases occur in individuals who have never smoked, and a
similar number are former or intermittent smokers
• Survival rate is significantly higher than other subtypes of
adenocarcinoma
Imaging – three basic patterns
• Solitary nodule
○○ Well-circumscribed with air bronchograms (may have spiculated
borders), located in the periphery of the lung (Fig. 10.10)
○○ Typically ground-glass attenuation on CT, with solid areas
within the lesion representing elements of adenocarcinoma
(Fig. 10.11)
○○ Often linear strands extending from the nodule to the pleura
(pleural tags, tail sign) (see Fig. e10.16)
○○ Characteristic bubble-like lucencies or pseudocavitation, reflect-
ing patent small bronchi or air-containing cystic spaces in papil-
lary tumors (see Fig. e10.17)
Fig. 10.10 Adenocarcinoma in situ. Large, well-circumscribed tumor mass

in the right lower lung [1]
Lung Cancer 129
Fig. 10.11 Adenocarcinoma in situ. Poorly marginated, ground-glass mass

with focal solid components [1]
Fig. 10.12 Adenocarcinoma in situ. Patchy, ill-defined lesion simulates an

area of focal pneumonia [1]
• Multiple nodules
○○ Random or peribronchovascular distribution (see Figs.
e10.18–e10.20)
○○ May mimic hematogenous metastases (see Fig. e10.21)
• Consolidation (Figs. 10.12 and 10.13; see Figs. e10.22 and
e10.23)
○○ Ill-defined area(s) of ground-glass opacity or consolidation mim-

icking pneumonia with air bronchograms (may be segmental or
involve an entire lobe), due to growth along the air spaces com-
bined with production of mucin by the tumor
○○ On CT, a large amount of mucin may cause the consolidation to
have low attenuation
○○ On contrast studies, blood vessels appear denser than the sur-
rounding opacified lung (CT angiogram sign), a highly sugges-
tive finding for this condition
• PET – frequent false negatives in tumors with low metabolic activity
Squamous Cell Carcinoma
• Second most common type of lung cancer, accounting for about

30% of all bronchogenic carcinomas
• Usually occurs in a central location (main, lobar, or segmental
bronchi), though about one-quarter may develop in a peripheral
location (like an adenocarcinoma)
• Strong association with cigarette smoking
• Grows rapidly
Fig. 10.13 Squamous cell carcinoma. Post-obstructive pneumonia presents

as homogeneous increased opacity of the right upper lobe due to a central
carcinoma. Patchy increased opacification at the right base is due to a
combination of atelectasis and consolidation secondary to extension of the
tumor into neighboring bronchi [1]
Lung Cancer 131
Imaging
• Post-obstructive atelectasis or pneumonia related to a radiographi-

cally occult central tumor causing partial or total bronchial obstruc-
tion (Fig. 10.13)
• Therefore, a patient with infectious symptoms and lobar collapse
should be followed with serial chest radiographs to ensure com-
plete clearing of the opacification and re-expansion of the affected
lobe
• Tumor mass in the right upper lobe bronchus produces the S sign of
Golden (see page 47)
• Peripheral type is the most frequent cause of Pancoast tumor (see
page 135)
• Most common type of lung cancer to cavitate (central necrosis is
caused by rapid tumor growth that exceeds the blood supply)
(Fig. 10.14; see Fig. e10.24)
• The appearance of a thick-walled cavity representing squamous
cell carcinoma may be impossible to distinguish radiographically
from a lung abscess
Fig. 10.14 Squamous cell carcinoma. Large cavitary mass in the right upper
lobe with an air-fluid level (arrows) and associated rib destruction [1]
Small Cell Lung Carcinoma (SCLC)
• Third most common type of lung cancer (about 20% of broncho-

genic carcinomas)
• Arises from neuroendocrine cells lining the proximal airways (lobar
and main bronchi) and thus associated with paraneoplastic syndromes
• Aggressive tumor that is the most rapidly growing lung cancer and
metastasizes early
• Usually occurs in cigarette smokers and more common in males
• Presenting symptoms include cough, chest pain, dyspnea, and
hemoptysis, as well as hoarseness (involvement of the recurrent
laryngeal nerve) and SVC syndrome
Imaging
• Large, bulky mediastinal mass (adenopathy) with associated hilar

involvement (Fig. 10.15; see Figs. e10.25 and e10.26)
• Obstructive changes of bronchial narrowing, lobar/total lung col-
lapse, and post-obstructive pneumonia
• Primary intrabronchial lesion rarely identified.
• Solitary pulmonary nodule in only about 5% of cases
• Elevation of a hemidiaphragm (if involvement of the recurrent
laryngeal nerve or subpulmonic pleural effusion)
Fig. 10.15 Small cell carcinoma. Tomographic image demonstrates bilateral,

bulky hilar adenopathy [1]
Lung Cancer 133
Large Cell Carcinoma
• Diagnosis of exclusion for all bronchogenic carcinomas that are not

adenocarcinoma, squamous cell carcinoma, or small cell carcinoma
• Represents about 3% of all lung cancers
• Strong association with cigarette smoking
• Grows extremely rapidly, metastasizes early, and has a poor prognosis
Imaging
• Usually a large peripheral lesion (Fig. 10.16)
Carcinoid Tumor
• Neuroendocrine tumor that is uncommon in adults but the most

common primary intrabronchial tumor in children
• Location
○○ 80% occur centrally, where they can cause post-obstructive
changes distally
○○ 20% occur peripherally and present as a solitary pulmonary nod-
ule (see Fig. e10.27)
Fig. 10.16 Large cell tumor. Well-defined peripheral mass in the right lower
lung [1]
• Major types
○○ “Typical” (low grade) – well differentiated, tends to grow slowly,
rarely metastasizes, and has an excellent prognosis (5-year sur-
vival >90%)
○○ “Atypical” (aggressive) – about 10% of carcinoids, which tend to
arise peripherally, often develop associated lymphadenopathy
and distant metastases, and have a poor prognosis (5-year sur-
vival of 50–70%)
• Carcinoid syndrome is rare with bronchial carcinoid tumors (only
if they have metastasized to the liver)
Imaging
• Central carcinoid appears as a hilar mass, which may produce asso-

ciated atelectasis or post-obstructive pneumonia (Fig. 10.17)
• Atypical tumors often show necrosis within the peripheral mass
(Fig. e10.28)
Fig. 10.17 Carcinoid tumor. Right hilar mass (arrow) in the lateral aspect of
the right main bronchus in a young woman with hemoptysis
Lung Cancer 135
Pancoast (Superior Sulcus) Tumor
• Non-small cell lung cancer arising at the extreme apex of the lung
• Represents about 5% of bronchogenic carcinomas (primarily squa-
mous cell)
• Frequently invades the chest wall, upper ribs, vertebral bodies, and
soft tissues of the thoracic inlet (subclavian vessels and brachial
plexus)
• Classically associated with Horner’s syndrome – ipsilateral ptosis
(drooping eyelid), miosis (constricted pupil), and anhidrosis (loss
of sweating)
Imaging
• Apical mass, often associated with destruction of adjacent ribs and

best seen on apical lordotic views (Fig. 10.18)
• In the absence of bone destruction, the tumor may be identified
only by asymmetry of presumed apical pleural thickening (>5 mm)
that has a convex margin (especially if increased since previous
studies) (Fig. 10.19)
• This appearance must be differentiated from apical pleural thicken-
ing related to old tuberculous disease, which has a concave margin
that parallels the adjacent ribs
a b
Fig. 10.18 Pancoast tumor. (a) Subtle area of increased opacification in the
left apical region (arrow), best identified by comparing similar levels of the
lungs on both sides. (b) Coronal CT clearly shows the irregular malignant lesion
invading the chest wall and mediastinum (arrow)
Fig. 10.19 Pancoast tumor. Increased opacification in the right apex (arrow).
Although this may simulate benign apical pleural thickening, the marked
asymmetry and irregularity should suggest the diagnosis of Pancoast tumor [1]
Metastases to the Lungs
Depending on the mode of spread to the lungs, metastases are divided
into three types: hematogenous, lymphangitic, and direct spread.
Hematogenous Spread
• Developing in up to one-third of patients with cancer, hematoge-

nous metastases are usually asymptomatic and only detected inci-
dentally during staging or follow-up of patients with a known
malignancy
• Malignancies that commonly spread hematogenously to the lung
are breast, colorectal, renal, bladder, testicular, head and neck, and
thyroid cancers, melanoma, and soft-tissue sarcomas
• Although usually multiple (Fig. 10.20), in about 10% of cases, a
metastasis may present as a solitary pulmonary nodule
• Metastases most likely to cavitate are squamous cell cancers of the
head and neck in men and the cervix in women, adenocarcinomas
of the large bowel, and sarcomas (see Fig. e10.29)
• Multiple large metastases (cannonball) usually result from tes-
ticular cancer in men or choriocarcinoma in women (Fig. 10.21)
Metastases to the Lungs 137
Fig. 10.20 Hematogenous metastases. Multiple, well-circumscribed nodules

scattered diffusely throughout the lungs [1]
Fig. 10.21 Cannonball metastases in choriocarcinoma [1]

Fig. 10.22 Osteosarcoma metastases. Multiple dense lesions bilaterally [1]
• Densely opaque metastases are virtually diagnostic of osteosar-

coma (which also can present with pneumothorax) (Fig. 10.22)
Imaging
• Single or multiple, well-defined nodules with smoother margins

than primary bronchogenic carcinoma
• Radiography
○○ Preferred screening technique (detects most metastases >15 mm
in diameter)
○○ May fail to detect smaller nodules (because of overlying ribs or
blood vessels) and nodules in specific areas (lung apices, inferior
recesses just above the dome of the diaphragm, subpleural region)
• CT (see Figs. e10.30–e10.32)
○○ Highly sensitive for detecting small discrete nodules, which have
a peripheral and basal predominance when limited in number but
a uniform distribution when there are innumerable lesions
○○ Ground-glass halos can reflect perilesional hemorrhage in metas-
tases from vascular tumors (melanoma, renal cell carcinoma,
choriocarcinoma, angiosarcoma)
• Radionuclide thyroid scan
○○ Strong uptake of I-131 is highly specific and much more sensi-
tive than chest radiographs for detecting metastases of papillary
or follicular thyroid cancer (medullary and anaplastic thyroid

carcinomas do not concentrate radioactive iodine)
• PET
○○ Many pulmonary metastases are FDG avid (SUV > 5 indicates
an aggressive neoplasm with a poor prognosis)
○○ Can identify the site of an unknown primary in almost 50% of cases
○○ False positive – active inflammatory or granulomatous processes;
primary lung malignancy
○○ False negative – small metastases (<1 cm) and those from low-
grade lung cancers (adenocarcinoma in situ, carcinoid) and
extrathoracic primaries that may have low FDG avidity (renal,
hepatic, testicular, mucinous adenocarcinomas of the breast and
gastrointestinal tract)
Indications for CT if chest radiograph is normal
• High propensity of tumor spread to the lung (such as melanoma,
testicular carcinoma, choriocarcinoma, head and neck tumors)
• Presence of metastases would alter treatment (usually by cancella-
tion of planned extensive surgery)
○○ Radical amputation for osteosarcoma
○○ Extensive lymph node dissection for melanoma
○○ Lobectomy or radiofrequency ablation for presumed solitary
metastasis or several small (<5) nodules
• Effective therapy available for metastases (osteogenic sarcoma,
choriocarcinoma, nonseminomatous testicular tumors, renal cell
carcinoma, certain functioning thyroid carcinomas)
• Detection of pulmonary metastases is of no clinical significance if
there is no effective treatment for metastases or if there already are
obvious extrathoracic metastases
Lymphangitic Spread
• Occurs most commonly with carcinomas of the colon, breast, lung,

stomach, and pancreas
• Usually results from hematogenous spread to the lung with subse-
quent interstitial and lymphatic invasion but can reflect direct lym-
phatic spread of tumor from mediastinal and hilar lymph nodes
• Bad prognosis, since usually a sign of end-stage disease (high
1-year mortality rate)
Imaging
• On radiographs, diffuse reticular or reticulonodular pattern that

predominantly involves the lung bases and is more common on the
right (Fig. 10.23; see Fig. e10.33)
○○ Septal lines mimicking interstitial pulmonary edema
○○ Bilateral enlargement of hilar or mediastinal lymph nodes (uni-
lateral distribution suggests bronchogenic carcinoma as the pri-
mary tumor)
○○ Pleural effusion in more than half of cases
○○ Imaging appearance may be difficult to distinguish from pulmo-
nary edema
• CT (Fig. 10.24; see Figs. e10.34–e10.36)
○○ Smooth or nodular thickening (“beaded chain” pattern) of the
peribronchovascular interstitium, interlobular septa, and fissures
○○ Nevertheless, generally preservation of normal lung architecture
at the lobular level
○○ Abnormalities frequently identified on CT in patients with nor-
mal chest radiographs (which do not well visualize the periph-
eral lung regions where involvement tends to occur)
Fig. 10.23 Lymphangitic metastases (breast carcinoma). Coarsened broncho-

vascular markings of irregular contour and poor definition that primarily involve
the right lower lung. Note the septal (Kerley) lines and left mastectomy [1]
Fig. 10.24 Lymphangitic metastases. Nodular thickening of the interlobular

septa (curved arrow) and interlobar fissures (straight arrows) [1]
Direct Spread (Fig. 10.25)
• Least common form of metastases to the lung

• Most frequently by direct invasion by a primary neoplasm of a con-
tiguous organ or structure (thyroid, esophagus, thymus, chest wall)
or spread from a neoplasm metastatic to another intrathoracic struc-
ture (rib or mediastinal lymph node)
• Direct extension also can occur through a vascular route, such as
the spread of renal cell cancer or testicular germ cell cancer as a
tumor thrombus to the lung via the inferior vena cava and the right
side of the heart
Fig. 10.25 Esophagorespiratory fistula. Direct communication between the

esophagus and bronchial tree (arrowheads), which developed by direct spread
from esophageal carcinoma
Lymphoma
• Involvement of the pleura and parenchyma usually occurs by direct

extension from mediastinal nodes along the lymphatics of the bron-
chovascular sheaths
• At times, it may be difficult to distinguish a superimposed infection
after radiation therapy or chemotherapy from the continued spread
of lymphomatous tissue
• However, any alveolar lung infiltrate in a patient with known lym-

phoma is more likely to represent an infectious than a lymphoma-
tous process
• Primary pulmonary lymphoma is rare and presents as single or
multiple, ill-defined homogeneous masses that rarely obstruct the
bronchial tree and thus almost invariably contain an air broncho-
gram (when most or all of a segment or lobe is involved, the appear-
ance may simulate acute pneumonia)
Imaging
• Patchy areas of parenchymal infiltrate that may coalesce to form a

large homogeneous nonsegmental mass (Fig. 10.26)
• May be multiple nodules with a bronchovascular and subpleural dis-
tribution (especially in the mid- and lower lungs) (see Fig. e10.37)
• Extensive dystrophic calcification of lymph nodes occurs in about 20%
of patients after radiation therapy or chemotherapy (see Fig. e10.38)
Fig. 10.26 Lymphoma. Secondary involvement in a patient with known non-

Hodgkin lymphoma shows marked nodular peribronchovascular thickening and
consolidation, in some areas demonstrating surrounding ground-glass opacity.
Clusters of nodules in both lungs (arrows) closely parallel the bronchovascular
structures [4]
Kaposi’s Sarcoma
• Most common AIDS-related multicentric neoplasm

• About one-third of AIDS patients, almost all of whom are homo-
sexual or bisexual men, have pulmonary involvement, though this
becomes clinically apparent in only 15%
• Propensity to involve the skin, lymph nodes, gastrointestinal tract,
and lungs
• Pulmonary manifestations are rare in the absence of cutaneous
involvement
Imaging (Fig. 10.27; see Fig. e10.39)
• Irregular (“flamed-shaped”) and ill-defined peribronchovascular

nodules and consolidations, combined with peribronchovascular
and interlobular septal thickening and pleural effusions
• Enhancing hilar/mediastinal lymphadenopathy (related to the
hypervascularity of Kaposi’s sarcoma)
• May be ground-glass attenuation (representing localized hemor-
rhage) around the periphery of lung nodules and masses
• Radionuclide gallium scan
○○ Kaposi’s sarcoma is not isotope avid (unlike lymphoma and pul-
monary infections)
○○ Therefore, diffuse parenchymal opacifications in an HIV-positive
patient that do not show gallium avidity likely represent Kaposi’s
sarcoma
Fig. 10.27 Kaposi’s sarcoma. Innumerable, bilateral, poorly defined peri-

bronchovascular micronodules, some of which exhibit coalescence [5]
Sequestration (Fig. 10.28)
• Area of aberrant, nonfunctioning lung that has no normal connec-

tion to the bronchial tree or pulmonary arteries and receives its
blood supply from the aorta or other systemic artery (usually detect-
able on contrast CT or MRI)
• Intralobar
○○ More common type (75%) and contained within the substance of
the lung (enclosed within the visceral pleura)
○○ Drains via the pulmonary veins
○○ Primarily involves the posterior basal segment (about two-thirds on
the left) and almost invariably arises contiguous to the diaphragm
○○ Presents in an adolescent or adult
○○ Often asymptomatic, though may present with recurrent pulmo-
nary infections (may develop secondary to chronic infection)
a b
Fig. 10.28 Sequestration. (a) Coronal CT shows a lobulated soft-tissue mass

at the right base medially (arrows). (b) Contrast study shows that the mass is
supplied by an artery (arrows) that arises directly from the aorta. (Courtesy of
Ritu Gill, MD, Boston)
Imaging
○○ Round, oval, or triangular mass or area of consolidation that typ-

ically is well circumscribed, occurs in a posterior-basal segment
of a lower lobe, and is contiguous with the diaphragm
○○ Usually contains air
○○ May appear as a thin- or thick-walled cystic mass (often multi-
locular) when a communication is established with contiguous
lung (usually the result of infection)
• Extralobar
○○ Enclosed within its own pleural layer (therefore seldom infected
or air containing)
○○ Drains via systemic veins (azygos system or inferior vena cava)
and usually receives its blood supply from the abdominal aorta
○○ About 90% are found in the left hemithorax, generally in close
proximity to the posteromedial aspect of the hemidiaphragm
○○ Typically presents during infancy (predominantly in males) and
is considered a congenital anomaly
References
2. Franquet E. Pneumonia. Semin Roentg. 2017;52:27–34.
the lung. AJR. 2013;200:712–28.
4. Bligh MP, Borgaonkar JN, Burrell SC, et al. Spectrum of CT findings in tho-
racic extranodal non-Hodgkin lymphoma. Radiographics. 2017;27:439–61.
5. Restropo CS, Martinez S, Lemos JA. Imaging manifestations of Kaposi’s
sarcoma. Radiographics. 2002;22:1169–85.
6. MacMahon H, Naidich DP, Goo JM, et al. Guidelines for management of
incidental pulmonary nodules detected on CT images: from the Fleischner
Society 2017. Radiology. 2017;284:228–43.
Pleural Neoplasms
11
Mesothelioma
• Most common primary tumor of the pleura (though a rare lesion

and much less frequent than pleural metastases)
• Primarily involves men age 50–70
• Related to asbestos exposure in about 80% of cases (latency time of
30–45 years)
• Lifetime risk of an asbestos worker developing mesothelioma is
about 10%
• Although surgery may be performed in patients with limited dis-
ease, mesothelioma is almost always fatal (mean survival time
<1 year)
Imaging
• An important distinction from metastases is that mesotheliomas are

always unilateral (Fig. 11.1), whereas metastases are frequently
bilateral (Fig. 11.2), and there generally is volume loss of the
affected hemithorax


https://doi.org/10.1007/978-3-030-16826-1_11
148 11 Pleural Neoplasms
Fig. 11.1 Mesothelioma. Extensive nodular pleural thickening with strictly

unilateral distribution (arrows) [1]
a b
Fig. 11.2 Pleural metastases (neuroendocrine lung carcinoma). (a) Two

large pleural masses with underlying rib lesions in the right apex and left upper
lung. (b) Coronal CT image demonstrates both metastases and clearly shows
destruction of the left sixth rib
• Radiographs (Fig. 11.3; see Fig. e11.1)

chapter’s website on SpringerLink: https://doi.org/10.1007/
978-3-030-16826-1_11)
○○ Diffuse irregular or nodular pleural thickening
○○ Coexisting calcified pleural plaques (20–50%) suggest asbestos
exposure
○○ Large pleural effusion may be the only finding (obscuring the
underlying neoplasm)
Metastases 149
Fig. 11.3 Diffuse pleural mesothelioma. Multiple masses thicken the right
pleura (arrows) in an elderly man with asbestos exposure [2]
• CT and MRI (see Fig. e11.2)

○○ Superior to radiography for precisely demonstrating tumor infil-
tration of other structures, such as the thoracic wall, vertebra,
mediastinum, diaphragm, and contralateral pleura, as well as dis-
tant metastases (all of which preclude surgical resection)
Metastases
• The pleura is a common site of metastases, especially from primary

adenocarcinomas
• Metastases may reach the pleura by hematogenous, lymphatic, or
direct spread
• Most commonly due to bronchogenic carcinoma (about 40%);
breast carcinoma and lymphoma are other major causes
• Pleural metastases are the second most common cause of pleural
effusion in adults (the first is left heart failure)
Imaging (Fig. 11.4; see Figs. e11.3–e11.7)
• Pleural effusion is the most common imaging finding

• Other manifestations include diffuse or focal nodular pleural thick-
ening, discrete mass, or circumferential pleural thickening with
infiltration into adjacent tissues
Fig. 11.4 Pleural metastases (bronchogenic carcinoma). Diffuse pleural

thickening is seen along the upper left chest wall (arrows). Elevation of the left
hemidiaphragm reflects involvement of the phrenic nerve and post-obstructive
atelectasis secondary to the left perihilar lesion [2]
• Metastatic deposits are often too small to be seen on chest radio-

graphs, and CT is far more sensitive for their detection
• PET-CT can distinguish benign from malignant pleural thickening
and effusion by demonstrating high FDG-uptake in the latter
Fibrous Tumor of the Pleura
• Uncommon pedunculated mesenchymal lesion with a variable

microscopic appearance and unpredictable biologic behavior
• Although most are benign, about 20% are aggressive with more
malignant features
• No association with asbestosis
• A classic, but rare, condition associated with benign fibrous tumor
of the pleura includes hypoglycemia and hypertrophic osteoar-
thropathy (Pierre-Marie-Bamberger Syndrome)
• Fibrous tumor should be included in the differential diagnosis of
any unilateral pleural lesion that shows gradual, but slow, growth
over many years
Pleural Lipoma 151
Fig. 11.5 Benign fibrous tumor of the pleura. Huge, homogeneous soft-tis-
sue mass (arrows) arising from the mediastinal pleura and projecting into the
right hemithorax [2]
Imaging
• Radiographs (Fig. 11.5)
○○ Solitary, peripheral, mobile (if attached to the visceral pleura by
a pedicle), sharply defined, and homogeneous nodule or mass
○○ Characteristic tail pointing to the hilum suggests an intrapleural
or fissural location
○○ May grow to huge size (often >7 cm in diameter)
○○ Malignant forms may demonstrate calcification and effusion
• CT
○○ Homogeneous attenuation in small tumors (see Fig. e11.8)
○○ Larger lesions tend to have more heterogeneous attenuation related
to areas of necrosis, hemorrhage, and cystic change (see Fig. e11.9)
○○ Almost all demonstrate contrast enhancement
Pleural Lipoma
• Most common benign tumor of the pleura

• Generally asymptomatic and discovered incidentally on imaging
for a different reason
Fig. 11.6 Pleural lipoma. Mediastinal window shows a smoothly marginated

mass with fat attenuation in the apex of the right lung [1]
• Usually well circumscribed and composed uniformly of fat on CT

and MRI (Fig. 11.6)
• If the mass contains an enhancing soft-tissue component, must con-
sider liposarcoma
References
1. Hussein-Jelen T, Bankier AA, Eisenberg RL. Solid pleural tumors. AJR.
2012;198:W512–20.
the lung. AJR. 2013;200:712–28.
Emphysema
12
• Abnormal permanent enlargement of air spaces distal to the termi-

nal bronchioles, accompanied by destruction of alveolar walls
• No obvious fibrosis except in end-stage disease, when it reflects a
reparative response
• Presenting symptoms include gradually progressive exertional dys-
pnea, productive cough, and abnormal pulmonary function tests
Centrilobular Emphysema (Fig. 12.1)
• Enlargement and destruction of alveoli in the central portion of the

secondary pulmonary lobule
• Strong association with cigarette smoking (severity of emphysema
increases with the number of cigarettes smoked)
• Upper lobe predominance


https://doi.org/10.1007/978-3-030-16826-1_12
154 12 Emphysema
Fig. 12.1 Centrilobular emphysema. (a, b) Multiple areas of low attenuation

(arrows) surrounded by normal parenchyma, grouped around the center of
secondary pulmonary lobules in the upper lobes [1]
Panlobular (Panacinar) Emphysema (Fig. 12.2)
• Enlargement and destruction of alveoli throughout the entire sec-

ondary pulmonary lobule
• Lower lobe predominance
• Often associated with alpha-1 antitrypsin deficiency
Paraseptal Emphysema 155
Fig. 12.2 Panlobular emphysema. Severe destruction of alveoli in both lower

lobes in a patient with alpha-1 antitrypsin deficiency
a b
Fig. 12.3 Paraseptal emphysema. (a, b) Destruction of lung parenchyma

with distinct bullous changes (arrows) that predominate in the subpleural
regions of the upper lobes [1]
Paraseptal Emphysema (Fig. 12.3)
• Focal or multifocal involvement of the periphery of the secondary

pulmonary lobule (least common form)
• Predominance in the periphery of the lung (along the fissures and
pleural reflections)
• Common causes include cigarette smoking, occupational disorders,
and alpha-1 antitrypsin deficiency
• Coalescence of emphysematous areas and the formation of bullae
in the subpleural region can lead to pneumothorax
156 12 Emphysema
Imaging
• Radiographs
○○ Hyperexpansion of the lungs (Fig. 12.4)
• Flattened or concave hemidiaphragms, especially on lateral
view
• Increased AP diameter of the chest
• Increased retrosternal clear space
○○ Lung destruction (generalized hyperlucency of the lungs with
marked attenuation and stretching of pulmonary vessels and the
presence of blebs/bullae, especially in the apices and subpleural
regions) (see Fig. e12.1)
978-3-030-16826-1_12)
○○ Often evidence of pulmonary arterial hypertension (enlargement
of central pulmonary arteries with rapid peripheral tapering) (see
Fig. 9.8)
○○ The heart tends to be small and relatively vertical (Fig. 12.4a)
a b
Fig. 12.4 Emphysema. (a) Severe hyperexpansion of the lungs with flattening
of the hemidiaphragms. Note the vertical appearance of the thin cardiac silhou-
ette. (b) Lateral radiograph also shows enlargement of the retrosternal air space
and a barrel chest. (Heilman/Wikimedia)
Bullous Disease 157
○○ Saber-sheath trachea (striking decrease in the coronal diameter

and increase in its sagittal diameter) (see Figs. 17.2 and e17.6)
○○ Once the diagnosis of emphysema is established, repeat chest
radiographs are indicated ONLY if there is clinical evidence of
supervening disease (e.g., infection, congestive heart failure)
• CT
○○ Far more sensitive and specific than chest radiographs for the
diagnosis of emphysema
○○ Initially, scattered, round or oval, low-attenuation areas within
the lung (<1 cm) that are easily separable from surrounding nor-
mal parenchyma despite the absence of clearly definable walls
(see Figs. e12.1 and e12.2)
○○ These cyst-like structures often contain a small “dot,” which rep-
resents the normal lobular artery
○○ With progression, whole zones of the lung become lucent, and
there is often a decrease in the number and caliber of associated
blood vessels
○○ Frequent secondary findings include subpleural blebs and bullae
and hyperinflated lungs (see Fig. e12.3)
○○ Large bullae can compress and distort the underlying paren-
chyma, sometimes into bizarre configurations (see Fig. e12.4)
○○ Can differentiate between:
• Centrilobular emphysema (lucencies scattered throughout the
lung parenchyma)
• Paraseptal emphysema (lucencies located in the subpleural
regions and adjacent to the interlobar fissures)
○○ Helpful in the preoperative assessment of potential candidates
for lung volume reduction surgery as treatment for upper lobe-
predominant emphysema (i.e., areas that contribute little to pul-
monary function but adversely affect respiratory mechanics)
Bullous Disease
• Blebs and bullae are sharply defined, air-containing spaces that are
bounded by curvilinear, hairline shadows
• According to the Fleischner Society Glossary of Terms for Thoracic
Imaging, a “bleb” is a cystic space ≤l cm in diameter; anything
larger than this is defined as a “bulla” (which can reach substantial
size and occupy an entire lobe)
158 12 Emphysema
• Blebs and bullae are commonly seen in both upper lobes in patients
with coexisting centrilobular or paraseptal emphysema
• Most commonly occur in young men, who usually are smokers
• In patients with a single huge bulla or recurrent pneumothoraces,
surgical bullectomy can improve pulmonary function or even be
curative (not effective in patients with severe generalized
emphysema)
Imaging
• Single or multiple, thin-walled, sharply demarcated, air-filled avas-

cular spaces in the lung that most commonly occur in the upper
lobes (see Figs. e12.5 and e12.6)
• At times, the very thin wall of a large bulla may not be apparent on
radiographs, and its presence can only be inferred by seeing a sub-
stantial portion of the lung with minimal lung markings
• If infected, bullae may present as cystic masses with air-fluid levels
(see Fig. e12.7)
Alpha-1 Antitrypsin Deficiency
• Inherited disorder (autosomal recessive) in which there are low lev-

els of alpha-1 protease inhibitor, a protein that prevents the damag-
ing effects of elastases released by macrophages and neutrophils
• Patients who are homozygous for this disorder have a 20% risk of
developing emphysema (cigarette smoking significantly increases
the rapidity of deterioration of pulmonary function)
• Panlobular emphysema that predominantly involve the lower lobes

(rather than the upper zones, as in conventional emphysema)
• Uniform involvement of the entire secondary lobule (no visualiza-
tion of the central arteriole and bronchiole, which are seen in cen-
trilobular emphysema)
References 159
Congenital Lobar Emphysema
• More accurately termed congenital lobar overinflation, it usually

occurs in infants or young children, most commonly in males and
involving the left upper lobe
• Progressive overdistention of a lobe probably results from bron-
chial obstruction with poststenotic air trapping, related to a one-
way, ball-valve mechanism
• Occasionally discovered incidentally in adults
Imaging
• Overinflation leads to hyperlucency of the involved lobe, which

may be associated with atelectasis and mediastinal shift (see Fig.
e12.9)
References
the lung. AJR. 2013;200:W222–37.
2. Eisenberg RL, Johnson NM. Comprehensive Radiographic Pathology. 6th ed.
St. Louis: Elsevier/Mosby; 2016.
3. Cantin L, Bankier AA, Eisenberg RL. Multiple cystlike lung lesions in the
adult. AJR. 2010;194:W1–W11.
Pulmonary Fibrosis
13
Chronic
Usual Interstitial Pneumonia (UIP)
• Most commonly seen in patients with idiopathic pulmonary fibrosis

(IPF)
• Also may occur with asbestosis, connective tissue disorders (espe-
cially rheumatoid arthritis and scleroderma), chronic hypersensitiv-
ity, and drug toxicity
• Insidious development of respiratory symptoms (primarily dyspnea
and nonproductive cough), which are similar to NSIP but affect an
older population (>age 50)
• History of cigarette smoking appears to be a risk factor for the
development of IPF, but does not seem to affect the course of the
disease
• Increased incidence of lung cancer (develops in 10–15% of patients
with IPF)

doi.org/10.1007/978-3-030-16826-1_13) contains supplementary m aterial, which

https://doi.org/10.1007/978-3-030-16826-1_13
162 13 Pulmonary Fibrosis
Imaging (Figs. 13.1 and 13.2; see Figs. e13.1, e13.2, e13.4–e13.6)

978-3-030-16826-1_13])
a b
Fig. 13.1 Severe diffuse interstitial fibrosis. (a, b) Coarse reticular pattern
indicating pronounced fibrosis. Intervening small areas of lucency produce the
appearance of honeycomb lung, especially in the right upper lobe [1]
Fig. 13.2 Usual interstitial pneumonia. Reticular opacities, moderate

ground-glass opacities, traction bronchiectasis, and basilar honeycombing [3]
Chronic 163
• Reticular pattern with traction bronchiectasis and extensive macro-

cystic honeycombing, which has a striking basilar and subpleural
distribution
• Progressive volume loss and disorganized pulmonary architecture
in advanced disease (highly specific for UIP)
• Ground-glass opacities are present in a majority of patients but
generally are limited in extent and rarely a prominent component
(unlike NSIP)
• Progression of these opacities to honeycombing is common and
indicates irreversible fibrosis
Nonspecific Interstitial Pneumonia (NSIP)
• Gradual development of respiratory symptoms (primarily dyspnea

and nonproductive cough), which is similar to UIP but usually
milder and affects a younger population (age 40–50)
• No relationship with cigarette smoking
• Two basic subtypes depending on the histologic infiltration of
alveolar septa:
○○ Cellular – inflammatory cells (plasma cells, lymphocytes); less
common, but much better response to steroids and more favor-
able prognosis
○○ Fibrotic – homogeneous septal thickening resulting from fibro-
sis; much poorer prognosis
• Although often idiopathic, NSIP tends to develop in patients with
connective tissue disorders (especially scleroderma, polymyositis,
and dermatomyositis)
• Other conditions causing NSIP include hypersensitivity pneumonia,
occupational exposure, and drug-induced lung disease
• Predominantly affects the middle and lower lungs

• Bilateral, relatively symmetric patchy areas of ground-glass opaci-
ties combined with irregular reticular opacities and scattered
micronodules
• Subpleural sparing is highly suggestive of NSIP and virtually
excludes UIP
• In advanced disease, associated areas of traction bronchiectasis and
consolidation
Fig. 13.3 Nonspecific interstitial pneumonia. Bilateral diffuse ground-glass

attenuation with inter- and intralobular lines (crazy-paving pattern) in a patient
on amiodarone therapy. Note the traction bronchiectasis [1]
Table 13.1 UIP vs. NSIP UIP NSIP

Honeycombing Yes No
Smoking-related Yes No
Peripheral/subpleural Yes No
distribution
Association with connective Some Yes
tissue disorders
Prognosis Poor Good
• May demonstrate the crazy-paving pattern

• Microcystic honeycombing (much less extensive than in UIP)
• May demonstrate findings consistent with underlying connective
tissue disease (pleural and pericardial effusion, soft-tissue calcifi-
cation, esophageal dilatation) (see Table 13.1)
Acute and Subacute
Cryptogenic Organizing Pneumonia (COP)
• Chronic inflammatory lung disease with peripheral air-space opac-

ities that increase over several weeks despite antibiotic therapy
Acute and Subacute 165
• Formerly known as bronchiolitis obliterans organizing pneumonia

(BOOP), the histologic finding is granulation tissue polyps within
the alveolar ducts and bronchial lumens that leads to inflammatory
intra-alveolar exudates and fibroblast proliferation
• Usually idiopathic but can occur as a reaction to bacterial or espe-
cially viral pneumonia, drug toxicity (bleomycin, gold salts, cyclo-
phosphamide, methotrexate), inhalation of toxic fumes, and lung
and bone marrow transplantation or as a complication of connec-
tive tissue disorder
• No association with cigarette smoking
• Most patients are 50–60 years of age with a history of a flu-like ill-
ness followed by about 3 months of cough, exertional dyspnea,
malaise, fever, and weight loss
• Diagnosis is usually confirmed by surgical biopsy or bron-
choalveolar lavage, and there is generally a good response to
steroid therapy (though there may be recurrence after treatment
stopped)
• Radiographs
○○ Patchy bilateral (occasionally unilateral) air-space consolida-
tions that resemble an active pneumonia but actually reflect intra-
alveolar fibroblast proliferation that may be associated with a
prior respiratory infection
○○ Usually subpleural, predominantly involving the lower lungs.
○○ About half of patients have small nodules
• CT
○○ Findings are far more than expected from chest radiographs
○○ Characteristic peripheral or peribronchial distribution with a
basilar predominance
○○ Lung abnormalities vary from ground-glass opacities to consoli-
dation (which may contain air bronchograms and cylindrical
bronchial dilatation)
○○ These tend to change location and size (sometimes involving an
entire lobe), even without treatment
Fig. 13.4 Cryptogenic organizing pneumonia (drug toxicity). (a) Diffuse

bilateral, subpleural areas of opacification. The large consolidation runs along
the minor fissure. (b) In another patient, there are diffuse areas of consolidation
containing air bronchograms. (MBq/Wikimedia)
Acute Interstitial Pneumonia (AIP)
• Only idiopathic interstitial lung disease with acute onset of symp-

toms (often a history of prior viral-like illness) and has the poorest
prognosis
• Most patients develop severe dyspnea with a need for mechanical
ventilation within 3 weeks
• Diffuse alveolar damage (caused by destruction of surfactant) with
rapidly progressing alveolar edema and hemorrhage is similar to the
appearance of acute respiratory distress syndrome (ARDS)
Smoking-Related 167
• Diffuse, bilaterally symmetric distribution of ground-glass opaci-

ties (typically a lower lobe predominance, unlike ARDS)
• Costophrenic angles are often spared
• Areas of consolidation are usually less extensive and limited to the
dependent regions of the lung
• In the late fibrotic phase, there is architectural distortion, traction
bronchiectasis, and honeycombing that are more severe in the non-
dependent areas of the lung
Fig. 13.5 Acute interstitial pneumonia (nitric acid inhalation). Extensive

bilateral air-space opacities with sparing of the medial and lateral costophrenic
angles [3]
Smoking-Related
Respiratory Bronchiolitis-Interstitial Lung Disease (RB-ILD)
• Smoking-related interstitial lung disease that represents the symp-

tomatic form of respiratory bronchiolitis
• With desquamative interstitial pneumonia, RB-ILD is considered
to be part of the spectrum of severity of interstitial lung disease
induced by cigarette smoking
• Develops primarily in men (especially age 30–50) and almost always in
individuals who are heavy smokers, especially of unfiltered cigarettes
Imaging (Fig. 13.6)
• Centrilobular nodules (3–5 mm) with patchy ground-glass opaci-

ties and bronchial wall thickening that predominantly involve the
upper lobes, especially on the right
• Commonly associated with centrilobular emphysema, though usu-
ally no signs of fibrosis
a b
Fig. 13.6 Respiratory bronchiolitis-interstitial lung disease. (a) Small nod-

ules and patchy areas of ground-glass opacities bilaterally. (b) After the cessa-
tion of smoking, there has been substantial clearing. (Courtesy of Jennifer Ni
Mhuircheartaigh, MD, Boston)
Desquamative Interstitial Pneumonia (DIP)
• Almost always occurs in cigarette smokers and is considered to

represent the most severe end of the spectrum of smoking-related
interstitial diseases, which includes pulmonary Langerhans cell
histiocytosis and RB-ILD
• May also develop in nonsmokers related to lung infections, expo-
sure to organic dust, and various drugs (nitrofurantoin, busulfan,
sulfasalazine)
• Primarily affects men age 30–40 years
• Alveolar spaces between bronchioles filled with macrophages
Imaging
• Patchy or diffuse ground-glass pattern, usually with peripheral and

lower lung predominance (see Fig. e13.12)
• Often patchy or generalized reticulonodular appearance with small
cystic spaces (related to fibrotic changes) (Fig. 13.7)
Smoking-Related 169
Fig. 13.7 Desquamative interstitial pneumonia. Diffuse reticulonodular pat-

tern indicating interstitial disease, combined with bibasilar air-space consolida-
tion that obscures the borders of the heart [1]
Pulmonary Langerhans Cell Histiocytosis (PLCH)
• Uncommon idiopathic disorder (formerly known as eosinophilic

granuloma or histiocytosis X), which is characterized histologi-
cally by a benign granulomatous infiltration of mature histiocytes
• PLCH occurs almost exclusively in smokers (young adults and
middle aged), probably representing an allergic reaction to ciga-
rette smoke in certain individuals
• Pneumothorax is a common presenting complaint (this complica-
tion occurs in up to 25% of patients with PLCH and is often bilat-
eral and recurrent)
• Stopping smoking leads to clinical improvement
Imaging
• Initially, multiple small (1–10 mm), indistinct granulomatous nod-

ules that have a peribronchiolar or centrilobular distribution and an
upper lobe predominance (Fig. 13.8)
• Progressive cavitation of the nodules eventually results in thick-
walled and then thin-walled cysts (see Figs. e13.13 and e13.14)
• Cysts may have bizarre shapes with little normal intervening lung
(unlike the round and uniform cysts in lymphangioleiomyomato-
sis) (Fig. 13.9)
• Upper lobe predominance (unlike the diffuse involvement in
lymphangioleiomyomatosis) and sparing of the costophrenic angles
Fig. 13.8 Pulmonary Langerhans cell histiocytosis. (a, b) Diffuse and innu-
merable microcystic changes [4]
References 171
Fig. 13.9 Pulmonary Langerhans cell histiocytosis. Innumerable thick-

walled cysts of various size with bizarre branching configurations [1]
References
2. Cantin L, Bankier AA, Eisenberg RL. Bronchiectasis. AJR. 2009;193:
W158–71.
the lung. AJR. 2013;200:712–28.
the lung. AJR. 2013;200:W222–37.
Inhalational Diseases
14
Pneumoconioses
• Generic term for occupational disorders related to the repeated

inhalation and retention of small particles in the lung
• More than 100 conditions have been described, of which only a few
will be covered in this section
• Most inhalational diseases predominantly involve the upper lobes,
because the particles are better cleared by the higher blood flow and
lymphatic drainage in the lower lobes (see Fig. e14.1)
(All electronic images (Figs. e14.1–e14.17) can be found
on this chapter’s website on SpringerLink: https://doi.org/
10.1007/978-3-030-16826-1_14)
• The one major exception is asbestosis, which predominantly affects
the lower lobes since the inhaled particles are too large to be
removed by alveolar macrophages and the lymphatic system


https://doi.org/10.1007/978-3-030-16826-1_14
174 14 Inhalational Diseases
Silicosis
• Irreversible occupational lung disease due to chronic inhalation of

dust containing crystalline silica or silicon dioxide, which deposits
in the alveoli, is taken up by macrophages and incites a diffuse
inflammatory reaction that leads to lung fibrosis and emphysema
• Silica exposure most often occurs in people who are employed in
construction, mining, sandblasting, stonecutting, tunneling, and the
manufacture of abrasives, as well as those who work with glass,
pottery, and on railroads
• Most who develop the disease are men over age 50, who have had
at least 20 years of exposure
• Some affected individuals are asymptomatic (simple silicosis),
while those with more severe disease (complicated silicosis) pres-
ent with cough, dyspnea, and increased sputum (black sputum in
coal workers)
Imaging
• Small, well-circumscribed, round nodules (1–10 mm) that predom-

inantly involve the posterior portions of the upper lungs and may
calcify (Figs. 14.1 and 14.2; see Fig. e14.2)
• Hilar and mediastinal lymphadenopathies are common, with char-
acteristic peripheral “eggshell” calcification of the enlarged nodes
virtually pathognomonic of silicosis (though it occasionally can
also occur in sarcoidosis and treated lymphoma) (Fig. 14.3; see
Fig. e14.3)
• The parenchymal pulmonary nodules increase in size and number
as the disease advances, eventually forming nonsegmental con-
glomerate masses (>1 cm) known as progressive massive fibrosis
(PMF), which are usually irregular and ill-defined with peripheral
stranding (Fig. 14.4; see Figs. e14.4 and e14.5)
• PMF is generally symmetric and located in the upper lobes or supe-
rior segments of the lower lobes, tending to progressively migrate
toward the hilum as the fibrotic process progresses
• The coalescent masses may undergo ischemic changes and cavi-
tate, serving as a breeding ground for superimposed infection
Silicosis 175
Fig. 14.1 Silicosis. Multiple small, well-circumscribed military nodules [2]
Fig. 14.2 Silicosis. Upper lobe distribution of small nodules [1]
• Coal workers’ pneumoconiosis (CWP) – similar imaging appear-

ance but caused by the inhalation of coal dust that does not contain
silica (see Figs. e14.6 and e14.7)
• Caplan syndrome – refers to patients with rheumatoid arthritis who
also have CWP (more common) or silicosis
Fig. 14.3 Silicosis. Diffuse eggshell calcifications are well seen on this tomo-
graphic view [3]
Fig. 14.4 Silicosis. Progressive massive fibrosis appears as large, irregular

masses in both perihilar regions [2]
Asbestosis
• Occupational disorder in individuals exposed to a high concentra-

tion of asbestos over a prolonged period
• Affected individuals typically have engaged in the mining and
manufacturing of asbestos, a fire-resistant silicate used in such
Hypersensitivity Pneumonitis 177
industries as construction, ship building, and the manufacture and

repair of brake linings, insulation, and electrical wiring
• After a long latency period (20 or more years), there is an insidious
onset of symptoms of exertional dyspnea and reduced exercise
tolerance
• Progressive reduction in pulmonary function tests is associated with
increasing symptoms of airway disease (cough, sputum, wheezing),
which occurs primarily in those who are also heavy smokers
• High incidence of mesothelioma (also bronchogenic carcinoma
and adenocarcinoma in situ)
Imaging
• In the early stages, a reticular pattern of pulmonary opacities that

primarily involve the lower lungs and may progress to honeycomb-
ing (see Figs. e14.8 and e14.9)
• Later, pleural thickening and plaque formation along the lateral
chest wall (Fig. 14.5; see Fig. e14.10)
• In patients with extensive interstitial fibrosis, the radiographic and
CT findings tend to be indistinguishable from idiopathic pulmo-
nary fibrosis (Fig. 14.6)
• Note that the characteristic appearance of calcified pleural plaques
actually is a component of asbestos-related disease rather than
asbestosis, since they do not lead to fibrosis and are usually asymp-
tomatic (see Fig. e14.11)
Hypersensitivity Pneumonitis
• Also known as extrinsic allergic alveolitis, a group of allergic lung

diseases that are caused by chronic inhalation of a variety of airborne
organic and chemical antigens that leads to a granulomatous immu-
nological response of the airways and pulmonary parenchyma
• Most common forms are farmer’s lung and bird fancier’s lung (also
a response to a variety of infectious organisms, chemicals, and
wood dusts)
• Acute – flu-like symptoms, which typically develop 4–12 hours
after dust exposure and include cough, fever, chills, and myalgia
• Chronic – insidious onset may prevent identification of a causative
antigen, so that this condition may be underdiagnosed
a b
Fig. 14.5 Asbestosis. (a) Extensive calcified plaques en face bilaterally as well
as in the left hemidiaphragmatic pleura. (b, c) Calcified plaques on pleural sur-
faces at the hemidiaphragms (black arrows) and anterior and posterior chest
walls (white arrows). Note the non-calcified plaque on the posterior chest wall
in C (striped arrow)
Imaging
• Acute/subacute
○○ Small, ill-defined centrilobular nodules and bilateral air-space
ground-glass opacities that are most prominent in the mid and
lower lungs (see Figs. e14.12 and e14.13)
○○ Air trapping on expiratory CT scans produces a mosaic attenua-
tion pattern in subacute disease (Fig. 14.7)
Hypersensitivity Pneumonitis 179
a b
Fig. 14.6 Asbestosis. (a, b) Extensive fibrotic changes, indistinguishable from

idiopathic pulmonary fibrosis [2]
• Chronic (see Fig. e14.14)

○○ Lung fibrosis produces honeycombing, traction bronchiectasis,
and architectural distortion
○○ There also may be reticular opacities randomly distributed in the
peribronchial and subpleural regions
○○ Unlike UIP, honeycombing is not common; when present, it
often involves the upper (rather than lower) lobes
Fig. 14.7 Hypersensitivity pneumonitis (subacute stage). Diffuse bilateral

ground-glass opacities produce a geographic pattern of mosaic attenuation
without architectural distortion, predominantly involving the upper lobes [1]
Allergic Bronchopulmonary Aspergillosis (ABPA)
• Hypersensitivity immune reaction to Aspergillus organisms (no

direct fungal invasion of the lungs or bronchi)
• This damages the bronchial wall, causing central bronchiectasis
and mucous plugs containing fungus and inflammatory cells
• Symptoms include chronic cough, wheezing, pleuritic chest pain,
fever, and expectoration of mucus plugs
• Often a history of asthma or cystic fibrosis
• Prominent local and peripheral eosinophilia and elevated IgE levels
Imaging
• Radiographs (Fig. 14.8, see Fig. e14.15a)

○○ “Finger-in-glove” sign of large airway impaction, most promi-
nently involving the upper lobes
○○ Often recurrent atelectasis and migratory patchy foci of air-space
consolidation
Fig. 14.8 Allergic bronchopulmonary aspergillosis. Patchy opacifications in

segmental bronchi of the upper lobes in a patient with asthma and pronounced
peripheral eosinophilia [2]
Allergic Bronchopulmonary Aspergillosis (ABPA) 181
Fig. 14.9 Allergic bronchopulmonary aspergillosis. (a) Lateral radiograph

in a patient with asthma shows basilar opacifications (arrow). (b) CT image
demonstrates extensive bronchiectasis and mucoid impaction on the left, pro-
ducing a dramatic finger-in-glove sign (black arrow). Less prominent findings
are seen at the right base. (c) Following scooping out of the impacted mucus and
aspergillus infestation, there is residual mild bronchiectasis at the bases (arrows).
(Courtesy of Ritu Gill, MD, Boston)
• CT (Fig. 14.9; see Figs. e14.15 and e14.16)

○○ Central bronchiectasis (which is most often varicoid) and mucoid
impactions
○○ Areas of peripheral bronchiolitis in small airways manifest as
bronchiolar nodules and/or tree-in-bud opacities
○○ Indirect signs of small airway disease include a mosaic pattern of
lung attenuation and air trapping on expiratory scanning
Crack Lung
• Respiratory complication of smoking crack cocaine, which causes

diffuse alveolar damage and hemorrhage followed by infiltration
by inflammatory cells, especially eosinophils
Images (see Fig. e14.17; see Fig. e8.15)
• Diffuse perihilar alveolar edema and hemorrhage, as well as inter-

stitial edema that primarily affects the perihilar regions
• May be associated with an eosinophil-rich empyema and evidence
of barotrauma (pneumothorax and abnormal air in the mediastinum
or pericardium)
References
the lung. AJR. 2013;200:W222–37.
the lung. AJR. 2013;200:712–28.
5. Gosset N, Bankier AA, Eisenberg RL. Tree-in-bud pattern. AJR. 2009;193:
W472–7.
Miscellaneous Diffuse
Pulmonary Diseases 15
Sarcoidosis
• Systemic inflammatory disease of unknown origin that is character-

ized by diffuse noncaseating granulomas
• Predominantly involves the lungs but also may affect the heart,
joints, eyes (uveitis), kidneys, central nervous system, and skin
(erythema nodosum)
• Most commonly develops between ages 25 and 40, especially in
African-American women (ten times more frequent than in Caucasians)
• About half of patients are asymptomatic, with the disease detected
incidentally on a chest radiograph obtained for unrelated symptoms
Imaging
• Radiographs
○○ Classic radiographic appearance of bilaterally symmetric, lobu-
lated enlargement of hilar and paratracheal nodes (1-2-3 sign)
develops in up to 90% of patients (Fig. 15.1; see Fig. e15.1)
978-3-030-16826-1_15])

https://doi.org/10.1007/978-3-030-16826-1_15
184 15 Miscellaneous Diffuse Pulmonary Diseases
○○ On lateral view, the donut sign with adenopathy circumferen-

tially encircling the trachea (Fig. 15.1b)
○○ Enlarged lymph nodes contain stippled or eggshell calcifications
in half the cases (Fig. 15.2; see Fig. e15.2)
Fig. 15.1 Sarcoidosis. (a, b) Enlargement of the right hilar, left hilar, and right
paratracheal lymph nodes, producing the classic 1-2-3 pattern of adenopathy [1]
Sarcoidosis 185
○○ About 50% of patients with hilar lymphadenopathy develop dif-

fuse parenchymal disease, most commonly a reticulonodular
pattern that is usually bilaterally symmetric and predominantly
involves the upper and mid-lung zones (Fig. 15.3; see Fig. e15.3)
○○ Nodal enlargement typically resolves as the parenchymal disease
develops (unlike lymphoma or tuberculosis)
Fig. 15.2 Sarcoidosis. Diffuse eggshell calcifications in hilar and mediastinal

lymph nodes bilaterally. (Courtesy of Jeffrey Klein, MD, Burlington, VT)
Fig. 15.3 Sarcoidosis. Diffuse reticulonodular pattern associated with hilar ade-
nopathy [1]
○○ In about 20%, the reticulonodular pattern leads to extensive

interstitial pulmonary fibrosis (coarse, linear opacities radiating
outward from the hila, which are pulled upward) (see Fig. 15.4)
○○ This eventually can result in end-stage disease, with severe fibrous
scarring, the formation of bullae, and emphysema (Fig. 15.5)
Fig. 15.4 Sarcoidosis. Chronic fibrotic changes with architectural distortion

of the upper lungs bilaterally
Fig. 15.5 Sarcoidosis. End-stage disease, with severe fibrous scarring, bleb
formation, and emphysema [1]
Sarcoidosis 187
Fig. 15.6 Sarcoidosis. “Alveolar” pattern of patchy, ill-defined areas of air-

space consolidation scattered throughout both lungs [1]
○○ “Alveolar” sarcoid produces bilateral, poorly defined, fluffy air-

space consolidations with air bronchograms in the peripheral
portions of the lungs (mimicking pneumonia), which represent
an interstitial process that compresses and obliterates alveoli
(Fig. 15.6)
CT
• Lymphadenopathy tends to be of homogeneous soft-tissue attenu-

ation without compression of adjacent bronchi and vessels (see
Fig. e15.4)
• Small irregular nodules (1–5 mm) with interstitial thickening in a
perilymphatic distribution (“beaded” pattern), which extends
along the bronchovascular bundles from the hilum to the periphery
and predominantly involves the upper- and mid-lung zones (see
Fig. e15.5)
• Coalescence of perilymphatic nodules may produce a mass, at
times surrounded by peripheral small nodules (galaxy sign) (see
Fig. e15.6)
• Less frequently, the nodules are located in the interlobular septa,
subpleural lymphatics, and along the fissures (see Fig. e15.7)
• In late stages, fibrous distortion of lung parenchyma may be seen on CT
before it is apparent on chest radiographs (see Figs. e15.8 and e15.9)
• Other CT manifestations include:

○○ Ground-glass opacities (50%), which may be associated with
superimposed interlobular septal thickening and interlobular
lines to produce the crazy-paving pattern (see Fig. e15.10)
○○ Alveolar sarcoidosis (airspace nodules and consolidation with
air bronchograms simulating pneumonia) (see Fig. e15.11)
○○ Masses simulating metastatic disease (see Fig. e15.12)
○○ Cysts and cavitation (in necrotizing sarcoid angiitis)
○○ Bronchial wall thickening and airway stenoses
• Fungus balls (mycetomas) may develop in cystic areas related to sar-
coid (second most common underlying cause, after tuberculosis)
• Mosaic attenuation pattern with air trapping on expiratory scans
may reflect extrinsic peribronchial fibrosis or intrinsic noncaseat-
ing granulomas in small airways
• The wide variety of manifestations on both radiographs and CT
images, which suggest other chest diseases, has led to sarcoidosis
being labeled the “great mimicker” (see Fig. e15.13)
• Intensive steroid therapy can result in dramatic clinical and imag-
ing improvement (see Fig. e15.14)
Lymphangioleiomyomatosis (LAM)
• Rare cystic lung disease related to bronchial obstruction and lung

destruction due to progressive smooth muscle proliferation in the
walls of bronchi, bronchioles, alveolar septa, pulmonary vessels,
lymphatics, and pleura (histologically similar to tuberous
sclerosis)
• Primarily affects women of childbearing age (symptoms may
develop or be exacerbated during pregnancy), with no relation to
smoking history
• May present after menopause in women undergoing estrogen hor-
monal treatment
• Spontaneous pneumothorax is the presenting appearance in more
than half of patients (caused by rupture of peripheral dilated air
spaces secondary to air trapping from obstructed airways)
• Chylothorax (secondary to dilated and obstructed lymphatics) often
occurs
• May be associated abdominal findings (chylous ascites, renal angi-
omyolipomas, and retroperitoneal lymphadenopathy)
Lymphangioleiomyomatosis (LAM) 189
Imaging (Figs. 15.7 and 15.8; see Figs. e15.15 and e15.16)
• Multiple well-defined, smooth, thin-walled cysts of varying size,

which initially are surrounded by normal pulmonary parenchyma
• Unlike pulmonary Langerhans cell histiocytosis (PLCH), in LAM:
○○ The cysts usually are round and regular (rather than having
bizarre shapes)
○○ Diffuse distribution with no sparing of the lower lungs and cos-
tophrenic angles (rather than an upper lobe predominance)
○○ Lung nodules (a hallmark of PLCH) are typically absent
• Low-attenuation (<0 HU) pleural or pericardial effusions in 60%
Fig. 15.7 Lymphangioleiomyomatosis. (a) Increased lung volumes and fine

linear opacities. (b) Multiple, well-defined, regular cysts interspersed with nor-
mal intervening lung [3]
Fig. 15.8 Lymphangioleiomyomatosis. Innumerable thin-walled cysts of

approximately equal size are uniformly distributed throughout both lungs [1]
Pulmonary Alveolar Proteinosis
• Rare condition of unknown etiology characterized by air-space

deposition of a periodic acid-Schiff (PAS)-positive granular mate-
rial that has high protein and lipid content
• Usually idiopathic, though may be related to an immunologic
abnormality or environmental exposure to silica
• Primarily affects men age 30–50 who have a smoking history and
progressive symptoms of dyspnea and nonproductive cough
• Increased susceptibility to pulmonary and extrapulmonary infec-
tions from both common and opportunistic organisms (most fre-
quently nocardiosis) and an increased incidence of lymphoma
• Bronchoalveolar lavage, which is usually performed to make the
diagnosis, is generally effective at ameliorating symptoms (often for
prolonged periods) until the typically self-limited disease resolves
Imaging
• Radiographs
○○ Bilateral and symmetric alveolar infiltrates that are identical in
distribution and character to those of pulmonary edema (batwing
pattern) (Fig. 15.9)
○○ However, no evidence of cardiac enlargement, pleural effusion,
or elevation of pulmonary venous pressure
ANCA-Associated Granulomatous Vasculitis 191
Fig. 15.9 Pulmonary alveolar proteinosis. Diffuse, bilateral air-space consoli-

dation predominantly involves the central portions of the lung and simulates pul-
monary edema. The patient was asymptomatic, and serial radiographs over several
months showed little change [1]
• CT
○○ Diffuse, bilateral ground-glass opacification (see Fig. e15.17)
○○ Classic cause of the “crazy-paving” pattern (smooth interlobular
septal thickening superimposed on a ground-glass background)
(see Fig. e15.18)
• Other causes of crazy-paving include Pneumocystis jiroveci pneu-
monia, adenocarcinoma in situ, cryptogenic organizing pneumo-
nia, lipoid pneumonia, and alveolar sarcoid
ANCA-Associated Granulomatous Vasculitis
• Formerly known as Wegener’s granulomatosis, ANCA (antineutro-

philic cytoplasmic antibody)-associated granulomatous vasculitis
is a rare inflammation of small-to-medium vessels without associ-
ated infection
• Positive C-ANCA is highly specific for this condition
• Of unknown etiology, the classic triad consists of abnormalities
involving the sinuses (febrile sinusitis), lungs (chest pain, cough, dys-
pnea, hemoptysis), and kidneys (glomerulonephritis and hematuria)
• About 90% of patients are of northern European descent (much less
common in blacks); primarily affects men
Imaging
• Radiographs
○○ Multiple round, fairly well-circumscribed nodules that may sim-
ulate metastases
○○ Thick-walled cavities with irregular, shaggy inner margins occur
in about half the patients (Fig. 15.10)
○○ Development of an air-fluid level within a cavity suggests super-
imposed infection
• CT
○○ Ground-glass opacities related to alveolar hemorrhage, necrotic
cellular alveolar infiltrates, or mosaic perfusion due to small-
vessel vasculitis
○○ Nodules with irregular margins, often in a peribronchovascular
distribution (see Fig. e15.19)
○○ Ground-glass halo sign surrounding the irregular nodules is an
indication of hemorrhage
○○ Thickening of tracheal or bronchial walls may cause focal or
more extensive stenotic areas that may require stenting
Fig. 15.10 ANCA- associated granulomatous vasculitis. Multiple thick-

walled cavities with irregular, shaggy inner linings [1]
Scleroderma 193
Scleroderma
• Connective tissue disorder is which there is fibrosis and atrophy of

multiple organ systems, primarily the skin, gastrointestinal tract,
heart, and kidneys (in addition to the lungs)
• Classic extrapulmonary findings include:
○○ Dilated esophagus with absent peristalsis in the lower two-thirds
(smooth muscle)
○○ Widely patent distal esophagus (in the region of the lower esoph-
ageal sphincter), predisposing to reflux esophagitis and repeated
lung aspiration
○○ Erosion of the terminal tufts of the fingers with associated soft-
tissue calcification
• Bilateral reticulonodular interstitial changes consistent with pul-

monary fibrosis, which typically has a predominantly subpleural
distribution in the bases of the lungs
• Severe esophageal dilatation (not seen in other causes of fibrotic lung
disease, such as UIP, NSIP, rheumatoid lung, and dermatomyositis)
a b
Fig. 15.11 Scleroderma. (a) Diffuse prominence of coarse interstitial mark-

ings at the bases bilaterally. (b) Coned view of the left lower lung in another
patient demonstrates a honeycomb pattern, with small emphysematous areas
combined with fibrosis and fine nodularity [1]
Cystic Fibrosis
• Hereditary disorder (autosomal recessive) characterized by abnormal

secretions from exocrine glands throughout the body (pancreas, large
bowel, salivary and sweat glands, and tracheobronchial tree)
• Block in chloride transport across cell membranes in the bronchial
lumen and the excessive resorption of sodium lead to the produc-
tion of a thick and dry mucus, resulting in decreased clearance of
the tenacious material and eventually mucous plugging in small
and large airways and subsequent bacterial infection
• Diagnosis of cystic fibrosis can be confirmed by an abnormal sweat
chloride test or molecular testing (polymerase chain reaction)
Imaging
• Radiographs (Fig. 15.12; see Fig. e15.23)

○○ Hyperinflation of the lungs with bronchial wall thickening (par-
allel linear opacities [“tram lines”]), which produces a diffuse
Fig. 15.12 Cystic fibrosis. Diffuse increase in interstitial markings radiating in

a bronchovascular distribution with tramlines (arrows) and peribronchial cuffing
(arrowhead) [1]
Drug Toxicity 195
coarse reticular pattern that is most prominent in the upper lung

zones (lower lobes have more efficient clearance of secretions)
○○ Ring shadows can be caused by cystic bronchiectasis, bullae,
microabscesses, or honeycombing
○○ Hilar enlargement may reflect post-pneumonia lymphadenopa-
thy or pulmonary artery hypertension
• CT (see Figs. e15.24 and e15.25)
○○ Superior to chest radiographs for demonstrating bronchial wall
inflammatory changes (bronchial wall and peribronchial thick-
ening), bronchiectasis, mucous plugging, and air trapping on
expiratory scanning
○○ Signet ring sign (dilated, thick-walled bronchus with adjacent
normal pulmonary artery seen on cross section)
○○ Large amounts of bronchiolar secretions result in the “tree-in-
bud” pattern
Drug Toxicity
• Systemic drugs can produce a spectrum of pulmonary manifestations:

○○ Cytotoxic drugs (largest and most important group of agents
associated with lung toxicity, especially cyclophosphamide and
busulfan)
○○ Non-cytotoxic drugs (amiodarone, gold salts, methotrexate,
nitrofurantoin)
• May be associated with eosinophilia
Imaging
• Although toxicity related to individual drugs has specific appear-

ances, a common pattern is the following:
○○ Initially, scattered or diffuse areas of ground-glass opacity (see
Fig. e15.26)
○○ Progressive fibrosis may lead to marked architectural distortion
and honeycombing, often with a predominantly basal distribu-
tion (Figs. 15.13 and 15.14; see Fig. e15.27)
○○ Toxicity to amiodarone, a tri-iodinated compound used to treat
cardiac arrhythmias, which occurs in almost 20% of patients and
is apparently dose-related
Fig. 15.13 Drug toxicity (methotrexate). Diffuse interstitial pattern with

patches of alveolar consolidation in a child treated for myelogenous leukemia.
After methotrexate therapy ended, there was rapid clinical and radiographic
improvement [1]
Fig. 15.14 Drug toxicity (busulfan). Severe coarse reticular pattern [1]
• Most commonly presents as a chronic interstitial pneumonitis

with a reticular pattern (Fig. 15.15) that may mimic congestive
failure (though at times it has an upper lobe predominance)
• Less commonly appears as solitary or multiple areas of con-
solidation and/or nodules (see Fig. e15.28)
Radiation-Induced Lung Disease 197
Fig. 15.15 Amiodarone toxicity. Severe pulmonary fibrosis. (James Heilman,

MD /Wikimedia)
Radiation-Induced Lung Disease
• Acute radiation pneumonitis and subsequent fibrosis are seen in

most patients who have received mantle radiation therapy for lym-
phoma and other malignant lesions in the chest
• Rarely detectable less than 1 month after the end of treatment
(usually observed at 6–8 weeks after therapy and peaks at
4 months)
• When complete resolution does not occur, the late or chronic
stage of radiation damage, which develops within 6–12 months
after the end of therapy, is characterized by extensive fibrosis and
loss of volume that becomes stable within 2 years after
treatment
• Dose-related:
○○ <20 Gy – rarely causes radiation pneumonitis
○○ >40 Gy – usually causes radiation pneumonitis
• Essential to differentiate the classic pattern of radiation therapy
changes from superimposed infection and recurrent malignancy
Imaging
• Acute (see Fig. e15.29)

○○ Patchy areas of irregular consolidation that are localized to the
radiation port and often are associated with considerable loss of
volume
○○ Typically, a sharp demarcation between the irradiated opacified
area and normal lung, which does not respect anatomic boundar-
ies (such as fissures)
• Late (Fig. 15.16; see Figs. e15.30–e15.32)
○○ Parenchymal opacities become more reticular and fibrotic (may
appear like a mass or scar)
○○ Associated volume loss and traction bronchiectasis
○○ Increase in size or density of a previously stable area of radiation
fibrosis, which may be accompanied by a more convex margin of
the lesion, is worrisome for tumor recurrence
Fig. 15.16 Radiation-induced lung disease. Following postmastectomy radi-

ation, a mass of fibrous tissue (arrows) extends from the right hilum to parallel
the right border of the mediastinum [1]
Lymphoid Interstitial Pneumonia (LIP) 199
• PET
○○ FDG uptake may increase within the first few months after radia-
tion therapy due to inflammatory changes but then usually
decreases over time
○○ The later development of focal areas of increased FDG uptake in
an area of radiation fibrosis suggests residual or recurrent tumor
Lymphoid Interstitial Pneumonia (LIP)
• Diffuse disorder typically associated with collagen vascular dis-

eases, especially Sjögren syndrome
• Histologically, diffuse infiltration of the interstitium by lympho-
cytes, plasma cells, and histiocytes
• More common in women and typically develops between ages 40
and 50
Imaging
• Diffuse or multifocal ground-glass opacities and nodules, often in the

periphery of the lung and in a bronchovascular distribution (Fig. 15.17)
Fig. 15.17 Lympho cytic interstitial pneumonia (Sjogren syndrome).

Diffuse ground-glass opacities and multiple small perivascular cysts (arrows)
with lower lung predominance [5]
• Eventually, chronic LIP appears as a diffuse cystic lung disease,

though the scattered perivascular, thin-walled cysts usually are less
numerous than in PLCH or LAM (see Fig. e15.33)
Amyloidosis
• Abnormal extracellular accumulation of insoluble amyloid mate-

rial within airway walls or the lung parenchyma
• Amyloidosis limited to the respiratory tract is uncommon
• May be primary or (much more commonly) secondary to a chronic
inflammatory disease (e.g., infection, bronchiectasis, neoplasm,
rheumatic disease) or merely advancing age
• Three basic types:
○○ Tracheobronchial
○○ Single or multiple pulmonary nodules (best prognosis)
○○ Diffuse parenchymal opacities
Imaging
• Tracheobronchial
○○ Submucosal deposition of proteinaceous amyloid material leads
to diffuse mural thickening and luminal narrowing, which may
result in obstructive hyperinflation, atelectasis, or recurrent
pneumonia (see Fig. e15.34)
○○ Usually found incidentally on chest radiographs in asymptom-
atic older adults
• Pulmonary nodules
○○ Single or multiple, sharply marginated, peripheral pulmonary
nodules that are more prominent in the lower lungs (Fig. 15.18)
• Diffuse parenchymal opacities
○○ Deposits originating in the muscular walls of small blood vessels
enlarge and spread diffusely into the interstitial tissues
(Fig. 15.19)
○○ Diffuse micronodular, reticulonodular, or miliary pattern (may
be honeycombing)
○○ Hilar and mediastinal lymph nodes may be markedly enlarged
○○ Calcification occurs in up to half of nodules and also may involve
lymph nodes
Amyloidosis 201
a b
Fig. 15.18 Amyloidomas. (a, b) Multiple nodular opacifications bilaterally,

mimicking pulmonary metastases. Notice that several of the nodules have
calcified
Fig. 15.19 Amyloidosis. Diffuse pattern of interstitial fibrosis [1]

References
the lung. AJR. 2013;200:W222–37.
3. Cantin L, Bankier AA, Eisenberg RL. Multiple cystlike lung lesions in the
adult. AJR. 2010;194:W1–W11.
W158–71.
the lung. AJR. 2013;200:712–28.
Mediastinal Masses
16
The mediastinum traditionally has been divided into three compart-

ments (Fig. 16.1), all of which are bounded superiorly by the thoracic
inlet and inferiorly by the diaphragm [1]:
Anterior Mediastinum
• Extends from the back of the sternum to the anterior border of the
heart and great vessels
• “Four Ts” – Thymic lesion, Teratoma, (extrathoracic) Thyroid
mass, and “Terrible” lymphoma (some add a fifth “T” – Thoracic
ascending aortic aneurysm)
Middle Mediastinum
• Extends from the anterior border of the heart and aorta to the pos-
terior border of the heart
• Contains the heart, origins of the great vessels, trachea and main
bronchi, and lymph nodes


https://doi.org/10.1007/978-3-030-16826-1_16
204 16 Mediastinal Masses
a b
Fig. 16.1 Drawings illustrating the mediastinal compartments (gray, out-

lined in black). (a) Anterior mediastinum. (a) Middle mediastinum. (c) Posterior
mediastinum [1]
Posterior Mediastinum
• Extends from the posterior border of the heart to the anterior border
of the vertebrae
• Contains the esophagus, descending aorta, thoracic spine, paraver-
tebral soft tissues, and lymph nodes
ITMIG Classification of Mediastinal Compartments 205
ITMIG Classification of Mediastinal Compartments
In 2017, a reclassification of the three mediastinal compartments was

issued by the International Thymic Malignancy Interest Group
(TIMIG) (Fig. 16.2) [2]:
Fig. 16.2 ITMIG definition of mediastinal compartments. (a) Sagittal refor-

matted and (b) axial images. Note that on the axial view, the prevascular compart-
ment (purple) wraps around the heart and pericardium, which are located in the
visceral compartment (blue). The area in yellow represents the paravertebral com-
partment, with the green line indicating the boundary line between the visceral
and paravertebral compartments [2]
PREVASCULAR (ANTERIOR)
• Contains the thymus, fat, lymph nodes, and left innominate vein
• Most common masses are thymic lesions, lymphoma and meta-
static lymphadenopathy, intrathoracic masses, and germ cell
neoplasms
VISCERAL (MIDDLE)
• Contains vascular structures (heart, aorta, intrapericardial pulmo-

nary arteries and veins, SVC, azygos vein, and thoracic duct), tra-
chea and carina, esophagus, and lymph nodes
• Most common abnormalities are hiatal hernia, lymphadenopathy,
esophageal tumors, tracheal lesions, cardiac lesions, and thoracic
ascending aortic aneurysm
PARAVERTEBRAL (POSTERIOR)
• Contains the thoracic spine and paravertebral soft tissues

• Most common abnormalities are neurogenic tumors, Bochdalek
hernia, lymphadenopathy, infections, and trauma
Cervicothoracic sign to separate anterior and posterior mediastinal

masses on frontal view (Fig. 16.3):
• Upper border of the anterior mediastinum lies at the level of the

clavicles
• Upper border of the posterior mediastinum extends much higher
• Therefore, any mediastinal mass clearly visible above the clavicles
on the frontal view must lie posteriorly
• Conversely, if the upper border of the lesion disappears as it
approaches the clavicles, the lesion must lie at least partly in the
anterior mediastinum
• The trachea is the dividing line, so that a juxtatracheal mass is vis-
ible part way above the clavicles
Anterior Mediastinal Masses (Superior Mediastinum) 207
Fig. 16.3 Cervicothoracic sign. (a) Huge upper mediastinal mass extends
well above the level of the clavicle and displaces the trachea to the right. (b) CT
image demonstrates that the large mass lies posteriorly. (Courtesy of Ritu Gill,
MD, Boston)
Anterior Mediastinal Masses (Superior

Mediastinum)
Thymoma
• Benign or low-grade malignant tumor that is the most common

anterior mediastinal mass, especially after age 40
• About 40% of patients with thymoma have myasthenia gravis (about
15% of patients with myasthenia gravis have thymomas) (Fig. 16.4)
Fig. 16.4 Thymoma. (a, b) Large mass in the anterior mediastinum (arrows) in
a patient with myasthenia gravis [3]
• Round or oval, smooth or lobulated mass that may protrude to

one or both sides of the mediastinum and obscure the heart bor-
der (best seen on lateral views) (see Fig. e16.1)
978-3-030-16826-1_16])
• Usually arises near the junction of the heart and great vessels, dis-
placing them posteriorly (see Fig. e16.2)
• CT
○○ Well-defined mass that generally has uniform soft-tissue attenu-
ation (see Fig. e16.3a)
○○ There may be high-fat content (Fig. e16.3b), areas of cystic or
necrotic degeneration in large lesions, and often calcification in
the capsule or throughout the mass
Thymoma Versus Thymic Carcinoma
• Sign of benignancy – preservation of a well-defined fat plane

between the thymoma and adjacent structures
• Signs suggesting malignancy
○○ Loss of the fat plane between the mass and adjacent mediastinal
structures (Fig. 16.5; see Figs. e16.4 and e16.5)
○○ Extension of tumor into the mediastinum (with encasement of
mediastinal structures) or lung parenchyma
○○ Pleural deposits (especially posteriorly and in the costophrenic
angles) from transpleural seeding of tumor (“drop” metastases)
○○ Irregular pericardial thickening (tumor implantation)
Fig. 16.5 Thymic carcinoid. Lobulated, heterogeneously enhancing mass.

Loss of the fat plane between the mass and the pericardium suggests tumor inva-
sion [3]
Thymic Hyperplasia
• Diffuse, symmetric enlargement of the thymus that must be distin-

guished from thymic neoplasm, which typically appears as a focal
mass (Fig. 16.6; see Fig. e16.6)
• There are two forms of thymic hyperplasia (indistinguishable on
imaging):
○○ True thymic hyperplasia – response to severe systemic stress
(burns, radiation therapy) and rebound hyperplasia to chemo-
therapy or steroids
○○ Lymphoid (autoimmune) hyperplasia – myasthenia gravis, SLE,
scleroderma, and rheumatoid arthritis
Fig. 16.6 Thymic hyperplasia. Triangular soft-tissue density (arrow) within

the mediastinal fat, which is situated adjacent to mediastinal vessels but without
signs of invasion
Thymic Cyst
• Well-circumscribed mass with homogeneous fluid attenuation

without contrast enhancement (Fig. 16.7; see Fig. e16.7)
• Curvilinear calcification of the cyst wall occurs in a small percent-
age of cases (see Fig. e16.8)
a b
Fig. 16.7 Thymic cyst. (a) Axial CT image shows an incidentally noted, well-
circumscribed mass of fluid attenuation (arrow) [5]. (b) Sagittal T1-weighted
MR image shows a low-signal cyst (arrow) in a thymic location [3]
Teratoma (Figs. 16.8–16.10; See Figs. e16.9–e16.12)
• Most common germ cell tumor of the anterior mediastinum, which

is usually benign and contains all three germ layers (endoderm,
mesoderm, and ectoderm)
• Well-marginated mass near the origin of the great vessels that is
most commonly cystic and may protrude to one or both sides of the
mediastinum
Fig. 16.8 Teratoma. Large lobulated mass confluent with the right border of
the heart [3]
Fig. 16.9 Mature cystic teratoma. Heterogeneous anterior mediastinal mass

with areas of fat (long arrow), calcification (short arrows), fluid attenuation, and
thin soft-tissue septa [3]
Fig. 16.10 Malignant germ cell tumor. Huge anterior mediastinal tumor that
is primarily solid, though there is a relatively large cystic component (arrow) [4]
• Pathognomonic calcification, ossification, teeth, or fat is infre-

quently identified within the lesion (more evident on CT)
• CT is valuable for differentiating benign tumors from malignant
teratomas, which are large nodular masses with indistinct margins,
thick enhancing capsule, extensive soft-tissue areas and a small

fatty component, and often necrosis and hemorrhage
• Malignant germ cell tumors (most commonly seminomas) tend to
grow rapidly and invade adjacent mediastinal structures
Thyroid Mass
• Benign, multinodular goiter is the most common cause of an ante-

rior mediastinal mass in the region of the thoracic inlet in an adult
(especially middle-aged or older women)
• Sharply defined, smooth or lobulated mass that occurs in the supe-
rior portion of the mediastinum and produces a characteristic
impression on the trachea (above the level of the aortic arch) and
deviates it to the contralateral side (Fig. 16.11)
• Usually evidence of a connection between the intrathoracic mass
and its origin in the thyroid gland in the neck (best seen on CT) (see
Figs. e16.13 and e16.14)
• CT – often demonstrates calcifications within the mass, which has
a high-attenuation value relative to adjacent muscles (≥20 HU) on
non-contrast scans, reflecting the high concentration of iodine
within the ectopic thyroid tissue (see Fig. e16.15)
• In about 20% of cases, the lesion extends posteriorly behind the
esophagus and adjacent to the trachea to involve the retrotracheal
space (see Fig. e16.16)
Fig. 16.11 Thyroid mass. Marked mass effect on the left of the trachea (arrow)
and displacement of the trachea to the right
Lymphoma – especially Hodgkin’s disease

• Radiographs
○○ Frontal view – mediastinal widening (Fig. 16.12)
○○ Lateral view – obliteration of the retrosternal clear space
• CT
○○ Homogeneous soft-tissue attenuation (see Fig. e16.17)
○○
Extensive dystrophic calcification of lymph nodes occurs in
about 20% of patients after radiation therapy or chemotherapy
(see Fig. e16.18)
○○ Large masses may have heterogeneous attenuation due to hem-
orrhage or necrosis (see Fig. e16.19)
○○ Lymphomatous masses tend to displace and encase mediastinal
structures, rather than narrow or invade them
○○ Lymphoma is FDG avid on PET-CT (this modality also is used
for initial staging and follow-up) (see Fig. e16.20)
a b
Fig. 16.12 Lymphoma. (a) Initial radiograph demonstrates marked widening

of the upper half of the mediastinum (arrows) due to pronounced adenopathy.
(b) After chemotherapy, there is a marked decrease in the width of the upper
mediastinum [3]
Lymphoma Lipoma (Fig. 16.13; See Fig. e16.21)
• Benign collection of fatty tissue that is most common in the ante-

rior mediastinum, although it can occur in the middle and posterior
mediastinum and adjacent to the diaphragm
• May be indistinguishable from thymolipoma
• Liposarcomas are extremely rare (most commonly occur in the
posterior mediastinum) and generally have a higher attenuation
than benign fat, are inhomogeneous, and tend to show features of
mediastinal invasion
Fig. 16.13 Lipoma. Well-demarcated fatty mass surrounds the right brachio-
cephalic artery [3]
Hemorrhage (Fig. 16.14; See Fig. e16.22)
• Widening of the mediastinum in a patient with a history of trauma,

surgery, or dissecting aneurysm
• CT may demonstrate a site of active bleeding
a b
Fig. 16.14 Mediastinal hemorrhage. (a) Initial study is within normal limits.
(b) Following a failed attempt at internal jugular central line insertion, there is
prominent widening of the mediastinum secondary to bleeding (arrows)
a b
Fig. 16.15 Ascending thoracic aorta aneurysm. (a, b) Marked dilatation of

both the ascending and descending portions of the thoracic aorta (arrows), pro-
ducing anterior and posterior mediastinal masses, respectively [3]
Aneurysm of the Ascending Aorta or Sinus of Valsalva

(Figs. 16.15; See Fig. e16.23)
• Saccular or fusiform mass that tends to extend anteriorly and to the

right
• May erode the sternum
Anterior Mediastinal Masses (Lower

Mediastinum)
Pericardial Cyst
• Benign, congenital cystic lesion, usually in the right cardiophrenic

angle (Fig. 16.16)
• Round or lobulated, sharply demarcated lower mediastinal mass
that typically touches both the anterior chest wall and the anterior
portion of the right hemidiaphragm (see Fig. e16.24)
• On MRI, may contain highly proteinaceous fluid that produces
high-signal intensity on T1-weighted images (see Fig. e16.25)
Anterior Mediastinal Masses (Lower Mediastinum) 217
a b
Fig. 16.16 Pericardial cyst. (a, b) Smooth mass (arrows) in the right cardio-
phrenic angle [3]
Fig. 16.17 Epicardial fat pad. Triangular, relatively lucent collection of fat at
the cardiac apex (arrow)
Epicardial Fat Pad (Fig. 16.17)
• Triangular fat collection, more prominent on the left, that silhou-

ettes the heart border at the cardiac apex on a frontal radiograph
and may simulate cardiomegaly
Morgagni Hernia (Fig. 16.18; See Figs. e16.26–e16.28)
• Herniation through the diaphragmatic foramen of Morgagni, which

is located adjacent to the xiphoid process of the sternum
• Round or oval mass that is almost invariably on the right
a b
Fig. 16.18 Morgagni hernia. (a, b) Bowel gas is seen within the anterolateral
hernia sac (arrows). (Courtesy of Gillian Lieberman, MD, Boston)
• Presence in the mass of gas-filled bowel (or contrast-filled colon

from an enema) is diagnostic
• Appears as a homogeneous opacity if the hernia is filled with liver
or omentum (mimics a fat pad or pericardial cyst)
Middle Mediastinal Masses

Lymphadenopathy (Fig. 16.19; See Figs. e16.29 and e16.30)
• Lymphoma (Hodgkin’s disease) – calcification in treated disease

• Sarcoidosis – dense or eggshell calcification (see page 185)
Fig. 16.19 Lymphadenopathy. Bilateral enlargement of hilar lymph nodes

(arrows) [3]
Middle Mediastinal Masses 219
• Silicosis/coal workers pneumoconiosis – eggshell calcification (see

Fig. 14.3)
• Old granulomatous disease – dense calcification (see Fig. e10.10)
• Small cell lung carcinoma (see Fig. 10.15)
• Metastases
• Infectious mononucleosis (see Fig. e6.31)
• Tuberculosis – usually unilateral (often the presenting finding in
children) (see Fig. 6.30); nodes typically have low attenuation on
CT (see Fig. e6.35)
Enlarged Pulmonary Artery (See Fig. 9.8)
Bronchogenic Cyst (Fig. 16.20; See Figs. e16.31 and e16.32)
• Smooth, round, homogeneous mass that is most commonly located

just inferior to the carina
• Often extends beyond the mediastinal confines and overlaps a hilar
shadow
• Tends to mold itself to surrounding structures because of its fluid
contents
• On CT, usually has a thin, imperceptible rim and does not show any
change in attenuation after contrast infusion
• May contain viscous mucoid or proteinaceous material, which pro-
duces a higher attenuation in the range of a solid neoplasm
• Rarely communicates with the tracheobronchial tree
a b
Fig. 16.20 Bronchogenic cyst. (a) Contrast CT scan shows a smooth mass
with uniform water attenuation and an imperceptible wall. (b) In another patient,
coronal T1-weighted MR image shows a cyst with high-signal-intensity con-
tents consistent with water [3]
Posterior Mediastinal Masses

Hiatal Hernia (Fig. 16.21; See Figs. e16.33 and e16.34)
• Soft-tissue mass that can protrude to one or both sides of the lower
mediastinum and often contains a virtually pathognomonic promi-
nent air-fluid level on upright images
a b
Fig. 16.21 Hiatal hernia. (a, b) Rounded soft-tissue mass (white arrows) con-
taining a large air-fluid level (black arrows). (Courtesy of Gillian Lieberman,
MD, Boston)
Bochdalek Hernia (Fig. 16.22; See Fig. e16.35)
• Round or oval, retrocardiac mass that is generally unilateral (much

more commonly on the left side)
• Usually small and contains only retroperitoneal fat but may include
the left kidney, liver, or spleen
• Radiographically, a smooth, well-circumscribed upward bulge at
the posterior aspect of the left hemidiaphragm
• Air-filled bowel loops in the mass are diagnostic
Posterior Mediastinal Masses 221
Fig. 16.22 Bochdalek hernia. Gas-filled loop of bowel (arrow) is situated pos-
teriorly in the thoracic cavity [3]
Foregut Duplication Cyst (Esophageal Duplication, Neurenteric,

or Bronchogenic Cyst)
• Smooth, thin-walled, fluid-attenuation mass (see Figs. e16.36–

e16.39a)
• May contain viscous fluid with an attenuation in the range of a solid
tumor (see Fig. e16.39b)
• Neurenteric cyst is often associated with a congenital defect of the
thoracic spine (butterfly vertebra, hemivertebra)
Esophageal Dilatation (Fig. 16.23; See Fig. e16.40)
• Esophagus motility disorders (achalasia, post-vagotomy syndrome,

Chagas disease, scleroderma, presbyesophagus, diabetic and alco-
holic neuropathy)
Fig. 16.23 Achalasia. (a) Lateral radiograph shows a mass-like appearance due
to a mixture of fluid and air density in the dilated esophagus (arrows). (b) In another
patient, axial CT image shows a dilated thoracic esophagus (arrow) that is filled
with food and contrast material and mimics a mass [3]
• Distal esophageal obstruction (benign or malignant stricture, com-

pression by an extrinsic mass)
• Broad vertical opacity on the right side of the mediastinum that
often contains an air-fluid level on upright images (especially in
achalasia)
• May produce anterior bulging of the trachea
Esophageal Neoplasm (Benign or Malignant)
• Abnormal convexity of the azygoesophageal recess, retrotracheal

mass, or generalized mediastinal widening
Esophageal Varices
• Dilated veins that enhance on contrast CT (see Fig. e16.41)
Neurogenic Tumor
• Children and young adults – sympathetic ganglion tumors (benign

ganglioneuroma; malignant neuroblastoma)
• Adults – peripheral nerve sheet tumors (see Fig. e16.42)
○○ Sharply marginated soft-tissue mass in the paravertebral gutter
○○ May be associated rib or vertebral erosion, calcification, and a
dumbbell appearance (part of the tumor is inside and part outside
the spinal canal, especially with neurofibromatosis)
○○ Schwannoma (most common) – benign, slow-growing, and typi-
cally occurs in the 20–50 age range
Spinal Neoplasm or Infection
• Paravertebral mass with associated bone destruction (Fig. 16.24;

see Figs. e16.43–e16.45)
Fig. 16.24 Tuberculous osteomyelitis of the spine. Large paravertebral

abscess produces a fusiform soft-tissue mass about the vertebrae (arrows).
There is poorly marginated destruction of the T9 vertebral body, along with loss
of the superior and inferior end plates [3]
Meningocele (Fig. 16.25)
• Protrusions of meninges through the spinal neural foramina (most

commonly associated with neurofibromatosis type 1)
• On radiography, widening of the neural foramen; smooth, well-
corticated pressure erosion/scalloping of adjacent vertebrae/ribs;
kyphoscoliosis of dorsal spine
Fig. 16.25 Intrathoracic meningocele (neurofibromatosis type 1). Large

fluid attenuation mass (M) in the posterior right hemithorax that communicates
with the spinal canal. Note the irregularity of the adjacent vertebral body and
expansion of the spinal canal [2]
Extramedullary Hematopoiesis (Fig. 16.26; See Figs. e16.46

and e16.47)
• Proliferation of red blood cells in extramedullary sites as a response

to conditions resulting in inadequate bone marrow production of
red blood cells by the bone marrow or excessive hemolysis
○○ Severe anemia (thalassemia, spherocytosis, sickle cell disease)
○○ Lymphoproliferative disorders (myelofibrosis, chronic myelog-
enous leukemia, lymphoma)
○○ Polycythemia vera
• Extensive, bilateral, often lobulated soft-tissue masses with smooth
margins in the paravertebral regions (below T6)
• May appear as a fat-attenuation mass
Fig. 16.26 Extramedullary hematopoiesis. Large bilateral soft-tissue masses

with smooth margins (arrows)
Descending Thoracic Aortic Aneurysm (Fig. 16.27;

See Fig. e16.48)
• Smooth or lobulated mass that typically projects from the postero-

lateral aspect of the aorta on the left side
• Frequently calcified and may become large enough to erode the
vertebral column
a b
Fig. 16.27 Descending thoracic aortic aneurysm. (a) Localized bulging of

the descending aorta (arrows). (b) In another patient, there is aneurysmal dila-
tion of the lower thoracic aorta (arrows). Note the marked tortuosity of the
remainder of the descending aorta [3]
Diffuse Mediastinal Processes

Mediastinal Lipomatosis (Fig. 16.28; See Fig. e16.49)
• Frequent cause of generalized mediastinal widening, especially in

the anterior mediastinum, conforming to the quip that the most
common cause of a wide mediastinum is a wide patient!
• In addition to obesity, excess fat deposition in the mediastinum
may be associated with steroid therapy, Cushing’s syndrome, or
diabetes, or it may be a normal variant in a non-obese patient
• Fat deposition localized to the superior part of the anterior com-
partment may simulate a mass or aortic dissection
Fig. 16.28 Mediastinal lipomatosis. Widening of the superior mediastinum

(arrows) in an obese patient
Acute Mediastinitis (See Fig. e16.50)
• Acute infection/inflammation of mediastinal structures and sur-

rounding fat and connective tissue, associated with high mortality
and morbidity
• On radiography, mediastinal widening with distortion of normal
mediastinal lines, stripes, and interfaces
• CT shows increased attenuation/stranding of mediastinal fat and
collections of gas or fluid within the mediastinum
Fibrosing Mediastinitis (Fig. 16.29; See Fig. e16.51)
• Rare benign form in which proliferation of acellular collagen and

fibrous tissue predominantly involves the middle mediastinum in
young patients
References 227
Fig. 16.29 Fibrosing mediastinitis. Soft-tissue mass diffusely infiltrates the

mediastinum. There is a subcarinal mass (M), encasement of the left main coro-
nary artery (arrow), and narrowing of the left superior pulmonary vein (S). (A,
ascending aorta; D, descending aorta; P, main pulmonary artery) [3]
• Presents with signs and symptoms of obstruction or compression of

the superior vena cava, pulmonary veins or arteries, central air-
ways, or esophagus
• Although often idiopathic, many cases are thought to be due to an
abnormal immunologic response to infection by Histoplasma
capsulatum
References
1. Whitten CR, Khan S, Munneke GJ, Grubnic S. A diagnostic approach to
mediastinal abnormalities. Radiographics. 2007;27:657–71.
2. Carter BW, Benveniste MF, Madan R, et al. ITMIG classification of medi-
astinal compartments and multidisciplinary approach to mediastinal masses.
4. Shahrzad M, Le TSN, Silva M, Bankier AA, Eisenberg RL. Anterior medias-
tinal masses. AJR. 2014;203:W128–38.
5. Molinari F, Bankier AA, Eisenberg RL. Fat-containing lesions in adult tho-
racic imaging. AJR. 2011;197:W795–813.
6. Wang ZJ, Reddy GP, Gotway MB, et al. CT and MR imaging of pericardial
disease. Radiographics. 2003;23:S167–80.
Trachea and Bronchi
17
Tracheobronchomegaly
• Also known as Mounier-Kuhn syndrome, a rare congenital disorder

that produces diffuse enlargement of the trachea and central
bronchi
• Strong male predominance, more common in blacks, and usually
first diagnosed at age 30–50
• Atrophy or absence of elastic fibers with thinning of smooth mus-
cle and abnormal cartilage
• Structural abnormality allows formation of diverticula between the
cartilage rings
• Abnormal respiratory dynamics (marked narrowing or collapse of
the trachea and main bronchi on expiration) results in retained
secretions and recurrent infections that may lead to bronchiectasis
and fibrosis
• Symptoms range from minimal with preservation of pulmonary
function to respiratory failure and death


https://doi.org/10.1007/978-3-030-16826-1_17
230 17 Trachea and Bronchi

978-3-030-16826-1_17)
• Tracheobronchomegaly (diameter of trachea >27 in men and

>23 mm in women) on inspiration, with collapse on expiration
• Corrugated appearance of the trachea and bronchial walls, with
focal diverticular outpouchings along the bronchi
• Thinning of the tracheal wall on CT
• Evidence of such complications as recurrent pneumonia, bronchi-
ectasis, and emphysematous changes with hyperinflation of the
lungs and pulmonary fibrosis
Relapsing Polychondritis
• Rare inflammatory disease, probably of autoimmune origin, that

destroys cartilage of the ear, nose, upper respiratory tract, and joints
(most common in middle-aged women)
• Inflammatory changes involve the pinna of the ear in about 90% of
cases
• Recurrent episodes of cartilage inflammation cause edema, granu-
lation tissue, and eventually fibrosis
• About half of patients demonstrate respiratory tract narrowing,
which is the major cause of symptoms (recurrent infections and
bronchiectasis related to impaired clearing of secretions) and death
• Diffuse smooth, symmetric wall thickening and luminal narrowing

of the larynx, trachea, and main bronchi
• Tracheal wall thickening that is anterior and lateral and spares the
posterior membranous portion (which contains no cartilage) is vir-
tually pathognomonic of relapsing polychondritis
• Tracheal narrowing may be focal (usually in a subglottic location)
or diffuse
• Thickened airway wall has increased attenuation, and calcification
frequently occurs
• Dynamic scanning can demonstrate expiratory collapse of affected
airways
Tracheomalacia 231
a b
Fig. 17.1 Relapsing polychondritis. (a) End-inspiration and (b) end-expiration

images show dynamic collapse of the trachea with expiration. Note the calcifi-
cation and thickening of the cartilaginous parts of the trachea (arrow), with
sparing of the posterior wall (arrowhead) [2]
Tracheomalacia
• Excessive focal or generalized collapsibility of the trachea on expi-

ration due to weakening of the supporting cartilage and muscles
• Symptoms of stridor intensify during times of increased airflow,
such as coughing, crying, or feeding
• Associated inefficient coughing mechanism and retained secretions
often lead to recurrent pulmonary infections and bronchiectasis
• May be primary in children or secondary
• In adults, tracheomalacia may be secondary to prior intubation,
chest trauma, COPD, extrinsic compression (vascular ring or
enlarged thyroid), chronic tracheobronchitis, or an intrinsic carti-
lage disorder (relapsing polychondritis)
• Concomitant involvement of the bronchi is termed tracheobroncho-
malacia (TBM)
• Hyperinflation of the lungs with excessive narrowing of the tra-

cheal lumen during expiration
• CT
○○ Inspiration – may be normal or only a “lunate” shape, with
reduced AP diameter of the airway
○○ Expiration – substantial anterior bowing of the posterior mem-
branous portion of the trachea (crescentic appearance with
decreased space between the anterior and posterior walls, known
as the frown sign)
○○ Tracheomalacia is now defined as narrowing >70% on
expiration
○○ In severe disease, there may be touching of the anterior and pos-
terior walls
Saber-Sheath Trachea
• Narrowing of the intrathoracic trachea, caused by deformity of tra-

cheal cartilage, is a highly specific sign of chronic obstructive pul-
monary disease
• Extrathoracic trachea is normal
• Marked decrease in the coronal diameter of the intrathoracic tra-

chea associated with an increase in its sagittal diameter (PA
diameter of the trachea ≤2/3 thirds of the diameter on the lateral
view)
Post-intubation Stenosis
• Focal narrowing that represents a late complication of intubation

• Reflects pressure necrosis of the wall of the trachea resulting from
overdistension of the cuff (exceeding the pressure in the capillaries
supplying the tracheal mucosa) or positioning the tip of the endo-
tracheal tube against the tracheal wall
• Most commonly, tracheal stenosis occurs at the level of a tracheos-
tomy stoma, secondary to fibrosis and granulation tissue at the site
Post-intubation Stenosis 233
a b
Fig. 17.2 Saber-sheath trachea. (a) In this patient with marked chronic
obstructive pulmonary disease, there is severe coronal narrowing of the intra-
thoracic trachea (small arrows) with an abrupt change to a more rounded cross-
sectional shape at the thoracic outlet (large arrows). (b) Lateral view shows the
sagittal diameter of the trachea to be within normal limits (arrow) [2]
• Presenting symptoms include cough, stridor, wheezing, and dys-

pnea on exertion (typically develop when narrowing of the lumen is
>50% of the cross-sectional area)
Imaging (Fig. 17.3)
• Short segment of tracheal narrowing, typically with an hourglass

configuration
• Frequently not appreciated on chest radiographs, so that the diag-
nosis requires CT (multiplanar and 3D rendering can demonstrate
narrowing not seen on axial images)
a b
Fig. 17.3 Tracheal stenosis after tracheostomy. (a) Frontal tomogram shows a
well-defined tubular area of tracheal narrowing at the tracheostomy cuff site. (b)
Lateral tomogram in a different patient demonstrates thickening of the anterior
tracheal wall (arrows), secondary to fibrosis and granulation tissue, at the site of the
tracheostomy stoma. This finding was of no clinical significance. (c) Coronal CT
image shows severe tracheal narrowing after tracheostomy (arrows) [a, b from 2]
Bronchiectasis 235
Other Causes of Tracheal Stenosis and Wall Thickening
• Amyloidosis – diffuse wall thickening/narrowing with focal nodu-

lar masses (see Fig. e15.34)
• ANCA-associated granulomatous vasculitis – focal or diffuse wall
thickening and narrowing (often renal and pulmonary involvement)
(see Fig. e17.7)
• Radiation fibrosis – tracheal narrowing associated with traction
bronchiectasis (see Fig. e17.8)
• Sarcoidosis – wall thickening, often with irregular or nodular ste-
nosis (may be enlarged lymph nodes compressing the airway)
• Tuberculosis – irregular wall thickening in the hyperplastic stage,
which leads to smooth narrowing in the fibrostenotic stage (usually
also hilar lymphadenopathy and pulmonary findings)
Bronchiectasis
• Progressive, irreversible localized or diffuse dilatation of the

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

tumor, arising before the bifurcation of left upper and lower lobe bronchi, causes
distal bronchiectasis (white arrows). Note the central carcinoid tumor (black
arrow) [1]
○○ Allergic bronchopulmonary aspergillosis (increased immuno-

logic response) (see page 180)
○○ Interstitial pulmonary fibrosis (loss of surrounding lung volume)
○○ Tuberculous scarring (upper lobes)
○○ Intrinsic bronchial disease (stenosis, extrinsic compression,
endobronchial mass)
• Classified into three categories (from least to most severe)
(Fig. 17.5):
○○ Cylindrical – uniform bronchial dilatation without tapering and
with parallel walls (Fig. 17.6)
Bronchiectasis 237
Fig. 17.5 Normal bronchus (arrow) [1]
Fig. 17.6 Cylindrical bronchiectasis. Lack of bronchial tapering (arrow) [1]

Fig. 17.7 Varicose bronchiectasis. “String-of-pearls” appearance (arrow) [1]
○○ Varicose – beaded appearance reflecting areas of bronchial dila-

tation and narrowing (Fig. 17.7)
○○ Cystic – severe bronchial enlargement and ballooning leading to
the formation of a string of multiple cysts that extend to the pleu-
ral surface and often contain air-fluid levels (Fig. 17.8; see Fig
e17.13)
Imaging
• Radiographs
○○ “Tram tracks” (parallel linear shadows representing the walls of
cylindrically dilated bronchi) (Fig. 17.9)
○○ Areas of multiple thin-walled cysts that may have air-fluid levels
and tend to be peripheral and cluster together in the distribution
of a bronchovascular bundle (Fig. 17.10)
Bronchiectasis 239
Fig. 17.8 Cystic bronchiectasis. Multiple cystic spaces, some with air-fluid
levels (arrows), predominantly involve the left lung [2]
Fig. 17.9 Tram track sign. Coned view of the right lower lung demonstrates
the characteristic parallel line shadows outside the boundary of the pulmonary
hilum. Note the coarse increase in interstitial markings in this patient with
chronic bronchitis [2]
Fig. 17.10 Bronchiectasis. Diffuse increase in interstitial markings with mul-

tiple thin-walled cysts radiating in a bronchovascular distribution with tramlines
(arrows) and peribronchial cuffing (arrowhead) [2]
• CT
○○ Multiple dilated, thin-walled circular lucencies (on cross-sec-
tion) and parallel linear opacities (bronchial walls sectioned
lengthwise)
○○ Signet ring sign – dilated bronchus adjacent to a normal pulmo-
nary artery branch (generally the same size) (Fig. 17.11)
○○ Lack of normal bronchial tapering
○○ Bronchi visible in the peripheral 1 cm of the lungs (see Fig.
e17.14)
○○ Mucoid impactions (simulating lung nodules or branching, fin-
ger-like opacities)
○○ Cystic bronchiectasis – classic “cluster of grapes” appearance
(see Fig. e17.15)
○○ Central varicose bronchiectasis – highly suggestive of allergic
bronchopulmonary aspergillosis (see Fig. e17.16)
Mucoid Impaction 241
Fig. 17.11 Signet ring sign. Multiple examples (arrows) in a patient with cys-
tic bronchiectasis. (Courtesy of Ritu Gill, MD, Boston)
Mucoid Impaction
• Airway filling by mucoid secretions that produce tubular or branch-

ing opacities that typically radiate from the hilum toward the
periphery of the lung
• Affects patients with bronchospasm (plugs present in dilated proxi-
mal segmental bronchi) and a sensitivity to Aspergillus fumigatus
• Almost always associated with asthma or pre-existing chronic
bronchial disease (especially cystic fibrosis)
• May also develop distal to a bronchial obstruction due to either
benign (tuberculosis, bronchostenosis) or malignant (lung cancer,
bronchial carcinoid) disease
• The affected portion of the lung remains aerated through collateral
air drift through interalveolar (pores of Kohn) and bronchiole-alve-
olar (canals of Lambert) connections
• Usually transient but may persist for months and even enlarge
Imaging
• Tubular or branching opacities that resemble fingers

• May have Y- or V-shaped configuration if there is plugging of a
bronchial bifurcation (Fig. 17.12; see Fig. e17.17)
• CT – bronchiectasis, low-attenuation mucus inspissated in the
bronchi, and a clear connection with the central airways
a b
Fig. 17.12 Mucoid impaction. (a) V-shaped and (b) Y-shaped masses
(arrows) [2]
Broncholithiasis
• Calcified or ossified material within the bronchial lumen

• Most commonly due to erosion or extrusion of a calcified adjacent
lymph node into the bronchial lumen
• Usually associated with a long-standing focus of necrotizing granu-
lomatous lymphadenitis, especially following tuberculosis (but the
frequency of broncholithiasis complicating granulomatous infection
is quite low)
• Most often involves the proximal right middle lobe bronchus and
the origin of the anterior segmental bronchi of the upper lobes
(because of airway anatomy and lymph node distribution)
• May be recurrent pneumonias related to episodes of bronchial
obstruction
• Broncholiths vary in size and are usually irregular, often possessing

spur-like projections or sharp edges
• Post-obstructive atelectasis, bronchiectasis, and air trapping
Bronchopleural Fistula (BPF) 243
Fig. 17.13 Broncholithiasis. Innumerable calcified masses scattered through-

out the lungs [2]
Bronchopleural Fistula (BPF)
• Abnormal connection between an airway and the pleural space, which

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

for aspergillus infection, more than half of the right hemithorax is filled with
fluid (air-fluid levels). (b) Four months later, the next follow-up image shows a
dramatic increase in the amount of air within the hemithorax. (c) CT demon-
strates a small focus of air immediately distal to the tracheal bifurcation (arrow),
adjacent to the stump of the bronchus intermedius or right lower lobe bronchus,
indicating the site of the leak
Foreign Body (Fig. 17.15)
• Aspirated foreign bodies are most common in young children,

especially under age 3
• In adults, they often occur in those with altered mental status or
represent teeth or dental devices
• Most frequently found in the lower lobe bronchi on the right,
because of the more direct angle of the right main bronchus with
the trachea
References 245
a b
Fig. 17.15 Bronchial foreign body. (a, b) Aspirated dental crown appears as
a dense metallic opacification (white arrow) causing collapse of the posterior
basal segment of the right lower lobe (black arrow). (Courtesy of Jennifer Ni
Mhuircheartaigh, MD, Boston)
Trauma
• Tracheal tear is an uncommon injury that tends to be associated

with fractures of the upper thorax, including the first three ribs,
clavicle, sternum, and scapula
• Bronchial tear, which may be a complication of surgical lobectomy,
presents as persistent pneumothorax (despite adequate placement
of one or more chest tubes), increasing subcutaneous emphysema
postoperatively, and focal peribronchial collections of air (see Fig.
e17.20)
• Collapsed lung due to complete rupture of a main bronchus pro-
duces the fallen lung sign (see Fig. 5.27)
References
W158–71.
3. Kaewlai R, Avery LL, Asrani AV, Novelline RA. Multidetector CT of blunt
thoracic trauma. Radiographics. 2008;28:1555–70.
Aorta
18
Acute Aortic Injury
• Serious complication of rapid deceleration injury or blunt chest

trauma and associated with a high mortality rate
• Cause of death in 15% of persons who die from motor vehicle acci-
dents; of these, up to 90% are fatal before arrival at the hospital,
and about half of short-term survivors die within the first 24 hours
• About 90% of acute aortic injuries visible on CT occur at the aortic
isthmus, just distal to the origin of the left subclavian artery
• About 2% of untreated cases eventually present as a chronic
pseudoaneurysm
Imaging
• Radiographs (Figs. 18.1 and 18.2)

○○ Normal chest radiograph has a 98% negative predictive value for
aortic injury
○○ Abnormal study has a low positive predictive value (<15%)
○○ Mediastinal widening seen at chest radiography may on CT be
shown not to result from an aortic injury, but rather from either a
hematoma secondary to sternal or vertebral body fracture or such


https://doi.org/10.1007/978-3-030-16826-1_18
248 18 Aorta
Fig. 18.1 Indirect signs of acute aortic injury. On a non-rotated frontal chest
radiograph, there is displacement of the trachea to the right (black arrow) with wid-
ening of the mediastinum and loss of the normal configuration of the aortic arch
(white arrow). (Case courtesy of Dr. Andrew Dixon, Radiopaedia.org, rID: 45368)
causes as mediastinal lipomatosis, tortuous vessels, vascular

anomalies, lymphadenopathy, or pleural fluid
○○ Indirect signs of acute aortic injury include:
• Deviation of the trachea to the right on a non-rotated image
• Displacement of an esophageal tube to the right of the T4 spi-
nous process
• Loss of the contour of the left margin of the aortic arch and
descending aorta
• Widened paraspinal lines and right paratracheal stripe
• Left apical pleural cap
• CT (see Fig. e18.1)
this chapter’s website on SpringerLink: https://doi.org/10.1007/
978-3-030-16826-1_18)
○○ Direct signs of aortic injury:
• Irregular contour of the aortic wall
• Intimal flap
• Intraluminal thrombus
• Pseudoaneurysm (contained rupture in which the majority of
the aortic wall has been breached, with luminal blood held in
only by a thin rim of the remaining wall or adventitia)
• Extravasation of contrast material
• Abrupt tapering of the descending aorta compared with the
ascending aorta (“pseudocoarctation”)
Acute Aortic Injury 249
Fig. 18.2 Mediastinal hemorrhage secondary to blunt chest trauma. (a)

Supine chest radiograph shows a widened right paratracheal stripe (arrows) mea-
suring 1 cm. (b) Aortography in the same patient demonstrates a pseudoaneu-
rysm at the level of the aortic isthmus (arrows). The arrowhead indicates an
intimal flap [1]
○○ Indirect sign – mediastinal hemorrhage (more specific if local-

ized to the periaortic region)
○○ Contrast-enhanced CT has a virtually 100% sensitivity and nega-
tive predictive value for traumatic aortic injury
250 18 Aorta
Aortic Dissection
There are two classification schemes to distinguish aortic dissections

that need emergency surgical repair from those that usually require
only medical management:
• Stanford classification:
○○ Type A (75%) – involves the ascending aorta (regardless of the
site of intimal tear or distal extent) (see Figs. e18.2 and e18.3)
○○ Type B (25%) – does not involve the ascending aorta (but tends
to propagate distally and obstruct arteries supplying the abdomi-
nal organs and lower extremities (see Fig. e18.4)
• DeBakey classification:
○○ Type I – originates in the ascending aorta and extends distally
throughout the aorta (Stanford A)
○○ Type II – confined to the ascending aorta (stops at the origin of
the brachiocephalic vessels) (Stanford A)
○○ Type III – originates in the descending aorta beyond the subcla-
vian artery and extends distally (Stanford B)
• Predisposing factors include atherosclerosis, hypertension (most
common cause in the elderly), cystic medial necrosis (e.g., Marfan
syndrome [most common cause in patients under age 40]), trauma,
aortic stenosis, bicuspid aortic valve, coarctation of the aorta,
Ehlers-Danlos syndrome, and cocaine use
• Sudden onset of “ripping” chest or back pain (male-female ratio
of 3:1)
Imaging
• Radiographs
○○ Progressive widening of the superior mediastinum on serial
images, often with an irregular or wavy outer border of the aorta
(Fig. 18.3a)
○○ Separation (>4 mm) between intimal calcification and the outer
border of the aortic shadow indicates widening of the aortic wall
(see Fig. e18.5)
Aortic Dissection 251
a b
Fig. 18.3 Huge aortic dissection. (a, b) Striking prominence of the entire
descending thoracic aorta (arrows). Note the long intimal flap in b
• CT
○○ Double-barrel aorta with an intimal flap separating the true
and false lumen (usually larger and more slowly filling)
(Fig. 18.3b)
○○ Intimal tears spiral down the aorta, with the false lumen lying
anterior and to the right in the ascending aorta and posterior and
to the left in the descending aorta
○○ Interruption of the continuous intimal flap indicates entry and
reentry points of the dissection (see Fig. e18.6)
○○ May be obstruction of one or more vessels arising from the aorta
(especially the left renal artery)
Management
• Type A – immediate surgical repair (because of a higher risk of

aortic rupture and tendency to extend to the aortic root, coronary
arteries, and pericardium)
• Type B – medical therapy for hypertension (unless development of
complications, especially rupture or occlusion of a major branch of
the aorta)
252 18 Aorta
• Without treatment, there is a high mortality rate (1–2% per hour for
the first 2 days)
• With prompt appropriate surgical intervention, the long-term sur-
vival is about 50%
Aortic Aneurysm
• Localized or diffuse dilatation of the aorta (≥50% of normal

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

density (Fig. 18.4)
Aortic Aneurysm 253
a b
Fig. 18.4 Aneurysm of the descending aorta. (a) Frontal view demonstrates
a localized bulging of the descending aorta (arrows). (b) Lateral view in another
patient shows aneurysmal dilatation of the lower thoracic aorta (arrows). Note
the marked tortuosity of the remained of the descending aorta [1]
• Curvilinear calcification may occur in the outer wall (ascending

aorta calcification suggests syphilis or hyperlipidemia and poses an
embolic risk in patients scheduled for CABG)
• CT:
○○ Crescent sign – high attenuation of the aortic wall or mural
thrombus on non-contrast images suggests acute or impending
rupture (see Fig. e18.7)
○○ Ruptured aneurysm produces high-attenuation blood in periaor-
tic tissues (see Fig. e18.8)
• MRI – increased T1 signal in a saccular aneurysm is consistent
with thrombosis or slow flow
Management
• Significant risk of rupture of a saccular aneurysm if:

○○ > 5.5 cm in the ascending aorta
○○ > 6.0 cm in the descending aorta
• Annual growth rate of >1 cm/year (or >0.5 cm/6 months) also is an
indication for surgical repair
254 18 Aorta
Pseudoaneurysm of the Aorta
• Contained rupture in which the majority of the aortic wall has been
breached and luminal blood is held in only by a thin rim of the
remaining wall or adventitia
• Typically secondary to focal aortic transection
• About 85% result from penetrating trauma (gunshot or stab
wounds); the remainder develops after blunt trauma (motor vehicle
accidents or falls)
• Relatively few develop from penetrating atherosclerotic ulcers
Imaging (see Fig. 18.2b)
• Generally occur along the undersurface of the aortic isthmus, at or

near the site of the ductus arteriosus
Coarctation of the Aorta
• Narrowing of the aortic arch with partial obstruction of blood flow

• In the more common “adult” type, aortic narrowing occurs at or
just distal to the level of the ductus arteriosus (double bulge repre-
sents prestenotic and poststenotic dilatation)
• In the “infantile” variety, there is a long segment of narrowing lying
proximal to the ductus (obligatory right-to-left shunt and early con-
gestive heart failure)
• Associated conditions include bicuspid aortic valve (75%), Turner
syndrome (20%), and cerebral aneurysms (10%)
• Characteristic difference in blood pressure between the upper and
lower extremities with decreased femoral pulses
Imaging
• Enlargement of the left ventricle with a characteristic double bulge

in the region of the aortic knob (figure-3 sign on plain chest radio-
graphs and reverse figure-3, or figure-E, sign on the barium-filled
esophagus) (see Fig. e18.9)
Reference 255
• Inferior rib notching (usually involving the posterior third to eighth

ribs), which rarely develops before age 6
• Angiographic demonstration of a pressure gradient >20 mm Hg
may indicate a need for intervention (surgery or balloon angio-
plasty with stent placement)
Reference

Cardiac-Pericardial Disease
19
It is usually easy to determine whether the heart is enlarged or of nor-

mal size. When unsure, one can measure the cardiothoracic ratio
(CTR). On a full inspiration PA image, the widest transverse diameter
of the heart should be <50% of the widest internal diameter of the rib
cage (ratio of 0.55 or greater suggests enlargement of the cardiac sil-
houette). Remember that in a normal patient, the CTR may be abnor-
mally high (mimicking cardiomegaly) on an AP or lordotic view, or if
there are low lung volumes.
Apparent enlargement of the cardiac contour does not necessarily
mean that the heart itself is large. For example, pericardial effusion
can enlarge the apparent size of the heart (and the CTR), even though
the heart size is within normal limits.
Enlargement of specific cardiac chambers can be suggested radio-
graphically, but an accurate evaluation requires CT or echocardiogra-
phy. The following are traditional observations suggesting enlargement
of specific cardiac chambers:
• Left ventricle (forms the left heart border) – displacement of the

cardiac apex to the left, inferiorly, or posteriorly (Figs. 19.1 and
19.2)


https://doi.org/10.1007/978-3-030-16826-1_19
258 19 Cardiac-Pericardial Disease
Fig. 19.1 Left ventricular enlargement. Downward and lateral displacement

of the cardiac apex. Note that the cardiac shadow extends below the dome of the
left hemidiaphragm (black arrow). The ascending aorta is strikingly dilated
(white arrows), consistent with an underlying component of stenosis in this
patient with aortic regurgitation [1]
Fig. 19.2 Left ventricular enlargement. Marked posterior prominence of the

left ventricle (arrows) in this patient with an acute myocardial infarction [1]
19 Cardiac-Pericardial Disease 259
a b
Fig. 19.3 Right ventricular enlargement. (a) Lateral and upward displace-
ment of the radiographic cardiac apex (arrow) in a patient with tetralogy of
Fallot. (b) On the lateral view, the enlarged right ventricle fills most of the
retrosternal space (arrows) [1]
• Right ventricle (most anterior chamber) – filling of the retrosternal

space on the lateral view; uplifted cardiac apex on the frontal view
(Fig. 19.3; see Fig. e19.1)

chapter’swebsiteonSpringerLink:https://doi.org/10.1007/978-3-030-
16826-1_19)
• Left atrium (most posterior chamber)

○○ Double density sign – right side of the enlarged left atrium
becomes visible as a “mass” superimposed over the right side of
the heart (Fig. 19.4a)
○○ Elevation of the left main bronchus that results in splaying of the
carina, with the interbronchial angle >90° (Fig. 19.4b)
○○ On the lateral view, bulge of the left atrial region (above the level
of prominence related to an enlarged left ventricle)
○○ Posterior displacement of the esophagus (can cause dysphagia)
(Fig. 19.5)
• Right atrium (forms the right heart border) – lateral bulging or
elongation of the right heart border (Fig. 19.6; see Fig. e19.2)
a b
Fig. 19.4 Left atrial enlargement. (a, b) Gross cardiomegaly with enlarge-
ment of the left atrium and left ventricle in this patient with mitral regurgitation.
Note the striking double contour configuration (arrows, a) and elevation of the
left main bronchus (arrows, b), characteristic signs of left atrial enlargement.
The aortic knob is normal in size, and there is no evidence of pulmonary vascu-
lar congestion [1]
If there is overall enlargement of the cardiac silhouette, an analysis of

the size of the left atrium and the aorta can suggest the diagnosis of an
underlying cardiac abnormality:
• Enlarged left atrium – mitral regurgitation (see Fig. 19.4)

• Enlarged aorta – aortic regurgitation (see Fig. 19.1)
• Neither enlarged – dilated cardiomyopathy, high-output state, or
pericardial effusion (Fig. 19.7)
Note: The radiographic appearance of a discordance between sub-

stantial enlargement of the cardiac silhouette and normal or mini-
mally elevated pulmonary venous pressure should suggest two
diagnostic possibilities – cardiomyopathy and pericardial effusion
(see Fig. e19.3; see Fig. 2.1a)
If the overall size of the cardiac silhouette is normal:
• Enlarged left atrium – mitral stenosis (see Fig. e19.4)

• Enlarged aorta – aortic stenosis or aneurysm (see Fig. e19.5)
• Neither enlarged – hypertrophic cardiomyopathy, pulmonary artery
hypertension, and acute myocardial infarction
19 Cardiac-Pericardial Disease 261
Fig. 19.5 Left atrial enlargement. The enlarged chamber produces a discrete
posterior indentation (arrows) on the barium-filled esophagus in a patient with
mitral stenosis [1]
a b
Fig. 19.6 Right atrial enlargement. (a, b) Striking prominence of the right
atrium in this patient with tricuspid insufficiency [1]
Fig. 19.7 Alcoholic cardiomyopathy. Generalized enlargement of the cardiac

silhouette involving all chambers, without special prominence of the left atrium
or aorta [1]
Mitral Annulus Calcification
• Degenerative, non-inflammatory process that primarily occurs in

persons over age 60, is more common in women, and usually is of
no clinical significance
• May be associated with aortic stenosis and hypertension (possibly
related to increased strain on the mitral valve due to pressure over-
load on the left ventricle) and an increased risk of stroke
Imaging (Fig. 19.8)
• Bandlike calcification typically in a pattern resembling a reverse

letter “C” or the letter “J”
• Can also appear like the letter “O” if there is involvement of the
anterior valve leaflet
Myocardial Infarction: Complications
Ventricular Aneurysm (True)
• Focal dyskinetic outpouching of the left ventricular wall that devel-

ops in fewer than 5% of ST elevation myocardial infarctions (STEMI).
• Involvement of all layers of the muscular wall
Myocardial Infarction: Complications 263
Fig. 19.8 Mitral annulus calcification (arrows) [1]
a b
Fig. 19.9 Ventricular aneurysm. (a, b) Bulging and curvilinear peripheral

calcification (arrows) along the lower left border of the heart near the apex. Note
the relatively anterior position of the aneurysm on the lateral view [1]
• Usually occurs along the anterolateral or apical wall of the left ven-
tricle and is associated with occlusion of the left anterior descend-
ing coronary artery
• Curvilinear calcification along the left ventricular contour (Fig. 19.9;
see Fig. e19.6)
Pseudoaneurysm (False)
• Contained ventricular rupture in which there is no myocardium in

the aneurysm wall, which is composed of pericardium
• Typically occurs on the upper diaphragmatic and posterior wall and

is associated with occlusion of the circumflex or right coronary
artery
• Danger of impending complete rupture, which is suggested by
interval increase in size of the pseudoaneurysm over sequential
images
Dressler Syndrome
• Autoimmune pericarditis, characterized by fever and pleuroperi-

cardial chest pain, beginning 1–6 weeks after an acute myocardial
infarction
• Striking response to steroid therapy
• Pleural effusion (transudate), which is bilateral in 50% of patients
(usually greater on the left), is the most common finding (80%) and
may occur alone
• Pericardial effusion
High-Output Failure
• Uncommon condition in which there is elevated cardiac output and

low systemic vascular resistance (due to peripheral vasodilatation
or arteriovenous shunting)
• May be associated with increased oxygen consumption that reflects
increased metabolic demand
• Most common causes:
○○ Anemia (especially sickle cell disease and thalassemia)
○○ Thyrotoxicosis (high metabolic rate)
○○ Paget’s disease (multiple microscopic arteriovenous malforma-
tions in affected bones)
○○ Pregnancy (increased blood volume and flow)
Imaging
• Enlargement of the heart with generalized engorgement of pulmo-

nary vessels (see Fig. e19.7)
Pericardial Disease 265
Pericardial Disease
Normally, there is up to about 40 mL of fluid within the pericardial
space, separating the parietal and visceral pericardial layers. An
abnormal accumulation of pericardial fluid initially collects posterior
to the left ventricle (dependent portion with the patient in a supine
position). As the amount of pericardial effusion increases further, it
tends to accumulate more along the right heart border until it fills the
entire pericardial space and encircles the heart.
Pericardial Effusion
• Severity of symptoms varies greatly depending on the underlying

cause, the rate at which the pericardial fluid accumulates, and the
total amount present
• Faint, distant heart sounds on auscultation
• Cardiac tamponade:
○○ May occur rapidly (trauma, myocardial rupture) or slowly
(cancer)
○○ Rapid accumulation of as little as 100–200 mL of pericardial
fluid can severely decrease ventricular filling during diastole
○○ Medical emergency because of such complications as pulmo-
nary edema, shock, and death
Causes
• Congestive heart failure – evidence of venous congestion and fre-

quently an associated pleural effusion (often unilateral on the right)
• Infection – most commonly viral (coxsackievirus) or mycobacterial
• Connective tissue disease – systemic lupus erythematosus, rheuma-
toid arthritis, scleroderma, and polyarteritis nodosa
• Neoplasm – lymphoma and lung, breast, or melanoma metastases
• Drug-induced – procainamide, hydralazine, and phenytoin
• Uremia – pericardial effusion develops in about 15% of patients on
prolonged hemodialysis (may collect rapidly and be life
threatening)
• Myxedema
• Trauma – rapid development may produce severe alteration of car-
diac function with minimal change in the radiographic cardiac
silhouette
• Idiopathic (diagnosis of exclusion)
Imaging
• Radiographs
○○ Rapid increase in the size of the cardiac silhouette on serial chest
films (suggests pericardial effusion rather than cardiomyopathy
as the cause of a large heart with normal pulmonary
vascularity)
○○ The heart often assumes a globular, water-bottle, or flask-shaped
configuration (both sides of the heart appearing rounded and dis-
placed laterally), especially when the lungs remain clear
(Fig. 19.10; see Fig. e19.8)
○○ Epicardial fat pad sign
• On a lateral projection, virtually pathognomonic widening
(>4 mm) of the normally thin soft-tissue opacity of the peri-
cardium between the lucent stripes representing the anterior
mediastinal and subepicardial fat (Oreo cookie sign)
(Fig. 19.11)
• Low sensitivity but high specificity for pericardial effusion
Fig. 19.10 Uremic pericardial effusion. Globular enlargement of the cardiac

silhouette in a child on prolonged hemodialysis [1]
Pericardial Disease 267
• CT/MRI
○○ Sensitive modalities for detecting and confirming pericardial
effusion (see Fig. e19.9)
○○ CT attenuation measurements and signal characteristics at MRI
can characterize pericardial effusions as serous or hemorrhagic/
proteinaceous (see Figs. e19.10 and e19.11)
Fig. 19.11 Epicardial fat pad sign in pericardial effusion, (a) On the lateral
view in a normal patient, a thin, relatively dense line (arrow) representing the
normal pericardium may be seen between the anterior mediastinal and subepi-
cardial fat. (b) In this patient, there is a wide soft-tissue density separating the
subepicardial fat stripe (arrows) from the anterior mediastinal fat. This is a vir-
tually pathognomonic sign of pericardial effusion or thickening [1]
○○ Signs of pericardial tamponade include:

• Compression of the right heart chambers
• Flattening or inversion of the wall of the right ventricle
• Inverted interventricular septum
• Enlargement of the SVC and IVC
Constrictive Pericarditis
• Fibrotic pericardial thickening limiting the ability of the heart to

function normally and leading to clinical signs of heart failure
• Most frequent causes are cardiac surgery and radiation therapy
• Less common etiologies include infection (viral or tuberculous),
connective tissue disease, uremia, and neoplasm
Imaging
• Pericardial thickening (≥4 mm) with a reduced cardiac volume and

a narrowed, tubular configuration of the right ventricle
• CT is exquisitely sensitive for detecting often-associated pericar-
dial calcification, which predominantly is seen in an inferior and
right-sided location
• MRI is more sensitive in distinguishing between pericardial effu-
sion and thickening (but cannot detect calcification)
• Contrast enhancement of the pericardium suggests an active inflam-
matory process
Pericardial Calcification
• Usually related to prior pericarditis (most commonly viral or ure-

mic) or trauma
• Occurs in about 50% of cases of constrictive pericarditis (strong
evidence to distinguish this condition from restrictive cardiomy-
opathy, which can have a similar clinical appearance)
Imaging
• Curvilinear calcification that conforms to the margins of the peri-

cardial sac and often is best visualized on lateral chest radiographs
(Fig. 19.12)
References 269
Fig. 19.12 Chronic constrictive pericarditis. Dense calcification in the peri-

cardium (arrows) surrounding a normal-sized heart [1]
• If thin and linear – typically viral or uremic pericarditis, but could

be prior trauma or surgery, or a connective tissue disorder
• If thick, irregular, and amorphous – most likely old tuberculous
pericarditis or asbestos plaques (as in pleural disease)
References
2. Shahrzad M, Le TSN, Silva M, Bankier AA, Eisenberg RL. Anterior medias-
tinal masses. AJR. 2014;203:W128–38.
3. Wang ZJ, Reddy GP, Gotway MB, et al. CT and MR imaging of pericardial
disease. Radiographics. 2003;23:S167–80.
Diaphragm
20
The two hemidiaphragms separate the thoracic and abdominal

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


https://doi.org/10.1007/978-3-030-16826-1_20
272 20 Diaphragm
Fig. 20.1 Big rib sign. (a) Lateral view shows that the magnified right ribs
appear larger and are projected more posteriorly (black arrows) when compared
with the smaller and more anterior left ribs (white arrow). Note that the lower
thoracic vertebrae appear whiter than those above, the opposite of the normal
pattern (spine sign), indicating an abnormality at the base. The hemidiaphragm
extending to the larger ribs (right) is sharply seen, unlike the other hemidia-
phragm (left) that is not well visualized posteriorly. Therefore, the spine sign
should be resulting from an abnormality at the left base. (b) Frontal view con-
firms the left basilar abnormality, representing a combination of pleural fluid
and underlying volume loss in the lower lung
Eventration 273
Eventration (Fig. 20.2; See Fig. e20.1)

website on SpringerLink: https://doi.org/10.1007/978-3-030-16826-1_20)
• Congenital elevation of a portion of the hemidiaphragm due to a
thin and weakened membranous sheet replacing a portion of the
normal diaphragmatic muscle
• Usually involves only the anteromedial portion of the right hemi-
diaphragm, through which a portion of the right lobe of the liver
bulges (unlike paralysis or weakness of the hemidiaphragm, which
generally affects the entire muscle uniformly)
• In a posterior eventration, upward displacement of the kidney can
produce a rounded mass
• Frontal view may show a “double diaphragm” appearance, which
can be confirmed as an eventration on the lateral projection
• No clinical significance
Fig. 20.2 Partial eventration. Elevation of the central portion of the right
hemidiaphragm (arrow) [1]
274 20 Diaphragm
Phrenic Nerve Paralysis (Fig. 20.3; See Fig. e20.2)
• Causes of phrenic nerve paralysis include:

○○ Process interfering with the normal function of the phrenic nerve
(inadvertent surgical transaction, primary bronchogenic carci-
noma, or mediastinal metastases)
○○ Intrinsic neurologic disease (poliomyelitis, Erb’s palsy, periph-
eral neuritis, hemiplegia)
○○ Injury to the phrenic nerve, thoracic cage, cervical spine, or bra-
chial plexus
○○ Pressure from a substernal thyroid or aneurysm
○○ Lung or mediastinal infection (paralysis may be temporary)
Imaging
• Unilateral (infrequently bilateral) diaphragmatic elevation with

characteristic paradoxical motion of the affected hemidiaphragm
(tends to ascend rather than descend with inspiration and the fluo-
roscopic “sniff test”)
a b
Fig. 20.3 Phrenic nerve palsy. (a, b) Images in two separate patients show
paralysis of the elevated right hemidiaphragm due to a primary bronchogenic car-
cinoma (arrows) involving the phrenic nerve (a From Ref. [1]; b From Ref. [2])
Traumatic Rupture of Hemidiaphragm 275
raumatic Rupture of Hemidiaphragm (Figs. 20.4 and

T
20.5; See Fig. e20.3)
• Uncommon, but serious, complication of blunt and penetrating

trauma that predominantly occurs in young men
• Much more frequent on the left (ascribed to either the protective
effect of the liver on the right hemidiaphragm or relative weakness
of the left hemidiaphragm)
• Initial chest radiograph is nondiagnostic in up to 50% of cases
• Rapid diagnosis is necessary to prevent such serious complications
as bowel obstruction and strangulation
• Congenital diaphragmatic hernia typically occurs on the left (see
Fig. e20.4)
Fig. 20.4 Left diaphragmatic rupture (motor vehicle accident). Initial

radiograph shows intrathoracic herniation of the stomach (S), a pleural effusion,
a pulmonary contusion, and contralateral mediastinal shift [3]
276 20 Diaphragm
Fig. 20.5 Left diaphragmatic tear. Sagittal CT demonstrates a large defect

(arrows) with herniation of the stomach (∗) into the thorax [4]
Imaging
• CT
○○ Multiplanar imaging and speed of acquisition make this the pre-
ferred modality to directly demonstrate a defect or discontinuity
of the hemidiaphragm in the setting of acute trauma
• Radiographs – indirect signs of left hemidiaphragm injury
○○ Nasogastric tube coiled in the thorax above the left hemidiaphragm
○○ Presence of gas-filled stomach or bowel in the thorax
○○ Apparently elevated hemidiaphragm with an unusual contour
(loss of normal dome shape)
○○ Changing hemidiaphragm levels on serial radiographs
○○ Shift of the mediastinum to the right
Diaphragmatic Herniation
• Hiatal – see page 219

• Paraesophageal
• Morgagni – see page 216
• Bochdalek – see page 219
References 277
Juxtaphrenic Peak (Fig. 20.6)
• Peak arising from the medial part of the hemidiaphragm, most

commonly caused by traction from the accessory oblique fissure in
patients with volume loss in the upper lobe related to collapse or
lobectomy
a b
Fig. 20.6 Juxtaphrenic peak. (a) Preoperative radiograph shows that the right
hemidiaphragm has a normal appearance. (b) After right upper lobectomy, the
patient developed a classic juxtaphrenic peak (arrow)
References
2. Nason LK, Walker CM, McNeeley MF, et al. Imaging of the diaphragm:
anatomy and function. Radiographics. 2012;32:E51–70.
3. Iochum S, Ludig WF, et al. Imaging of diaphragmatic injury: a diagnostic
challenge? Radiographics. 2002;22:S103–18.
Esophagus
21
Achalasia
• Functional obstruction of the distal esophagus with proximal dila-

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


https://doi.org/10.1007/978-3-030-16826-1_21
280 21 Esophagus
Imaging
• Dilatation and tortuosity of the esophagus can produce a widened

mediastinum (double contour) (Fig. 21.1)
• Often an air-fluid level in the retrotracheal region, which on the
frontal view projects to the right side adjacent to the cardiac shadow
(see Fig. e21.1a)
978-3-030-16826-1_21)
• Anterior bowing of the trachea (see Fig. e21.1b)
• Small or absent gastric air bubble
• Esophagram – characteristic smoothly tapered, conical narrowing
of the distal esophagus (beak sign) (Fig. 21.2)
• CT – filling of the dilated esophagus with food (see Figs. e21.2 and
e21.3)
a b
Fig. 21.1 Achalasia. (a) The margin of the dilated, tortuous esophagus
(arrows) parallels the right border of the heart. (Courtesy of James Heilman,
MD, Vancouver, Canada). (b) In another patient, a lateral view shows dramatic
dilatation of the esophagus (arrows) [1]
Boerhaave Syndrome 281
Fig. 21.2 Achalasia. Beak sign (arrow) [1]
Boerhaave Syndrome
• Transmural perforation of the distal esophagus (relatively unsup-

ported by connective tissue), which is related to severe vomiting
that produces a sudden increase in intraluminal pressure
• Most frequently occurs in males and usually follows heavy drink-
ing and a large meal
• The tear is classically vertical and involves the posterolateral wall
of the esophagus
• Patients usually present with sudden retrosternal or epigastric pain,
which often radiates to the neck or shoulder blades and is associ-
ated with fever and leukocytosis
• Frequently misdiagnosed as myocardial infarction, aortic dissec-
tion, pulmonary embolism, pancreatitis, or perforated peptic
ulcer
• High morbidity and mortality (70%) if there is a delay of more than
24 hours in making the diagnosis and instituting appropriate treat-
ment (intravenous volume resuscitation, broad-spectrum antibiot-
ics, and generally prompt surgical intervention)
282 21 Esophagus
Fig. 21.3 Boerhaave syndrome. Pneumomediastinum along the outer margin

of the descending thoracic aorta (white arrows) and extending into the soft tis-
sues of the neck (black arrows). (https://commons.wikimedia.org/wiki/
File:CXR_Pneumomediastinum.jpg to410/Wikimedia)
Imaging
• Pneumomediastinum that surrounds the aorta and extends into the

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

agus, predominantly in the cervical region (at or just about the level
of the thoracic inlet) or proximal to an esophageal stricture
Foreign Body 283
Fig. 21.4 Boerhaave syndrome. Esophagram with water-soluble contrast

shows substantial extravasation (white arrow) through the transmural perfora-
tion of the esophagus (black arrow). (Courtesy of Gillian Lieberman, MD,
Boston)
• Sharp swallowed objects that transiently lodge in the esophagus

can abrade the esophageal mucosa, so that patient symptoms can
persist long after the foreign material has passed (until the mucosal
abrasion has healed)
• Radiographs easily demonstrate metallic objects (pins, coins,

small toys) that are frequently swallowed by infants and young
children
• Two views are always necessary to make certain the dense object
projected over the esophagus that truly lies within it
• Nonopaque objects made of wood or aluminum (and some light
alloys) are usually impossible to detect radiographically because
the density of these structures is almost equal to that of soft
tissue
284 21 Esophagus
Fig. 21.5 Foreign body. (a) Frontal and (b) lateral views of a child show a
coin lodged in the esophagus. (Courtesy of Edward Lee, MD, Boston, MA)
References
Pathology. 6th ed. St Louis: Elsevier/Mosby; 2016.
2. Franquet T, Erasmus JJ, Giménez A, et al. The retrotracheal space: normal
anatomic and pathologic appearances. Radiographics. 2002;22:S231–46.
Abnormal Air
22
Pneumothorax
• Air in the pleural space that produces volume loss in the ipsilateral

lung
Common causes
• Spontaneous (rupture of a small, usually apical bleb, especially in

tall, asthenic individuals) (Fig. 22.1)
• Trauma (penetrating or blunt, rib fracture, tracheobronchial injury)
• Complication of mechanical ventilation (barotrauma)
• Chronic obstructive pulmonary disease
• Chronic pulmonary disease (e.g., sarcoidosis, Langerhans cell
histiocytosis)
• Pneumocystis jiroveci pneumonia (formerly Pneumocystis carinii)
and other infections (see Figs. e22.1 and e22.2)
978-3-030-16826-1_22)
• Lung abscess with bronchopleural fistula
• Rupture of the esophagus (Boerhaave syndrome)


https://doi.org/10.1007/978-3-030-16826-1_22
286 22 Abnormal Air
a b
Fig. 22.1 Spontaneous pneumothorax. Complete collapse of the right (a)

and left (b) lungs in two different patients [1]
• Iatrogenic (surgery, lung or pleural biopsy, thoracentesis, central

line placement) (see Figs. e22.3 and e22.4)
Imaging
• Most commonly apical and lateral air without peripheral lung

markings, which parallels the curvature of the lateral chest wall
and is separated from normal lung by a sharp pleural margin
(Fig. 22.2)
• Accentuated on expiration views, as the volume of the normal lung
decreases and gas fills the pleural space (see Fig. e22.5)
• Supine view:
○○ Deep sulcus sign – air in the pleural space predominantly col-
lects in the anteromedial and subpulmonic portions of the chest
and may produce an unusually deep and lucent costophrenic
sulcus or upper abdomen (may be the only finding on supine
radiographs); highly specific, though not sensitive (Fig. 22.3;
see Fig. e22.6)
○○ Pneumothorax also may cause an unusually sharp outline of the
cardiac and mediastinal contours (because of adjacent free air
rather than aerated lung), or air may accumulate in a subpul-
monic location to produce a sharply defined hemidiaphragm
Pneumothorax 287
Fig. 22.2 Small pneumothorax. Collection of air in the left apex and along
the left lateral chest wall. The pleural line (arrows) is somewhat difficult to visu-
alize on this image. (Courtesy of Jeffrey Klein, MD, Burlington, VT)
Fig. 22.3 Pneumothorax. Deep sulcus sign on the left (arrows) representing an
anterior pneumothorax in a supine patient
288 22 Abnormal Air
a b
Fig. 22.4 Hydropneumothorax. (a, b) Multiple air-fluid levels (black arrows) in

the right hemithorax representing areas of loculated pneumothorax related to bron-
chopleural fistula. The large right superior mediastinal mass (white arrow) reflects
metastatic spread from a previously resected carcinoma of the right lung [1]
• Hydropneumothorax – presence of an air-fluid level in the pleural

space on an upright view (Fig. 22.4)
• Selective resorption of pleural fluid can result in a loculated pneu-
mothorax (see Fig. e22.7)
• Size of pneumothorax – in general, if the distance between the lung
margin and the apex of the chest wall is <2 cm, no chest tube is
required (often inserted if distance is >2 cm)
• Note that the decision whether to insert a chest tube is primarily
based on the clinical status of the patient
Mimics of Pneumothorax
• Apparent pleural line simulating pneumothorax

• Skin fold (relatively unsharp and thicker band of opacity rather
than the thin white line of visceral pleura) (Fig. 22.5a–c)
• Monitoring or support lines (Fig. 22.5d)
• Medial margin of the scapula
• Bullous emphysema (margin of a large cyst may simulate a pleural
line, and CT may be necessary to make this distinction)
Mimics of Pneumothorax 289
c d
Fig. 22.5 Skin fold. (a) Curvilinear line (arrows) mimicking a right pneumo-
thorax. (b) Image obtained 1 minute later shows that there is no pneumothorax,
indicating that the previous finding represented only a skin fold. (c) Prominent
skin fold on the left (white arrows) mimics a pneumothorax in a patient who has
a small right pneumothorax (black arrow) after a biopsy. The opaque area
medial to the pneumothorax represents post-procedure hemorrhage. (d) Outer
margin of a chest tube mimics a left pneumothorax (arrows). (c, Courtesy of
Ritu Gill, MD, Boston)
290 22 Abnormal Air
Tension Pneumothorax
• Medical emergency, in which there is shift of mediastinal structures

to the contralateral side
• Continually increasing intrathoracic pressure may compromise venous
return to the heart and lead to cardiopulmonary collapse (Fig. 22.6)
• Note that there may be complete collapse of a lung without any
midline shift to suggest tension (Fig. 22.7)
Fig. 22.6 Tension pneumothorax. Substantial collapse of the right lung

(white arrows) with shift of the mediastinum to the contralateral side. Black
arrow points to a malpositioned endotracheal tube in the right main bronchus,
with early volume loss in the left lower lung
Fig. 22.7 Total pneumothorax. Complete collapse of the right lung, without
any midline shift to suggest tension
Pneumomediastinum 291
Pulmonary Interstitial Emphysema (See Fig. e22.8)
• Alveolar rupture due to increased pressure/volume, which primar-

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

pressure ventilation in a child with hydrocarbon poisoning, there is the
development of a pneumomediastinum (white arrows) and small right
pneumothorax (black arrow). Note that the stiffness of the lungs has prevented
substantial collapse [1]
Pneumomediastinum
• Air within the mediastinum

292 22 Abnormal Air
Causes of air within the mediastinum
• Extension of pulmonary interstitial emphysema (in about one of

three patients)
• Trauma
○○ Chest wall – closed chest trauma causing abrupt increase in
intrathoracic pressure
○○ Esophagus – most frequently occurs during episodes of severe
vomiting (Boerhaave syndrome), with the tear typically involv-
ing the posterolateral wall of the lower portion of the esophagus
(relatively unsupported by connective tissue)
○○ Bronchi/trachea – caused by shearing force or a sudden increase
in pressure against a closed glottis
• Iatrogenic – surgery or instrumentation of the esophagus, trachea,
bronchi, or neck; overinflation during anesthesia and respiratory
therapy
• Extension of gas from the neck or retroperitoneum – trauma, surgi-
cal procedures, or penetrating cervical lesions
• Asthma – primarily in children
Fig. 22.9 Pneumomediastinum. The mediastinal pleura is displaced laterally

and appears as a long linear opacity (arrows) parallel to the heart border but
separated from it by air [3]
Pneumopericardium 293
a b
Fig. 22.10 Severe pneumomediastinum. (a, b) Large amounts of mediastinal

air (white arrow) along with extensive subcutaneous air, both anteriorly and
laterally (black arrows)
Images
• Linear, streak-like lucencies surrounding mediastinal structures

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

surgery or penetrating trauma
Images (Fig. 22.11, see Fig. e22.11)
• Continuous band of lucency surrounding the heart

• To distinguish from pneumomediastinum, pneumopericardium does
not extend beyond the root of the great vessels at the level of the main
pulmonary artery (upper limit of the parietal pericardial layer)
294 22 Abnormal Air
Fig. 22.11 Pneumopericardium. Gas filling the pericardial sac causes car-
diac tamponade. This newborn with respiratory distress syndrome developed
pneumopericardium associated with barotrauma from mechanical ventilation
[4]
Subcutaneous Emphysema
• Dissection of air into the soft tissues of the chest wall, which can
extend upward into the neck and downward into the upper abdomi-
nal wall
• Usually related to a thoracotomy drainage tube or penetrating chest
wall injury (including surgery)
Images (Fig. 22.12)
• Streaks of air outlining muscle bundles produce a striated appear-

ance along the chest wall
• Involvement of the pectoral muscles causes streaks projected across
the chest, making it difficult to evaluate the underlying lung
• No clinical significance and typically resolves within a few days
• Progressive increase in subcutaneous emphysema after thoracic
surgery is worrisome for bronchial leak
References 295
Fig. 22.12 Subcutaneous emphysema. Streaks and bubbles of subcutaneous

air (black arrows) are evident in the soft tissues along the lateral borders of the
thorax, especially on the right. Broad lucencies outlining pectoral muscle bun-
dles (open arrows) overlie the anterior chest wall. Note the fracture of the left
scapula (white closed arrow) and multiple rib fractures [3]
References
2. Agrons GA, Courtney SE, Stocker JT, Markowitz RI. Lung disease in
premature neonates: radiologic-pathologic correlation. Radiographics.
2005;25:1047–73.
4. Restropo CS, Lemos DF, Lemos JA, et al. Imaging findings in cardiac tam-
ponade with emphasis on CT. Radiograpics. 2007;27:1595–610.
Abnormalities Outside the Thorax
23
Although the vast majority of abnormalities on chest radiographs and

CT scans involve the heart and lungs, it is important to also examine
all other areas on the images. The following are examples of the broad
spectrum of pathology outside the heart and lungs that may be evident
on chest examinations.
Mass Impressing/Displacing the Lower Cervical

Trachea (Fig. 23.1)
• Most commonly a thyroid adenoma or goiter (95% benign and of

no clinical significance)
• Usually detected as an incidental finding on a frontal chest radio-
graph (confirmation can be made clinically by palpation of the
neck)
• Peripheral rim of calcification suggests a benign lesion (adenoma)
• Ultrasound, CT, or radionuclide studies can indicate the precise
nature of the mass


https://doi.org/10.1007/978-3-030-16826-1_23
298 23 Abnormalities Outside the Thorax
b
Fig. 23.1 Thyroid goiter. (a) Right thyroid mass (arrows) impresses the lower
cervical trachea and displaces it to the left. (b) Left thyroid mass impresses the
trachea (arrow)
Cervical Rib (See Fig. e23.1)

this chapter’s website on SpringerLink: https://doi.org/10.1007/
978-3-030-16826-1_23)
Gastrointestinal Abnormalities 299
• Extra rib arising from the seventh cervical vertebra (less than 0.5%
of the population)
• Usually of no clinical significance and discovered incidentally
• Pressure on underlying vessels and nerves can cause thoracic outlet
syndrome
Gastrointestinal Abnormalities
• Enlarged spleen – soft-tissue mass in the left upper abdomen caus-

ing medial displacement of the stomach (Fig. 23.2)
• Gallstones – characteristic opacifications in the right upper quad-
rant of the abdomen (see Fig. e23.2)
Fig. 23.2 Splenomegaly. (a) Marked medial displacement of the gastric air
shadow (arrows), consistent with enlargement of the spleen. (b) CT confirms
the presence of a huge spleen in this patient with cirrhosis
Fig. 23.3 Gastric outlet obstruction. Severe dilatation of the gas-filled stom-
ach (arrows)
• Dilated stomach (Fig. 23.3)

• Gastric pull-through following esophagectomy (Fig. 23.4)
• Pseudopolyposis in ulcerative colitis (see Fig. e23.3)
• Opaque foreign body (Fig. 23.5; see Fig. e23.4)
• Chilaiditi syndrome (Fig. 23.6)
○○ Interposition of the colon between the liver and right
hemidiaphragm
○○ Demonstration of haustra eliminates the possibility that the air
density is due to pneumoperitoneum
Pneumoperitoneum (Figs. 23.7–23.9; See Figs.

e23.5–e23.8)
• Characteristic curvilinear collection of air beneath one or both

hemidiaphragms
• Double wall (Rigler) sign on supine view, caused by peritoneal gas
outlining both the inner mucosal and outer serosal margins of the
bowel wall (the latter normally obscured by adjacent mesentery)
Pneumoperitoneum 301
Fig. 23.4 Gastric pull-through following esophagectomy (arrows)
Fig. 23.5 Foreign body. Retention of a swallowed dental crown (arrow) in a

gastric fundal diverticulum
• Supine view (no air-fluid level in the gastric fundus) can confirm
pneumoperitoneum, but not exclude it
• If there is strong clinical suspicion of free intraperitoneal gas, the
report should indicate that an upright image or CT is needed to
eliminate the possibility of pneumoperitoneum
Fig. 23.6 Chilaiditi syndrome. Interposition of colon (arrows) between the

liver and hemidiaphragm. Note the haustral markings within the dilated colon
Fig. 23.7 Pneumoperitoneum. Gas accumulating beneath the dome of the

right hemidiaphragm appears as a sickle-shaped lucency (arrow) on this erect
chest radiograph
Pneumoperitoneum 303
Fig. 23.8 Rigler sign of pneumoperitoneum. The white arrow points to the
outer wall of the stomach, which is seen because there is air both within the
stomach and outside it (a massive pneumoperitoneum). The patient suffered an
esophageal perforation during a dilation procedure. There is extensive subcuta-
neous gas in the right lower neck (black arrow) and a small medial pneumotho-
rax (gray arrow)
Fig. 23.9 Massive pneumoperitoneum (black arrows). This developed fol-

lowing insertion of a PEG tube (white arrow)
• If pneumoperitoneum is detected, it is essential to check whether

the patient has undergone recent surgery, peritoneal dialysis, or
insertion of a percutaneous endoscopic gastrostomy (PEG) tube; if
not, must worry about a perforated viscus
Injuries to the Bones of the Thorax
• Ribs (Fig. 23.10)
○○ On frontal radiographs, rib fractures are only seen when they are
displaced
Fig. 23.10 Rib fracture. (a) Displaced right rib fracture (arrow) (Courtesy of
Jim Wu, MD, Boston). (b) CT image in another patient shows a displaced left
posterior rib fracture (arrow) with a subpleural hematoma (arrowheads) [2]
Injuries to the Bones of the Thorax 305
○○ In patients from the emergency room, artifacts from a trauma

board make it even more difficult to detect a rib fracture
○○ If there is a strong clinical suspicion of rib fracture, dedicated
oblique views can be obtained
○○ Always check for an associated pneumothorax or visceral injury,
which are serious complications of rib fracture (much better
demonstrated on CT)
○○ Flail chest (Fig. 23.11; see Figs. e23.9 and e23.10)
• Three or more contiguous rib fractures that are segmental
(fractures in two or more places)
• This disrupts the normal respiratory mechanics of the chest
wall and leads to inadequate ventilation of the underlying lung
• Prompt identification of a flail chest is critical, and open reduc-
tion and internal plate fixation of the rib fractures appear to
speed the recovery process
Fig. 23.11 Flail chest. Note the associated right-sided pulmonary contusion
and subcutaneous emphysema (https://commons.wikimedia.org/wiki/File:
Pulmonary_contusion.jpg)
• Sternum and clavicle (Figs. 23.12 and 23.13; see Figs. e23.11–
e23.13)
○○ Radiographs are notoriously poor for detecting nondisplaced
sternal fractures
○○ Lateral view may demonstrate a displaced fracture
○○ If there is strong clinical suspicion for a radiographically occult
sternal fracture, CT is far more sensitive for making the diagnosis
○○ Clavicular fractures are easily demonstrated on radiographs
Fig. 23.12 Sternal fracture. (a) On the lateral radiograph, the fracture (arrow)
is very difficult to see. (b) Corresponding sagittal CT image clearly shows the
fracture (arrow). (Courtesy of Jennifer Ni Muircheartaigh, MD, Boston)
Injuries to the Bones of the Thorax 307
a b
Fig. 23.13 Clavicle fracture. (a) Frontal radiograph and (b) coned mage show
a comminuted fracture of the midshaft of the clavicle (arrow). (Courtesy of
Jeffrey Klein, MD, Burlington, VT)
○○ Acromioclavicular (AC) dislocation:

• Widening of the AC joint
○○ Normal distance is 5–8 mm
○○ Concerning if >2–4 mm asymmetry when compared to the
contralateral side
• >5 mm asymmetry of coracoclavicular distance (normal,
10–13 mm)
• Superior displacement of the clavicle (normally, the undersur-
faces of the clavicle and acromion are at the same level, though
mild clavicular elevation can be normal)
• If there is a strong clinical suspicion of AC separation, stress
views with weight-bearing can be performed
○○ The sternoclavicular articulation is difficult to assess on radio-
graphs, and CT is far more sensitive for detecting fractures and
dislocations in this region
• Thoracic spine (Fig. 23.14)

○○ Radiographic signs:
• Loss of vertebral body height (usually anterior wedge com-
pression fracture)
• Displaced paraspinal line (reflecting bleeding in the paraverte-
bral space)
• Widened interpedicular distance
• Absence of a pedicle
○○ Often fractures of multiple vertebral bodies (frequently non-
contiguous)
a b
Fig. 23.14 Spinal fracture. (a) Compression fracture of a lower dorsal verte-
bral body. (b) CT image shows loss of height of a mid-thoracic vertebral body
(arrow) with mild retropulsion. Note the vertical striations in the vertebral body
above it, characteristic of a hemangioma (of no clinical significance). (Courtesy
of Jim Wu, MD, Boston)
○○ Burst fracture – compression fracture of a vertebral body with

posteriorly displaced fragment(s) that may injure the spinal
cord
○○ CT clearly demonstrates the extent of the fracture and injury to
the spinal cord
○○ MRI is the best imaging modality for evaluating the full extent of
spinal cord and ligamentous injury
○○ If unclear whether an isolated thoracic spinal collapse represents
fracture (post-traumatic or postmenopausal) or metastatic dis-
ease, radionuclide bone imaging is the least expensive imaging
modality of choice for further work-up. Although all three condi-
tions will produce increased isotope uptake, the key is to assess
for multiple lesions, which strongly suggest metastases. If only
the one vertebral fracture shows isotope uptake, MRI can assess
the underlying marrow and determine whether the process is
benign or malignant
Miscellaneous 309
Miscellaneous
• Mastectomy – unilateral absence of a breast shadow (Fig. 23.15)

• Bullet fragments – metallic opacities (Fig. 23.16)
• Pectus excavatum – can silhouette the right hear border and mimic
a middle lobe abnormality (see Fig. e23.14)
• Sickle cell disease (see Fig. e23.15)
a b
Fig. 23.15 Mastectomy. Asymmetric loss of the breast shadow on the right
(a) and left (b). The arrows point to the normal breast shadows. (Courtesy of
Jennifer Ni Muircheartaigh, MD, Boston)
a b
Fig. 23.16 Bullet fragments. (a) Metallic opacifications overlie the lower left
chest (circle). (b) Lateral view shows that the fragments are in the posterior soft
tissues (circle)
○○ Localized steplike central depressions of multiple vertebral end

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

in multiple vertebral bodies in this patient with secondary hyperparathyroidism
related to chronic renal disease
Miscellaneous 311
Fig. 23.18 DISH. (https://commons.wikimedia.org/wiki/File:Forestier%27s_

disease,_X-ray_of_thoracic_column.jpg)
• Carotid artery calcification (See Fig. e23.20)

• Expansile rib lesion – fibrous dysplasia, myeloma
• Rotator cuff calcification – homogeneous opacification, often glob-
ular and amorphous with poor margins, adjacent to the greater
tuberosity of the humerus (see Fig. e23.21a)
• Shoulder fracture (see Fig. e23.21b)
• Hair/hair band – can produce an artifact in the upper lungs (see Fig.
e23.22)
References
3. Restropo CS, Martinez S, Lemos DF, et al. Imaging appearances of the ster-
num and sternoclavicular joints. Radiographics. 2009;29:839–59.
Index
A B
Abnormal air Bochdalek hernia, 220–221
pneumomediastinum, 291 Boerhaave syndrome, 281–282
pneumopericardium, 293–294 Bronchogenic cyst, 219–220
pneumothorax, 285–291 Bronchopleural fistula (BPF), 243–244
pulmonary interstitial emphysema,
291–293
subcutaneous emphysema, C
294–295 Carcinoid tumor, 133–135
Achalasia, 222 Cardiac edema vs. noncardiac edema, 98
Acute interstitial pneumonia Cardiothoracic ratio (CTR), 257
(AIP), 166–167 Cardiac chamber enlargement
Acute radiation pneumonitis, 197 left atrium, 259
Adult respiratory distress syndrome (ARDS), left ventricle, 257
101–103 right atrium, 259
Allergic bronchopulmonary aspergillosis right ventricle, 259
(ABPA), 180–182 Carotid artery calcification, 311
Alveolar sarcoidosis, 188 Cervical rib, 299
Amiodarone toxicity, 197 Cervicothoracic sign, 207
Amniotic fluid emboli, 110 Chest tube, 40–42
Amyloidosis, 201 Chylothorax, 91
ANCA-associated granulomatous vasculitis, Coccidioidomycosis, 124
126, 191–193 Community-acquired pneumonia (CAP), 56
Anterior junction line, 8–9 Crack lung, 182
Aorta Cryptogenic organizing pneumonia (COP),
acute aortic injury, 247–250 164–166
aneurysm, 252–253 Cystic fibrosis, 194–195
ascending thoracic, 216
descending thoracic, 225–226
coarctation, 254–255 D
dissection, 250–252 Desquamative interstitial pneumonia (DIP),
pseudoaneurysm, 254 168–169
Aorticopulmonary (AP) window, 11 Diaphragm
Apical pleural cap, 86 eventration, 273–274
ARDS, 101–103 herniation, 276
Asbestosis, 176–177 juxtaphrenic peak, 277
Automatic implantable cardiac defibrillator phrenic nerve paralysis, 274
(AICD), 38 traumatic rupture, 275–276
Azygoesophageal line and recess, Dobhoff (feeding) tube, 36–39
15–16 Drug toxicity, 195–197

https://doi.org/10.1007/978-3-030-16826-1
314 Index
E K
Emphysema Kaposi’s sarcoma, 144
alpha-1 antitrypsin deficiency, 158
bullous disease, 157–158
centrilobular, 153–154 L
congenital lobar, 158–159 Lipoma, 214–215
panlobular (panacinar), 154–155 Lobar collapse, 46–53
paraseptal, 155–157 left upper lobe, 50–51
Endotracheal (ET) tube, 25–27 lingula, 48
Enlarged spleen, 299 lower lobe, 48–50
Epicardial fat pad, 217 right middle lobe, 48
Esophagus right upper lobe, 46
achalasia, 279–281 total lung, 51–53
Boerhaave syndrome, 281–282 Loculated effusion, 89, 90
dilatation, 221–222 Lung cancer
foreign body, 282–284 adenocarcinoma, 127–130
neoplasm, 222 carcinoid tumor, 133–135
varices, 223 large cell carcinoma, 133
Expansile rib lesion, 311 metastases, 136
Extramedullary hematopoiesis, 224–225 direct spread, 141–142
hematogenous spread, 136–139
Kaposi sarcoma, 144–145
F lymphangitic spread, 139–141
Fallen lung sign, 52 lymphoma, 142–144
Fat embolism syndrome, 110, 111 pancoast (superior sulcus)
Fissural pseudotumor, 90 tumor, 135–136
Fissures, 7–8 small cell carcinoma (SCLC), 132–133
Fleischner sign, 107 squamous cell carcinoma, 130–132
Focal oligemia, 106 Lymphadenopathy, 218–219
Foregut duplication cyst, 221 Lymphangioleiomyomatosis
Foreign body emboli, 110 (LAM), 188–190
Lymphoid interstitial pneumonia (LIP),
199–200
G Lymphoma, 142, 143, 214
Galaxy sign, 187
M
H Mass impressing/displacing the lower cervical
Hamartoma, 125 trachea, 297–299
Hampton hump sign, 106 Mediastinal hemorrhage, 215
Hemorrhage, 215–216 Mediastinal lipomatosis, 226
Hemothorax, 90, 91 Mediastinal masses
Hiatal hernia, 220 anterior mediastinum, 203, 207–218
High-output failure, 264 cervicothoracic sign, 206
Hilum convergence sign, 113 diffuse mediastinum, 226–227
Hilum overlay sign, 9 middle mediastinum, 203, 218–220
Histoplasmosis, 124 posterior mediastinum, 204–205, 220–226
Hospital-acquired pneumonia Mediastinitis
(HAP), 57 acute, 226
Hypersensitivity pneumonitis, fibrosing, 226–227
177–180 Meningocele, 224
Mitral annulus calcification, 262
Morgagni hernia, 217–218
I Mosaic attenuation, 21–22
Intra-aortic balloon pump (IABP), 34 Mounier-Kuhn syndrome, 229
Index 315
Myocardial infarction complications, 262–264 empyema, 64–66

Dressler syndrome, 264 lung abscess, 63–64
pseudoaneurysm, 263 pneumatocele, 62–63
ventricular aneurysm, 262 follow-up of, 62
fungal pneumonia, 70–74
actinomycosis, 72
N aspergillosis, 70, 72
Nasogastric/orogastric tube, 35 candidiasis, 72
Neurogenic tumor, 223 coccidioidomycosis, 72
Nonspecific interstitial pneumonia histoplasmosis, 72
(NSIP), 163–164 mucormycosis, 72
pneumocystis jiroveci, 72–73
sporotrichosis, 72
O hospital-acquired pneumonia, 57
Obstructive atelectasis, 45 interstitial pneumonia, 59
lobar pneumonia, 57–58
lobular pneumonia, 58
P round pneumonia, 59–60
Pacemaker, 38 ventilator-acquired pneumonia, 57
Pancoast tumor, 135–136 viral pneumonia, 74–75
Paraspinal lines, 11–14 infectious mononucleosis, 74
Pericardial cyst, 216–217 tree-in-bud pattern, 75
Pericardial disease, 265 varicella (chickenpox) pneumonia, 74
calcification, 268–269 Pneumoperitoneum, 300
constrictive pericarditis, 268 Port-a-Cath and other tunneled catheters, 32
effusion, 265–268 Posterior junction line, 9
Peripherally inserted central catheters Posterior tracheal stripe, 14–15
(PICC lines), 28–32 Pulmonary alveolar proteinosis, 191
Pleural effusion, 52, 83, 85 Pulmonary arterial hypertension, 112–114
causes, 84 Pulmonary arteriovenous fistula
chylothorax, 91 (AVM), 125
fissural pseudotumor, 90 Pulmonary artery hypertension, 113
hemothorax, 90, 91 Pulmonary edema, 5
lateral decubitus view, 86 cardiac, 93–97
layering, 86 neurogenic, 97–101
loculated effusion, 89 Pulmonary embolism, 105–109
subpulmonic effusion, 88 Pulmonary hemorrhage, 101
supine view, 85 Pulmonary Langerhans cell histiocytosis
ultrasound, 88 (PLCH), 169–171
Pleural neoplasms Pulmonary veno-occlusive disease, 115
fibrous tumor, 150–151
mesothelioma, 147–149
metastases, 149–150 R
pleural lipoma, 151–152 Radiation-induced lung disease, 197–199
Pneumoconioses, 173 Relaxation (compressive) atelectasis, 44
Pneumonia, 56–57 Respiratory bronchiolitis-interstitial lung
aspiration, 60–62 disease (RB-ILD), 167–168
bacterial pneumonia Retrosternal stripe, 14
chronic eosinophilic Rheumatoid necrobiotic nodule, 125–126
pneumonia, 69 Rib
klebsiella, 66–67 expansile lesion, 311
Loeffler’s syndrome, 68–69 fracture, 304
septic emboli, 67 Right paravertebral stripe, 9–11
community-acquired pneumonia, 56 Rotator cuff calcification, 311
complications, 62–66 Round atelectasis, 45–46
316 Index
S thymoma, 207–210
Saddle embolus, 109 Thyroid mass, 213–214
Sarcoidosis, 183–188 Trachea and bronchi
Scleroderma, 193–194 amyloidosis, 235
Sequestration, 145–146 ANCA-associated granulomatous
Shoulder fracture, 312 vasculitis, 235
Silhouette sign, 22 bronchiectasis, 235–241
Silicosis, 174–176 broncholithiasis, 242–243
Sinus of Valsalva, 216 bronchopleural fistula, 243–244
Solitary pulmonary nodule (SPN), 117 foreign body, 244–245
age effect, 117 mucoid impaction, 241–242
air bronchogram, 123 post-intubation stenosis, 232–235
calcification, 119 radiation fibrosis, 235
cavitation, 122 relapsing polychondritis, 230–231
clinical risk factors, 118 saber-sheath trachea, 232
doubling time, 122 sarcoidosis, 235
Fleischner criteria, 124 tracheobronchomegaly, 229–230
granuloma, 124–125 tracheomalacia, 231–232
hamartoma, 125 trauma, 245
margins, 118 tuberculosis, 235
mimics, 123–124 Tracheostomy tube, 27
PET-CT, 123 Tree-in-bud pattern, 20–21
size effect, 117 Tuberculosis
Spinal neoplasm, 223–224 miliary, 80
Spine (vertebral fade-off) sign, 22–23 postprimary (reactivation/active), 78–80
Subsegmental/discoid/platelike atelectasis, primary, 75–77
43–44 Tuberculous osteomyelitis, 223
Swan-Ganz catheters, 32 Tumor emboli, 110
T U
Teratoma, 211–213 Usual interstitial pneumonia
Thorax bone injuries (UIP), 161–163
ribs, 304
soft-tissue abnormalities, 309
sternum and clavicle, 306 V
thoracic spine, 307 Ventilator-acquired pneumonia (VAP), 57
Thymus
carcinoid, 209
carcinoma, 209–210 W
cyst, 210–211 Westermark sign, 107
hyperplasia, 210

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What Radiology

Residents Need to Know:

What Radiology Residents

ISBN 978-3-030-16825-4 ISBN 978-3-030-16826-1 (eBook)

© Springer Nature Switzerland AG 2020

Each first-year rotation is a scary experience for new radiology resi-

Boston, MA, USA Ronald L. Eisenberg

Special thanks for image editing go to Michael Larson, Department of

1 Introduction �������������������������������������������������������������������������� 1

Mosaic Attenuation Pattern ���������������������������������������������� 21

Interstitial Pneumonia�������������������������������������������������������� 59

9 Pulmonary Vascular Diseases���������������������������������������������� 105

Pleural Lipoma���������������������������������������������������������������������� 151

Cystic Fibrosis���������������������������������������������������������������������� 194

Esophageal Neoplasm (Benign or Malignant)������������������ 222

Pericardial Disease���������������������������������������������������������������� 265

It is essential to develop a rigorous search pattern to ensure that you

Electronic Supplementary Material The online version of this chapter (https://

© Springer Nature Switzerland AG 2020 1

Some experienced readers prefer to first examine everything out-

Comparison with Old Studies/Reports: Better or Worse

The Value of Symmetry

All Abnormalities Can Look the Same

An important limitation of chest radiography is that most disorders

to distinguish among various diagnostic possibilities. The classic

possibilities. In the appropriate clinical setting, there also could be an

Special Areas for Focus

Apices – overlapping ribs and clavicle and cartilage calcification in

Hila – the overlapping tangle of normal arteries and veins makes it

Consider your report as a conversation between you and the referring

Fig. 1.4 Pulmonary edema. Characteristic diffuse bilateral pulmonary opaci-

• Lines composed of layers of visceral and parietal pleura that sepa-

Electronic Supplementary Material The online version of this chapter (https://

© Springer Nature Switzerland AG 2020 7

○○ Inferior accessory fissure – separates the medial basal segment

Anterior Junction Line (See Figs. e2.1 and e2.2)

(All electronic images (Figs. e2.1–e2.14) can be found on this chapter’s

• Formed by apposition of the visceral and parietal pleura of the

• Appears on up to 50% of radiographs as an oblique line crossing the

Posterior Junction Line (See Figs. e2.3 and e2.4)

• Formed by the apposition of the visceral and parietal pleura of the

Hilum Overlay Sign (Fig. 2.2; See Figs. e2.5 and e2.6)

• To distinguish true cardiomegaly from a large anterior mediastinal

Right Paratracheal Stripe (Figs. 2.3 and 2.4; See Fig. e2.7)

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

• It begins superiorly at the level of the clavicles and extends inferiorly

Fig. 2.4 Abnormal right paratracheal stripe. Paramediastinal opacification

• Widening or obliteration of the right paravertebral stripe is an indi-

 orticopulmonary (AP) Window (Figs. 2.5 and 2.6;

• Shallow concave interface between the aorta and pulmonary artery.

Paraspinal Lines (Figs. 2.7 and 2.8; See Fig. e2.9)

Fig. 2.6 Abnormal AP window (bronchogenic carcinoma). (a) In addi-

RIGHT PARASPINAL LINE

• Seen on about 25% of PA radiographs, it appears straight and typi-

LEFT PARASPINAL LINE

• Seen on about 40% of PA radiographs, it extends vertically from

Retrosternal Stripe (See Figs. e2.10 and e2.11)

Posterior Tracheal Stripe (Figs. 2.9 and 2.10; See Fig. e2.12)

• Thin vertical stripe, posterior to the trachea, which is formed by air

Fig. 2.9 (a, b) Normal posterior tracheal stripe (arrows)

• Typically measures up to 2.5 mm in thickness

Azygoesophageal Line and Recess (See Figs. e2.13 and e2.14)

• Interface formed by the right lower lobe outlining the mediastinum

Boston, MA, USA Ronald L. Eisenberg

1 Introduction �� 1

Mosaic Attenuation Pattern �� 21

Interstitial Pneumonia�� 59

9 Pulmonary Vascular Diseases�� 105

Pleural Lipoma�� 151

Cystic Fibrosis�� 194

Esophageal Neoplasm (Benign or Malignant)�� 222

Pericardial Disease�� 265

Comparison with Old Studies/Reports: Better or Worse

The Value of Symmetry

All Abnormalities Can Look the Same

Special Areas for Focus

Anterior Junction Line (See Figs. e2.1 and e2.2)

Posterior Junction Line (See Figs. e2.3 and e2.4)

Hilum Overlay Sign (Fig. 2.2; See Figs. e2.5 and e2.6)

Right Paratracheal Stripe (Figs. 2.3 and 2.4; See Fig. e2.7)

orticopulmonary (AP) Window (Figs. 2.5 and 2.6;

Paraspinal Lines (Figs. 2.7 and 2.8; See Fig. e2.9)

RIGHT PARASPINAL LINE

LEFT PARASPINAL LINE

Retrosternal Stripe (See Figs. e2.10 and e2.11)

Posterior Tracheal Stripe (Figs. 2.9 and 2.10; See Fig. e2.12)

Azygoesophageal Line and Recess (See Figs. e2.13 and e2.14)

Other Classic Patterns and Signs

Tree-in-Bud Pattern (Fig. 3.5)

Mosaic Attenuation Pattern (Fig. 3.6)

Silhouette Sign (Fig. 3.7; See Fig. e3.13)

Spine (Vertebral Fade-Off) Sign (Fig. 3.8)

Endotracheal (ET) Tube

Peripherally Inserted Central Catheters (PICC lines)

Port-a-Cath and Other Tunneled Catheters

Intra-Aortic Balloon Pump (IABP)

Dobhoff (Feeding) Tube

Relaxation (Compressive) Atelectasis

Round Atelectasis (Fig. 5.3; See Figs. e5.1 and e5.2)

Right Upper Lobe (Fig. 5.4; See Fig. e5.3)

Golden S Sign (Fig. 5.5)